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THE 


PRACTICE  OF  MEDICINE 


A  GUIDE  TO  THE  NATURE,  DISCRIMINATION 
AND   MANAGEMENT  OF  DISEASE 


BY 

A.  O.  J.  KELLY,  A.M.,  M.D. 

ASSISTANT      PROFESSOR      OP      MEDICINE      IN      THE      UNIVERSITY     OF     PENNSYLVANIA    AND    ASSISTANT 

PHYSICIAN    TO    THE    UNIVERSITY     HOSPITAL,    PHILADELPHIA;    PROFESSOR     OF    THE    THEORY    AND 

PRACTICE  OF    MEDICINE    IN    THE    UNIVERSITY  OF  VERMONT;    PROFESSOR    OF    PATHOLOGY    IN 

THE     woman's     medical     COLLEGE     OF     PENNSYLVANIA  ;     PHYSICIAN     TO     ST.     AGNEs' 

HOSPITAL,    PHILADELPHIA;    CHIEF    OF    THE    PATHOLOGICAL    DEPARTMENT  OF  THE 

GERMAN     HOSPITAL,    PHILADELPHIA;    MEMBER    OF     THE    ASSOCIATION    OF 

AMERICAN    PHYSICIANS     AND    OP     THE     INTERURBAN     CLINICAL 

club;    EDITOR    OP    THE    AMERICAN    JOURNAL    OP 

THE    MEDICAL     SCIENCES. 


ILLUSTRATED 


LEA  &  FEBIGEK 
PHILADELPHIA   AND  NEW  YORK 


Entered  according  to  Act  of  Congress,  in  the  year   1910,  by 

LEA  &  FEBIGER, 
in  the  Office  of  the  Librarian  of  Congress.     All  rights  reserved. 


O 

O 


C^X 


TO  MY  WIFE 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/practiceofmediciOOkell 


PREFACE. 


The  following  pages  represent  an  effort  to  prepare  for  the  student 
and  the  junior  practitioner  of  medicine  a  guide  to  the  nature,  discrim- 
ination, and  management  of  disease  that  should  contain  the  essentials 
unadorned  with  great  detail.  Since  the  determination  of  what  is  really 
essential  must  be  a  matter  of  individual  judgment,  the  greatest  problem 
encountered  was  what  to  exclude,  so  that  the  book,  without  exceeding 
a  convenient  limit,  should  be  comprehensive,  properly  balanced,  and 
in  good  perspective.  An  acquaintance  with  the  present  development 
and  the  trend  of  medical  education,  and  a  teacher's  appreciation  of  the 
needs  of  students,  make  one  realize  the  embarrassment  of  riches,  the 
large  number  of  facts,  too  often  placed  before  minds  not  yet  qualified 
to  sort  them  in  their  order  of  importance  and  grasp  their  mutual  bear- 
ings. This  defect  of  medical  pedagogy  violates  the  physiology  of  the 
mind,  which  is  so  constituted  that  the  natural  stimulus  to  interest,  and 
therefore  to  recollection,  is  the  tracing  of  rational  connection.  The 
resulting  mental  indigestion  and  lethargy  appear  at  examination  time 
and  when  the  student  or  junior  practitioner  is  confronted  with  the 
necessity  of  applying  at  the  bedside  principles  ill  understood.  A  book, 
of  course,  cannot  replace  actual  clinical  experience,  but  it  should  in 
fairness  offer  its  readers  a  well-ordered  statement  of  existing  knowledge 
as  a  basis  for  training  their  powers  of  observation  and  reasoning,  espe- 
cially in  conformity  with  opportunities  presented  at  the  bedside. 

These  considerations  determined  me  to  devote  most  space  and  atten- 
tion to  the  practical  aspects  of  medicine;  to  the  elucidation  of  those 
principles  exemplified  in  disease  at  the  bedside,  in  hospital  wards  and 
clinics,  and  in  the  consulting  room;  and  to  the  clinically  important  and 
more  common  disorders  rather  than  to  the  rarer  diseases,  however 
interesting.  Such  a  plan  seemed  to  offer  more  of  value  to  students  in 
recitations  and  in  hospital-ward  and  dispensary  work,  and  to  practi- 
tioners desiring  to  recall  elusive  facts.  A  systematic  arrangement  of 
the  subject  matter  has  been  adopted  to  facilitate  comprehension  of  the 
mutual  relations  of  different  clinical  and  pathological  entities.  P^mpha- 
sis  has  been  laid  upon  the  definition  of  processes  of  disease — to  impress 
upon  the  student  the  necessity  of  accuracy  in  his  use  of  terms  and  in 
his  clinical  descriptions.  Inasmuch  as  the  final  object  of  medicine  is 
practice,  most  space  has  been  devoted  to  symptomatology,  diagnosis, 
and  treatment;  and  to  ensure  a  rational  grasp  of  these  main  objectives, 
they  are  presented   in  their  natural  relationship  by  means  of  brief 


vi  PREFACE 

connecting  sections  on  etiological  factors,  essential  anatomical  lesions, 
and  pathological  physiology.  The  sections  on  pathological  physiology 
might  have  been  considerably  expanded;  but  I  venture  to  hope  that, 
although  limited  to  a  statement  of  the  main  facts,  they  may  prove 
serviceable  to  students  in  affording  them  a  broad  view  of  disease  and 
of  disturbed  functions  in  general.  Throughout  the  book  an  endeavor 
has  been  made  to  portray  the  nature  and  natural  history  of  disease, 
to  correlate  disturbed  or  perverted  function  with  altered  structure,  to 
explain  the  development  of  symptoms,  and  to  elucidate  the  sequence 
of  cause  and  effect.  Such  knowledge  is  essential  to  a  correct  and 
intelligent  comprehension  and  interpretation  of  morbid  phenomena 
(symptomatology  and  diagnosis),  to  the  ability  to  forecast  and  provide 
against  contingencies,  to  judgment  of  the  course,  duration,  and  termina- 
tion of  disease  (prognosis),  and  to  skill  in  rational  treatment  and  pro- 
phylaxis. Under  the  individual  diseases,  I  have,  as  a  rule,  emphasized 
at  least  one  method  of  treatment  that  I  know  to  be  of  value  from  my 
own  experience;  beyond  this  point,  however,  I  have  depended  upon 
the  recommendations  of  acknowledged  competent  authorities.  A 
few  formulse  have  been  included  as  an  aid  to  the  junior  practitioner; 
these  with  the  other  instructions  mentioned  should  serve  him  in  times 
of  stress  until  his  experience  and  judgment  warrant  his  making  his 
own  modifications.  Intentional  limitation  of  space  and  the  primarily 
clinical  purpose  of  the  book  have  made  it  seem  desirable  to  omit 
discussions  of  the  biological  characteristics  of  the  infectious  micro- 
organisms and  of  the  technique  of  laboratory  methods  of  diagnosis. 

A  book  on  such  a  boundless  subject  as  Medicine  must  be  evolved 
out  of  the  collective  experience  of  the  masters  of  all  times  and  all  parts 
of  the  world,  tinctured  by  the  study,  investigation,  judgment,  and 
experience  of  the  author.  Although  this  book,  in  large  part,  is  based 
upon  my  own  clinical  and  pathological  experience,  I  must  acknowledge 
my  indebtedness  to  the  many  writers  of  many  tongues  whose  contribu- 
tions to  medicine  form  the  basis  of  my  own  knowledge.  My  experience 
with  those  disorders  known  as  tropical  has  been  almost  limited  to  the 
rather  few  imported  cases  that  an  active  hospital  physician  encounters 
in  a  large  seaport.  I  have,  nevertheless,  included  a  brief  account  of 
these  diseases,  because  of  the  widespread  interest  recently  shown  in 
their  investigation,  and  on  account  of  the  increasing  number  of  stu- 
dents who  purpose  practising  in  our  tropical  possessions;  the  clinical 
descriptions,  however,  are  largely  a  reflection  of  those  of  such  highly 
esteemed  authorities  as  Manson,  Cantlie,  Jackson,  and  others.  The 
descriptions  of  the  metazoan  parasites  have  been  taken,  in  many 
instances  verbatim,  from  Stiles  —  the  recognized  authority  in  this 
country.  Elsewhere  the  attentive  reader  will  note  my  indebtedness 
to  other  authors — to  all  of  whom,  I  hope,  I  have  given  due  credit. 

A.  O.  J.  K. 

Philadelphia,  1910. 


CONTENTS 


SECTION  I 

INFECTIOUS  DISEASES 

General  Observations  and  Pathological  Physiology    ........  17 

BACTERIAL  INFECTIONS 

Typhoid  Fever 32 

Paratyphoid  Fever 60 

Pyogenic  Infections 61 

Erysipelas 67 

Pneumococcic  Infections 70 

Pneumococcic  Infection  of  the  Lung;  Pneumonia        .            71 

Meningococcic  Infection;  Cerebrospinal  Fever 86 

Gonococcic  Infection 90 

Tuberculosis 92 

Acute  Miliary  Tuberculosis 96 

Tuberculosis  of  the  Lymphatic  System 100 

Tuberculosis  of  the  Circulatory  System 106 

Tuberculosis  of  the  Respiratory  System 106 

Tuberculosis  of  the  Digestive  System 117 

Tuberculosis  of  the  Genito-urinary  System 120 

Tuberculosis  of  the  Nervous  System 122 

Tuberculosis  of  the  Bones  and  Joints 124 

Diphtheria 131 

Influenza 143 

Bacillary  Dysentery 145 

Tetanus 149 

Cholera 153 

Plague 156 

Glanders 159 

Anthrax 161 

Malta  Fever 164 

Leprosy '. 166 

NON-BACTERIAL  FUNGUS  INFECTIONS 

Actinomycosis 169 

Mycetoma 170 

Nocardiosis 171 

Pulmonary  Aspergillosis ' 171 

Oidiomycosis 172 

ZOOPARASITIC  INFECTIONS 

Protozoan  Infections 

Amoebiasis 175 

Relapsing  Fever 178 

Syphihs 180 


vm  CONTENTS 

Yaws 193 

Trypanosomiasis ■ 194 

Kala-azar 195 

Oriental  Sore 196 

Malarial  Infections 197 

Metazoan  Infections 

Distomatosis      .    ' 211 

Pulmonary  Distomatosis 211 

Hepatic  Distomatosis -.  211 

Intestinal  Distomatosis 212 

Venal  Distomatosis 213 

Teniasis 214 

Intestinal  Teniasis ;  Tapeworm  Infection 214 

Somatic  Teniasis 217 

Nemathelminthiasis 218 

Uncinariasis 218 

Strongyloidosis 219 

Ascariasis 219 

Oxyuriasis 220 

Trichocephaliasis 221 

Acanthocephaliasis 221 

Trichinosis _ 221 

Dracunculosis 223 

Filariasis 223 

Acariasis 224 

Ixodiasis 224 

Sarcoptic  Acariasis 224 

Parasitic  Insects 225 

Phthiriasis;  Pediculosis 225 

Fleas 225 

Bed-bugs    .      .      .      .  \ 225 

Myiasis 226 


INFECTIONS  OF  UNKNOWN  OR  DOUBTFUL  ETIOLOGY 

Variola 226 

Vaccinia 233 

Varicella 235 

Typhus  Fever 237 

Scarlet  Fever 240 

Measles 247 

Rotheln 250 

Glandular  Fever 252 

Rheumatic  Fever 253 

Pertussis 257 

Infectious  Parotitis 260 

Yellow  Fever 261 

Dengue 265 

Hydrophobia 266 

Rocky  Mountain  Spotted  Fever 269 

Epidemic  Poliomyelitis 270 

Acute  Infectious  Jaundice     . 272 

Foot-and-Mouth  Disease 273 

MiUary  Fever 274 

Milk  Sickness 274 

Beriberi 275 

Epidemic  Dropsy 277 

Nasha  Fever 278 

Japanese  River  Fever 278 

Ponos 279 


CONTENTS  IX 

Hill  Diarrhoea 280 

Sprue • 281 

Epidemic  Gangrenous  Proctitis 281 

Tropical  Phagedena 282 

Tropical  Bubo 283 

Ulcerating  Granuloma  of  the  Genitals 283 

Verruga 284 

Kubisagari 285 

Gangosa 286 

Ainhum 287 

Goundou 287 

Psittacosis ' 287 


SECTION   II 

INTOXICATIONS 

Alcoholism 289 

Opium  Habit 292 

Cocaine  Habit 293 

Lead  Poisoning 294 

Arsenical  Poisoning 296 

Mercurial  Poisoning 297 

Snake-venom  Poisoning     .      .' 298 

Food  Poisoning 299 


SECTION  III 
DISORDERS  OF  METABOLISM 

Pathological  Physiology 303 

Auto-intoxications 303 

Diabetes 305 

Diabetes  Insipidus 318 

Gout 320 

Obesity , 327 

Rickets 329 

Scurvy 331 

Amyloidosis       .      ^ .* 334 

Infantihsm •.      .      .  335 


SECTION  IV 

DISEASES  OF  THE  DUCTLESS  GLANDS  AND  OF 
INTERNAL  SECRETION 

Pathological  Physiology 337 


CONTENTS 


DISEASES  OF  THE  THYROID  GLAND 

Pathological  Physiology 339 

Acute  Thyroiditis 340 

Goitre 340 

Hyperthyroidism  and  Exophthalmic  Goitre 342 

Hypothyroidism;  Cretinism;  Myxcedema .      .  346 

Tumors  and  Cysts  of  the  Thyroid 349 

DISEASES  OF  THE  PARATHYROID  GLANDS 

Pathological  Physiology         349 

Tetany 350 

DISEASES  OF  THE  ADRENALS  AND  THE  CHROMAFFIN  SYSTEM 

Pathological  Physiology 351 

Addison's  Disease 353 

DISEASES  OF  THE  PITUITARY  BODY 

Pathological  Physiology 355 

Akromegaly 356 


SECTION  V 
DISEASES  OF  THE  BLOOD  AND   HEMOPOIETIC  SYSTEM 

Pathological  Physiology        .      ; 359 

Acute  Secondary  Anemia 365 

Chronic  Secondary  Anemia     . 367 

Chlorosis 369 

Pernicious  Anemia 373 

Leukemia ....  378 

Erythremia 385 

THE  HEMORRHAGIC  DISEASES 

Hemorrhage  in  the  Newborn 387 

Purpura 387 

Hemophilia , 390 

DISEASES  OF  THE  LYMPH  NODES  AND  LYMPH  VESSELS 

Pathological  Physiology 393 

Lymphangitis  and  Lymphadenitis 393 

Lymphangiectasis 395 

Tumors  and  Tumor-like  Formations 397 

Hodgkin's  Disease 398 

Diseases  of  the  Thoracic  Duct 401 

DISEASES  OF  THE  THYMUS  BODY 

Pathological  Physiology 402 

Enlargement  of  the  Thymus •  403 


CONTENTS  XI 


DISEASES  OF  THE  SPLEEN 


Pathological  Physiology 405 

Anomalies  of  Form  and  Position  of  the  Spleen 406 

Rupture  of  the  Spleen 406 

Thrombosis,  EmboHsm,  and  Abscess  of  the  Spleen 406 

Enlargement  of  the  Spleen 407 

Splenomegaly;  Splenic  Anemia 407 

Tumors  and  Cysts  of  the  Spleen 410 


SECTION  VI 
DISEASES  OF  THE  CIRCULATORY  SYSTEM 

Pathological  Physiology         411 

NEUROMUSCULAR  DISORDERS  OF  THE  HEART 

Cardiac  Pain 415 

Palpitation  of  the  Heart , 416 

Arrhythmia 416 

Tachycardia 421 

Bradycardia 422 

DISEASES  OF  THE  MYOCARDIUM 

The  Weak  or  Insufficient  Heart 424 

The  Overstrained  or  Irritable  Heart 427 

The  Fatty  Heart 430 

The  Infectious  Febrile  Heart        .            431 

The  Fibroid  Heart 434 

Hypertrophy  and  Dilatation  of  the  Heart 437 

Aneurysm  of  the  Heart 443 

Rupture  of  the  Heart 444 

Tumors  and  Parasites  of  the  Heart 444 

Disease  of  the  Coronary  Arteries 444 

DISEASES  OF  THE  ENDOCARDIUM 

Acute  Endocarditis 445 

Chronic  Endocarditis 450 

Chronic  Valvular  ©isease  of  the  Heart 452 

Mitral  Insufficiency 455 

Mitral  Stenosis 459 

Aortic  Insufficiency 462 

Aortic  Stenosis 466 

Tricuspid  Insufficiency    . , 468 

Tricuspid  Stenosis 469 

Pulmonary  Insufficiency 470 

Pulmonary  Stenosis 470 

Combined  Valvular  Lesions 471 

DISEASES  OF  THE  PERICARDIUM 

Pericarditis 478 

Fibrinous  Pericarditis 478 


xii  CONTENTS 

Serofibrinous  Pericarditis 480 

Purulent  Pericarditis 483 

Chronic  Pericarditis 484 

Hydropericardium 487 

Hemopericardium 487 

Pneumopericardium;  Pyopneumopericardium 488 

Chylopericardium 488 

DISEASES  OF  THE  ARTERIES 

Acute  Aortitis 489 

Arteriosclerosis 489 

Angina  Pectoris 493 

Aneurysm 497 


SECTION  VII 

DISEASES  OF  THE  RESPIRATORY  SYSTEM 

Pathological  Physiology 505 

DISEASES  OF  THE  NOSE 

Epistaxis 511 

Acute  Rhinitis 512 

Chronic  Rhinitis 514 

Hay  Fgver 515 

DISEASES  OF  THE  LARYNX 

Acute  Catarrhal  Laryngitis 517 

QCdemat  ovis  Laryngitis 519 

Spasmodic  L  aryngitis 520 

Chronic  Laryngitis 521 

Laryngeal  Perichondritis 522 

Tumors  of  the  Larynx 523 

DISEASES  OF  THE  TRACHEA  AND  BRONCHI 

Acute  Bronchitis 524 

Chronic  Bronchitis 527 

Fibrinous  Bronchitis 530 

Bronchiectasis 532 

Bronchial  Asthma 534 

Tracheal  and  Bronchial  Obstruction 537 

DISEASES  OF  THE  LUNGS 

Hemoptysis 539 

Congestion  of  the  Lungs 541 

CEdema  of  the  Lungs 543 

Pulmonary  Embolism  and  Thrombosis 545 

Atelectasis  and  Collapse  of  the  Lung 547 

Bronchopneumonia 549 

Chronic  Interstitial  Pneumonitis 552 

Pneumonokoniosis ■      •  554 

Emphysema •  555 


CONTENTS  xiii 

Abscess  of  the  Lung 559 

Gangrene  of  the  Lung 561 

Tumors  of  the  Lung 562 

DISEASES  OF  THE  PLEURA 

Pleuritis 564 

Fibrinous  Pleuritis 564 

Serofibrinous  Pleuritis 566 

Purulent  Pleuritis 574 

Hemorrhagic  Pleuritis 576 

Chronic  Pleuritis 577 

Hydrothorax 579 

Pneumothorax 580 

Chylothorax 583 

Tumors  of  the  Pleura 584 

DISEASES  OF  THE  MEDIASTINUM 

Mediastinitis 584 

Tumors  of.the  Mediastinum 585 


SECTION  VIII 

DISEASES  OF  THE  DIGESTIVE  SYSTEM 

DISEASES  OF  THE  MOUTH 

Stomatitis 587 

Gangrene  of  the  Cheek;  Noma 593 

DISEASES  OF  THE  TONGUE 

Glossitis 594 

Eczema 595 

Leukoplakia 595 

Black  Tongue 595 

Macroglossia 596 

Acute  Oedema 596 

Ranula 596 

'  DISEASES  OF  THE  SALIA'ARY  GLANDS 

Ptyalism 596 

Xerostomia 596 

Parotitis 596 

Gaseous  Distention 597 

Calculi 597 

Ludwig's  Angina 597 

DISEASES  OF  THE  FAUCES,  TONSILS,  AND  PHARYNX 

Acute  TonsilHtis 598 

Chronic  TonsilHtis 601 

Pharyngitis 603 

Ulceration  of  the  Pharynx 603 

Acute  Infectious  Phlegmon  of  the  Ph&rynx;      , 604 


xiv  CONTENTS 

Retropharyngeal  Abscess 604 

Elongation  of  the  Uvula   . 604 

The  Lingual  Tonsils 604 

DISEASES  OF  THE  (ESOPHAGUS 

Acute  (Esophagitis 605 

Chronic  (Esophagitis 605 

Ulceration 605 

Varices 606 

Rupture 606 

Dilatation 606 

Diverticula 606 

Spasm 606 

Paralysis 607 

Stenosis 607 

Carcinoma 607 

DISEASES  OF  THE  STOMACH 

Pathological  Physiology 608 

Symptomatic  Disorders  of  the  Stomach 610 

The  Appetite 610 

Thirst 611 

Nausea  and  Vomiting 612 

Hematemesis 613 

-^otor  Disorders 614 

Sensory  Disorders 616 

Secretory  Disorders 618 

Nervous  Dyspepsia 621 

Acute  Catarrhal  Gastritis 622 

Phlegmonous  Gastritis 624 

Toxic  Gastritis 624 

Infectious  Gastritis 625 

Chronic  Gastritis 626 

Acute  Dilatation  of  the  Stomach 629 

Chronic  Dilatation  of  the  Stomach 630 

Ulcer  of  the  Stomach  and  Duodenum 632 

Carcinoma  of  Stomach 638 

Non-carcinomatous  Tumors 643 

Hypertrophic  Stenosis  of  the  Pylorus 643 

DISEASES  OF  THE  INTESTINE 

Pathological  Physiology 643 

Symptomatic  Disorders  of  the  Intestine 646 

Motor  Disorders 647 

Sensory  Disorders 649 

Secretory  Disorders 650 

Intestinal  Indigestion 650 

Intestinal  Hemorrhage 652 

Mucous  Cohc     . 654 

Constipation 655 

Acute  Enteritis ' 657 

Chronic  Enteritis 659 

Diarrhoeal  Disorders  of  Children 661 

Croupous  or  Diphtheritic  Enteritis 667 

Phlegmonous  Enteritis 667 

Appendicitis 668 

Sigmoid  Diverticuhtis .  672 

Ulceration  of  the  Intestine 673 

Intestinal  Obstruction       , .      .      .      .      ,      .  674 


CONTENTS  XV 

Dilatation  of  the  Colon 682 

Infarction  of  the  Mesenteric  Vessels 682 

Intestinal  Sand 683 

Hemorrhoids 683 

Visceroptosis 685 


DISEASES  OF  THE  LIVER 

Pathological  Physiology 687 

Jaundice 689 

Anomalies  of  Form  and  Position  of  the  Liver 695 

Diseases  of  the  Bloodvessels  of  the  Liver 696 

Fatty  Liver 697 

Acute  Yellow  Atrophy  of  the  Liver 698 

Active  Congestion  of  the  Liver 702 

Passive  Congestion  of  the  Liver 703 

Perihepatitis 704 

Acute  Perihepatitis .      .      ...  704 

Local  Chronic  Perihepatitis 705 

General  Chronic  Perihepatitis 705 

Acute  Hepatitis 705 

Acute  Non-suppurative  Hepatitis 705 

Suppurative  Hepatitis 707 

Chronic  Interstitial  Hepatitis:  the  Cirrhoses  of  the  Liver 709 

Portal  Cirrhosis 710 

Biliary  Cirrhosis 717 

Tumors  of  the  Liver 719 


DISEASES  OF  THE  GALL-BLADDER  AND  BILIARY  DUCTS 

Congenital  Obliteration  of  the  Biliary  Ducts 721 

Acute  Catarrhal  Cholangitis 722 

Suppurative  Cholangitis .  724 

Chronic  Catarrhal  Cholangitis 725 

Acute  Cholecystitis ....  726 

Chronic  Cholecystitis 728 

Cholelithiasis 728 

Carcinoma  of  the  Gall-bladder  and  Biliary  Ducts 736 


DISEASES  OF  THE  PANCREAS 

Pathological  Physiology 737 

Hemorrhages  into  the  Pancreas 737 

Acute  Pancreatitis 738 

Chronic  Pancreatitis 741 

Cysts  of  the  Pancreas 743 

Tumors  of  the  Pancreas 744 

Pancreatic  Calculi 745 


DISEASES  OF  THE  PERITONEUM 

Ascites 746 

Acute  Peritonitis 748 

Chronic  Peritonitis 749 

Multiple  Serositis 750 


XYl  CONTENTS 

SECTION  IX 

DISEASES  OF  THE  URINARY  SYSTEM 

Pathological  Physiology 755 

Anuria 763 

Albuminuria 764 

Albumosuria 767 

Cylindruria 768 

Hematuria 769 

PjTiria 769 

AnomaUes  of  Form  and  Position  of  the  Ividneys 770 

Circulatory  Disturbances  of  the  Ividneys 770 

Nephritis 772 

Active  Diffuse  Xephritis 773 

Acute  Suppurative  Nephritis 779 

Chronic  Diffuse  Non-indurative  Nephritis 780 

Chronic  Diffuse  Indurative  Nephritis 783 

Cj'stitis;  Ureteritis;  Pj'ehtis;  Pyelonephritis;  Pyelonephrosis 788 

Perinephritis  and  Paranephritis 792 

Hydronephrosis 793 

Nephrolithiasis        .      .      .      .    / 794 

CYsts  of  the  Kidney 797 

Tumors  of  the  Kidnev 798 

Tumors  of  the  Bladder 799 


SECTION  X 
DISEASES  OF  THE  NERVOUS  SYSTEM 

Pathological  Phj'siology 801 

DISEASES  OF  THE  NERVES 

Neuralgia 808 

Neuritis 811 

Herpes  Zoster 813 

Neuromas 814 

Diseases  of  the  Cranial  Nerves 814 

Olfactorj'  Nerve 814 

Optic  Nerve 815 

Oculomotor  Nerve 816 

Trochlear  Nerve 816 

Abducens  Nerve 816 

Trigeminal  Nerve 817 

Facial  Nerve 817 

Auditor}'  Nerve 819 

Glossophars-ngeal  Nerve 819 

Pneumogastric  or  Vagus  Nerve 819 

Spinal  Accessor}'  Nerve         820 

Hypoglossal  Nerve 820 

Diseases  of  the  Spinal  Nerves 821 

C'er\'ical  Plexus  821 

Brachial  Plexus 821 

Lumbar  Plexus 824 

Sacral  Plexus         824 

Diseases  of  the  Cervical  Sympathetic  Nerves 82^ 


CONTENTS  xvii 


DISEASES  OF  THE  CEREBROSPINAL  MENINGES 

Meningeal  Hemorrhage 825 

External  Pachymeningitis 826 

Internal  Pachymeningitis 827 

Leptomeningitis 828 

DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

Cerebrospinal  Localization 831 

Aphasia , 840 

SYSTEM  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

Diseases  of  the  Upper  (Central)  Motor  Neuron 

Lateral  Sclerosis 845 

Spastic  Paralysis  of  Infants 846 

Hereditary  Spastic  Spinal  Paralysis 847 

Amaurotic  Family  Idiocy 847 

Unilateral  Ascending  and  Unilateral  Descending  Paralysis 848 

Diseases  op  the  Lower  (Peripheral)  Motor  Neuron 

Chronic  Anterior  Poliomyelitis 848 

Progressive  Neural  Muscular  Atrophy .  849 

Bulbar  Paralysis 850 

Ophthalmoplegia 851 

Disease  of  the  Upper  (Central)  and  the  Lower  (Peripheral) 

Motor  Neurons 

Amyotrophic  Lateral  Sclerosis 852 


Diseases  of  the  Sensory  Neuron 

Tabes  DorsaUs 853 

Interstitial  Hypertrophic  Progressive  Neuritis  of  Childhood 856 

Combined  System  Diseases 

Hereditary  or  Family  Ataxia 857 

Hereditary  or  Family  Cerebellar  Ataxia 857 

Ataxic  Paraplegia 858 

Toxic  Combined  Sclerosis 858 


NON-SYSTEM  DISEASE  OF  THE  BRAIN  AND  SPINAL  CORD 

Multiple  Sclerosis 859 

DIFFUSE  AND  FOCAL  DISEASES  OF  THE  BRAIN 

Hyperemia  of  the  Brain 861 

Anemia  of  the  Brain 861 

CEdema  of  the  Brain 862 


xviii  CONTENTS 

Cerebral  Hemorrhage 862 

Cerebral  Thrombosis 868 

Cerebral  Embolism 869 

Thrombosis  of  the  Cerebral  Sinuses 870 

Acute  Hemorrhagic  Encephalitis 871 

Abscess  of  the  Brain 871 

Tumors  of  the  Brain 873 

Hydrocephalus 875 


DIFFUSE  AND  FOCAL  DISEASES  OF  THE  SPINAL  CORD 

Vascular  Disorders  of  the  Spinal  Cord 876 

Hemorrhage  into  the  Spinal  Cord 876 

Caisson  Disease 878 

MyeUtis 879 

Compression  of  the  Spinal  Cord 882 

Tumors  of  the  Spinal  Cord 883 

SyringomyeUa 884 


.     NERVOUS  DISEASES  OF  FUNCTIONAL  OR  UNKNOWN  NATURE 

Migraine 886 

Epilepsy 888 

Hysteria 892 

Neurasthenia  and  Psychasthenia 895 

Occupation  Neuroses 897 

Paralysis  Agitans 898 

Acute  Chorea 900 

Hereditary  Chorea 902 

Convulsive  Tics 903 

Choreiform  Disorders 904 

Family  Periodical  Paralysis 904 

Heatstroke 905 


VASOMOTOR  AND  TROPHIC  DISORDERS 

Angioneurotic  (Edema 907 

Erythromelalgia 907 

Acroparesthesia 908 

Raynaud's  Disease 908 


SECTION  XI 
DISEASES  OF  THE  MUSCLES 

Muscular  Rheumatism 911 

Myositis 912 

Progressive  Muscular  Dystrophy 912 

Myoclonus 914 

Congenital  Myotonia 915 

Congenital  Amyotonia 916 


CONTENTS  xix 

SECTION  XII 
DISEASES  OF  THE  BONES  AND  JOINTS 

Acute  Arthritis 917 

Chronic  Atrophic  Arthritis 918 

Chronic  Hypertrophic  Osteo-arthritis 920 

Osteomalacia 921 

Osteitis  Deformans 922 

Hypertrophic  Pulmonary  Osteo-arthropathy 923 

Osteogenesis  Imperfecta 923 

Achondroplasia       .      .      .    • 923 

Facial  Hemiatrophy 923 

Leontiasis  Ossea 924 


THE  PRACTICE  OF  MEDICINE. 


SECTION   I. 
INFECTIOUS  DISEASES. 


The  infectious  diseases  comprise  a  series  of  disorders  that  result 
from  the  growth  within  the  hving  body  of  divers  pathogenic  vegetable 
and  animal  parasites.  These,  the  so-called  infectious  agents  (coiitagium 
vivum),  include  certain  bacteria,  certain  non-bacterial  fungi,  and  certain 
zooparasites  (protozoa,  worms,  and  arthropods).  In  consequence, 
one  may  divide  the  known  infectious  diseases  into  three  classes:  (1) 
The  bacterial  infections;  (2)  the  non-bacterial  fungus  infections;  and 
(3)  the  zooparasitic  infections;  but  to  these  one  must  at  present  add 
a  fourth  class,  that  of  infections  of  unknown  or  doubtful  etiology— 
which  comprise  diseases  undoubtedly  infectious  that  have  not  yet 
yielded  up  to  scientific  inquiry  their  specific  etiological  factors.  Perhaps 
the  causative  agents  of  many  of  these,  as  has  been  demonstrated  of  some 
of  them  (yellow  fever,  hydrophobia,  epidemic  poliomyelitis,  pleuro- 
pneumonia of  cattle,  foot-and-mouth  disease,  etc.),  are  certain  ultra- 
microscopic  parasites,  microorganisms  that  pass  through  a  fine  porous 
filter  impervious  to  ordinary  bacteria,  but  elude  detection  by  the  highest 
powers  of  the  microscope.  Additional  reasons,  however,  for  the  non- 
discovery  of  these  organisms  are  that  they  may  be  difficult  to  stain, 
difficult  or  impossible  to  cultivate  in  artificial  media  outside  the  body, 
and  present  in  small  numbers  in  the  diseases  they  provoke. 

Infectious  and  Contagious  Diseases. — In  times  past  the  diseases  now 
recognized  as  infectious  were  divided  into  two  classes — the  miasmatic 
and  the  contagious.  The  miasmatic  diseases  were  those  surmised  to 
be  due  to  some  cause,  a  miasm,  arising  without  the  body  and  capable 
of  provoking  disease  without  the  intervention  of  another  individual 
thus  affected;  the  contagious  diseases  were  those  caused  by  some 
factor,  a  contagion,  developed  within  the  diseased  body  and  capable 
of  transmitting  the  disease  to  another  individual  (man  or  animal),  either 
directly  or  indirectly  (through  the  medium  of  a  third  person  or  an 


18  INFECTIOUS  DISEASES 

object,  or  the  air).  Since  a  miasm  has  become  a  myth  of  the  past,  <he 
miasmatic  diseases  have  completely  disappeared;  but  the  terms  con- 
tagious and  infectious  still  obtain.  Perhaps  a  satisfactory  distinction 
may  be  drawn  between  them:  The  term  infectious  diseases  is  the 
broader,  and  includes  the  contagious  diseases.  The  term  contagious 
was  and  still  may  be  used  to  designate  diseases  readily  transmissible 
from  the  sick  to  the  well  by  direct  or  indirect  contact;  diseases  which 
seem  to  be  transmitted  through  the  medium  of  the  air  and  in  which 
(as  in  smallpox,  measles,  scarlatina,  etc.)  a  zone  of  "contagious  atmos- 
phere" seems  to  surround  the  patient;  and  diseases  of  which  the  causal 
infectious  agent,  or  contagium  vivum,  seems  to  be  ill-adapted  to  lead 
a  prolonged  existence  outside  the  living  body.  This  distinction,  which 
is  based  upon  the  ability  or  lack  of  ability  of  the  infectious  agent  to 
lead  respectively  a  parasitic  or  a  saprophytic  existence,  is  largely  artificial, 
since  borderland  cases  occur  and  diseases  ordinarily  not  contagious 
in  the  aforementioned  sense  may  become  so  (pneumonia,  typhoid 
fever,  etc.).  The  distinction,  however,  has  a  practical  bearing,  in  that 
the  diseases  thus  called  contagious  may  be  effectually  controlled  by 
isolation  of  the  patient  and  strict  hygienic  precautions,  whereas  those 
that  may  be  called  the  non-contagious  infectious  diseases  are  not  thus 
so  readily  controlled;  but  in  this  respect  also  borderland  cases  occur 
(some  cases  of  typhoid  fever,  pertussis,  measles,  scarlatina,  etc.).  The 
terms  transmissible  and  non-transmissible  and  communicable  and  non- 
communicable  have  been  proposed  to  surmount  the  supposed  difficulty 
— which  also  is  largely  artificial;  the  term  infectious  diseases  is  a  satis- 
factory and  all-inclusive  term. 

Transmission  of  the  Infectious  Diseases. — The  records  of  antiquity, 
as  well  as  of  more  modern  times,  definitely  prove  that  many  of  the 
infectious  diseases,  notably  plague,  cholera,  dysentery,  typhoid  fever, 
yellow  fever,  Malta  fever,  malaria,  influenza,  and  many  so-called 
tropical  disorders,  have  a  permanent  habitat,  are  endemic,  in  certain 
parts  of  the  world.  Some  of  these  diseases  are  seldom  or  never  en- 
countered beyond  the  confines  of  their  permanent  habitat;  others, 
from  time  to  time,  under  various  influences,  spread  from  these  endemic 
centres  to  more  or  less  distant  regions,  or  they  increase  in  number  and 
perhaps  virulence  in  regions  where  they  prevail  continuously — the 
disease  becomes  epidemic.  The  epidemic  may  be  local,  as  in  familial, 
house,  school,  barracks,  jail,  and  town  epidemics,  or  it  may  be  widespread, 
extending  throughout  several  adjoining  States  or  countries;  the  disease 
even  may  become  pandemic,  as  has  frequently  happened  in  connection 
with  plague,  cholera,  influenza,  etc.,  originating  in  the  Orient. 

The  infection  may  be  spread  by  aerial  convection,  by  contamination 
of  the  water  supply,  by  infected  persons,  by  a  third  person,  by  fomites 
(caravans,  cargoes,  baggage,  rags,  money,  especially  along  lines  of 
travel  and  commerce,  as  well  as  public  drinking  vessels,  personal  cloth- 
ing, bed-linen,  room  furnishings,  table  utensils,  children's  toys,  etc.), 
and  by  domestic  animals,  rats,  mosquitoes,  flies,  fleas,  bedbugs,  ticks, 


PATHWAYS  OF  INFECTION  19 

aiul  other  insects.  Each  of  these  modes  of  infection  may  be  active 
under  varying  circumstances;  but  from  time  immemorial  special 
importance  has  been  attributed  to  transmission  by  means  of  fomites. 
Unquestionably,  fomites  are  of  importance;  but  since  it  has  been 
definitely  proved  that  malaria  and  yellow  fever  are  transmitted  by  the 
bites  of  mosquitoes,  that  the  personal  and  bed-linen  and  even  the  dis- 
charges of  yellow-fever  patients  are  not  infectious,  and  that  plague  is 
transmitted  by  means  of  fleas  that  infest  plague-infected  rats,  the  fomites 
theory  has  been  robbed  of  much  of  its  former  importance;  and  since 
it  also  has  been  definitely  proved  that  many  persons  convalescent  from 
certain  infectious  diseases,  as  well  as  others  long  since  recovered  and 
apparently  healthy,  are  unconscious  "carriers"  of  the  specific  infectious 
agent  (typhoid  fever,  dysentery,  diphtheria,  scarlatina,  meningococcic 
infection,  cholera,  etc.),  the  prime  importance  of  direct  infection  from 
person  to  person  has  become  more  fully  realized.  The  simultaneous 
infection  of  many  persons  in  a  community  suggests,  as  a  rule,  aerial 
convection  of  the  infectious  agent  (as  in  influenza)  or  contamination 
of  the  water  supply  (as  in  typhoid  fever,  cholera,  dysentery,  etc.);  but 
many,  usually  small,  but  also  widespread,  epidemics  may  often  be 
traced  to  a  single  individual.  In  prophylaxis,  to  be  presently  men- 
tioned, the  significance  of  all  modes  of  infection  must  be  duly  appre- 
ciated; but  it  is  unwise  to  overestimate  the  significance  of  fomites,  and 
to  overlook  the  slight  sore  throat  (diphtheria),  persisting  oral  and  nasal 
discharges  (diphtheria  and  scarlatina),  and  the  chronic  carriers  of  typhoid 
and  dysentery  bacilli  in  the  stools — all  of  which  are  frequently  respon- 
sible for  more  or  less  serious  and  widespread,  though  usually  local, 
epidemics. 

Pathways  of  Infection. — In  health,  the  blood,  the  viscera,  and  the 
tissues  generally  are  free  from  pathogenic  bacteria,  although  the  bronchial 
lymph  nodes  may  contain  more  or  less  quiescent  tubercle  bacilli  and 
the  liver  partly  disintegrated  colon  and  perhaps  other  bacilli;  but  the 
skin,  the  nose,  mouth,  and  throat,  the  intestinal  tract,  and  the  female 
genital  tract  harbor  an  extensive  bacterial  flora.  This  for  the  most 
part  consists  of  non-pathogenic  bacteria,  largely  organisms  of  putre- 
faction; but  sometimes  pathogenic  bacteria  also  are  found,  leading  a 
saprophytic  existence — pyococcic  on  the  skin  and  in  the  nose,  mouth,  and 
throat.  Bacillus  coli,  Bacillus  pyocyaneus,  pyococci,  various  anaerobic 
bacteria,  etc.,  in  the  intestinal  tract,  and  so  forth. 

Infection  of  the  body  with  pathogenic  bacteria  may  occur  during 
intra-uterine  life — so-called  congenital  or  transplacental  infection ;  after 
birth  infection  may  occur  by  way  of  the  skin,  especially  through  the 
hair  follicles,  the  sebaceous  or  sweat  glands,  or  abrasions  or  wounds; 
by  way  of  the  respiratory  tract,  the  digestive  tract,  or  the  urogenital 
tract;  or  directly  into  the  blood  (direct  inoculation,  bites  of  insects, 
etc.).  Bacteria  that  do  not  succumb  in  the  body  are  eliminated  largely 
through  the  intestinal  and  the  urinary  tracts  (feces  and  urine),  but 
some  also  are  eliminated  with  discharges  from  the  genital  tract  in  women, 


20  INFECTIOUS  DISEASES 

by  expectoration,  coughing,  sneezing,  etc.,  and  from  open,  especially 
suppurating,  wounds,  etc.  Outside  the  body  the  bacteria  may  die, 
chiefly  under  the  influence  of  sunlight,  desiccation  (absence  of  suitable 
moisture),  inappropriate  temperature,  and  insuflacient  or  inappropriate 
nourishment.  Many  bacteria,  however,  live  for  varying  periods, 
especially  if  they  pass  into  the  spore  stage,  and  contaminating  the  air, 
soil,  or  water,  or  attaching  themselves  to  persons,  places,  or  things, 
may  subsequently  give  rise  to  new  infections. 

Nature  and  Lesions  of  the  Infections. — ^^^len  exposed  to  infection, 
the  body  may  be  in  a  receptive  or  a  refractory  state,  that  is,  it  may 
be  susceptible  to  or  immune  to  the  infection.  The  severity  of  an  ensuing 
infection  is  determined  somewhat  by  the  pathway  of  infection,  but 
largely  by  the  number  and  virulence  or  the  infecting  microorganisms, 
by  the  presence  or  absence  of  associated  microorganisms  (mixed, 
double,  concurrent,  or  secondary  infections),  and  by  the  resistance  of 
the  subject,  that  is,  by  a  natural  or  acquired,  active  or  passive,  partial 
or  complete  immunity.  This  resistance  or  immunity,  which  is  an 
expression  of  the  phagocytic,  antitoxic,  and  bactericidal  properties  of 
the  blood,  is  of  much  importance,  and  serves  to  explain  the  exemption 
from  infection  of  certain  individuals  exposed  thereto.  It  may  become 
reduced  under  varying  circumstances,  such  as  exposure  to  cold  and 
dampness  (catching  cold),  fatigue,  improper  or  insufficient  food,  hemor- 
rhage, and  debilitating  diseases  like  chronic  cardiac  and  pulmonary 
disorders,  diabetes,  nephritis,  malignant  disease,  etc.  In  the  last-named 
conditions,  secondary  or  terminal  infections,  due  usually  to  the  pyococci, 
Bacillus  coli,  etc.,  are  common,  and  are  often  directly  responsible  for 
the  fatal  issue. 

The  pathogenic  activity  of  the  infectious  bacteria  is  exerted  almost 
exclusively  through  the  production  of  specific  poisons.  These  bacteria, 
therefore,  are  included  with  the  substances  known  collectively  as  antigens 
(antibody  generators),  that  is,  organic  agents,  which,  when  introduced 
into  the  body,  not  only  give  rise  to  the  presence  in  the  blood  serum  of 
toxic  substances,  but  also  provoke  the  formation  by  the  cells  of  the 
body  of  various  antibodies  which  also  pass  over  into  the  blood  serum. 
These' comprise:  (1)  Pathogenic  bacteria;  (2)  the  poisonous  secretions 
or  products  of  certain  zooparasites  (Treponema  pallidum,  trypanosomes, 
etc.);  (3)  animal  cells,  extracts,  or  fluids  (erythrocytes,  blood  serum, 
snake  venom,  cells  or  extracts  of  different  organs,  etc.);  and  (4)  vege- 
table cells  or  extracts  (ricin,  abrin,  etc.).  The  term  toxin  is  often  used  to 
include  all  the  poisonous  products  of  bacteria,  of  which,  however,  several 
kinds  may  be  distinguished,  although  they  are  not  always  separable  the 
one  from  the  other.  Of  the  different  toxins  and  antibodies,  the  follow- 
ing are  the  most  important:  (1)  Toxins  (extracellular  toxins),  prod- 
ucts of  the  secretory  (or  excretory)  activity  of  the  bacteria  (especially 
Bacillus  diphtheria^.  Bacillus  tetani,  the  pyococci,  etc.).  These  are 
enzyme-like  bodies,  separable  by  filtration  from  the  bacteria,  and 
are  rendered  inactive  by  heating  to  56°  C;   they  exert  a   destructive 


NATURE  AND  LESIONS  OF  THE  INFECTIONS  21 

(degenerative)  action  on  the  body  cells;  and  they  provoke  the  formation 
in  the  body  of  substances  that  inhibit  their  action,  so-called  antitoxins, 
with  which  they  probably  unite  chemically.  Some  of  these  toxins 
have  a  special  affinity  for  certain  tissues — the  tetanus  toxin,  the  hydro- 
phobia virus,  and  the  lepra  bacillus  for  the  nervous  system;  the  menin- 
gococcus for  the  meninges;  the  gonoccocus  and  its  toxin  for  the  serous 
lining  of  the  joints,  etc.  (2)  Endotoxins  (intracellular  toxins),  either 
a  part  of  or  intimately  bound  to  the  bacteria,  and  liberated  only  upon 
lysis  or  destruction  of  the  bacteria.  These  also  exert  a  destructive 
(degenerative)  action  on  the  body  cells;  they  probably  give  rise  to  little 
if  any  antitoxin  formation,  but  they  do  provoke  the  formation  in  the 
body  of  bacteriolytic  substances.  (3)  Mycoprotein  (bacterial  protein), 
the  bacterial  substance  itself,  the  chief  action  of  which  seems  to  be 
exerted  locally — in  the  production  of  inflammation  and  leukocytic  in- 
filtration (chemotaxis).  (4)  Lysins,  substances  that  give  rise  to  solution 
not  only  of  the  provoking  bacteria,  but  also  of  the  body  cells — whence 
one  speaks  of  bacteriolysins,  cytolysins,  especially  hemolysins,  endo- 
theliolysins,  hepatolysins,  nephrolysins,  etc.  The  lysins  of  certain 
bacteria  have  been  definitely  demonstrated,  especially  those  of  the 
staphylococci  (staphylolysin),  streptococci  (streptolysin),  Bacillus  tetani 
(tetanolysin),  Bacillus  coli,  etc.  In  infections  with  these  bacteria 
an  antilysin  is  formed,  and  may  be  found  in  the  blood  serum.  For 
the  occurrence  of  an  effective  lytic  action,  such  as  hemolysis,  it  is 
necessary  to  have  the  interaction  of  an  antigen  (bacteria,  alien  erythro- 
cytes, etc.),  specific  antibodies  (so-called  immune  bodies,  or  ambo- 
ceptors), and  an  active  complement  (completing  substance,  cytase, 
alexin)  which  is  present  in  the  blood  serum  of  all  normal  animals. 
The  union  of  the  amboceptor  and  the  complement  constitute  the  lysin. 
(5)  Agglutinins,  substances  that  give  rise  to  the  agglutination  or  clump- 
ing of  the  specific  infecting  microorganism,  as  well  as  the  agglutination 
or  fusion  of  erythrocytes.  The  agglutination  of  pathogenic  micro- 
organisms constitutes  the  so-called  Pfeiffer  phenomenon,  and  is  utilized 
in  the  Gruber-Widal  reaction,  of  much  diagnostic  importance  in  typhoid 
fever,  paratyphoid  fever,  bacillary  dysentery,  Malta  fever,  etc.  Agglu- 
tination or  fusion  of  erythrocytes  is  believed  to  be  the  cause  o£  certain 
hyaline  thrombi  found  in  typhoid  fever  and  other  disorders.  (G)  Pre- 
cipitins, substances  that  lead  to  the  precipitation  of  bacteria,  or  to 
the  formation  of  a  sediment  (precipitate)  when  added  to  a  solution  of 
the  antigen  that  provoked  their  formation.  This  forms  the  basis  of 
a  test  serviceable  in  the  recognition  of  human  blood.  If  a  foreign 
protein,  such  as  human  blood  serum,  be  injected  into  a  rabbit,  the 
rabbit's  blood  serum  is  presently  found  to  contain  a  substance  (precipi- 
tin) which,  when  the  rabbit's  serum  is  added  to  a  suspension  of  some 
human  blood  (the  one-thousandth  part  of  a  milligram  or  less),  gives  rise 
to  a  visible  precipitate;  this  phenomenon  does  not  occur  if  the  rabbit's 
serum  is  added  to  other  than  human  serum,  except  that  of  some  of  the 
anthropoid  apes,  and  with  these  the  reaction  does  not  occur  in  such 


22  INFECTIOUS  DISEASES 

high  dilutions  as  with  human  serum.  (7)  Opsonins,  substances  that 
so  act  upon  the  infecting  bacteria  that  they  are  readily  destroyed  by 
the  phagocytes.  (8)  Aggressins,  substances  that  act  upon  the  phagocytes 
and  other  protecting  agencies  so  as  to  inhibit  or  destroy  their  power  of 
protecting  the  body  from  infection.  In  addition  to  the  aforementioned 
predominant  toxic  influences,  bacteria  may  provoke,  usually  relatively 
minor  lesions,  directly  by  obstructing  small  capillary  or  other  vascular 
areas  (bacterial  emboli),  or  by  being  present  in  excessive  numbers  in 
the  circulating  blood  (anthrax). 

An  established  infection  may  be  localized,  that  is,  confined  to  the 
point  of  inoculation  or  some  other  point  whence,  immediately  following 
inoculation,  the  bacteria  are  transported,  or  it  may  become  generalized. 
In  some  local  infections  the  body  generally  may  be  not  at  all  affected, 
although  the  local  lesions  may  increase  somewhat  in  extent  by  con- 
tinuity or  contiguity  of  tissue.  In  other  cases,  the  toxins  formed 
locally  gain  access  to  the  blood  stream  and  the  lymph  stream  and 
occasion  a  toxemia  (bacterial  intoxication)  and  certain  general  lesions 
and  symptoms;  this  is  especially  marked  in  typhoid  fever,  diphtheria, 
scarlatina,  tetanus,  pyococcic  infections,  variola,  etc.  In  still  other 
cases  the  bacteria  themselves  invade  the  blood  stream  or  the  lymph 
stream,  and  give  rise  to  a  general  hematogenous  or  lymphogenous 
infection  (as  the  case  may  be),  to  a  so-called  bacteremia;  this  is  notably 
the  case  in  typhoid  fever,  syphilis,  glanders,  anthrax,  many  pyococcic 
infections,  etc.  Although  some  infections,  such  as  tetanus,  diphtheria, 
tuberculosis,  etc.,  are  almost  if  not  quite  always  pure  toxemias,  and 
others,  such  as  typhoid  fever,  syphilis,  anthrax,  etc.,  are  always  bac- 
teremias, in  the  majority  of  infections  no  sharp  line  of  demarcation 
can  be  drawn  between  toxemias  and  bacteremias.  In  most  cases, 
as  already  stated,  the  lesions  and  symptoms  are  due  to  the  bacterial 
intoxication,  but  bacteremia  is  much  more  common  than  is  generally 
supposed;  the  bacteria,  being  carried  to  the  different  organs  of  the 
body,  set  up  disseminated  foci  of  disease  (so-called  bacterial  metastases), 
analogous  to  those  of  the  primary  lesion. 

The  local  and  general  results  of  infection  vary  with  the  nature  of 
the  infecting  microorganism  and  its  toxin,  and  with  the  tissues  especially 
involved.  In  general,  the  local  results  consist  of  toxic  degeneration 
of  the  cells  and  tissues,  which  may  progress  to  complete  necrosis,  and 
of  reactive  changes  comprised  within  the  term  inflammation.  The 
inflammatory  phenomena  may  be  simple  and  non-specific,  and  serous, 
serofibrinous,  fibrinous,  purulent,  or  hemorrhagic  in  character,  the 
same  bacterium  under  varying  circumstances  giving  rise  to  varying 
grades  of  exudation  or  proliferation;  in  other  cases,  the  inflammatory 
phenomena  may  be  specific,  that  is,  so  characteristic  as  to  enable  one 
thereby  to  postulate  the  nature  of  the  initiating  microorganism  (tuber- 
culosis, syphilis,  glanders,  etc.).  In  chronic  infections  there  is  likely 
to  be  also  considerable  formation  of  new  connective  or  cicatricial  tissue. 

The  general  results  of  bacterial   intoxication  vary  considerably  in 


PATHOLOGICAL  PHYSIOLOGY  OF  THE  INFECTIONS  23 

different  cases,  but  the  most  constant  and  conspicuous  lesions  consist 
of  parenchymatous  and  sometimes  fatty  degeneration  of  the  viscera, 
especially  the  myocardium,  the  liver,  the  kidneys,  and  the  muscles. 
In  addition,  one  may  encounter  focal  necroses  of  the  liver  and  the 
lymphoid  tissues  (the  lymph  nodes,  the  spleen,  and  the  bone  marrow), 
the  result  of  the  local  action  of  the  toxins  or  of  occlusion  of  small  vascular 
areas  by  large  phagocytic  cells  or  thrombi  made  up  of  fused  erythro- 
cytes (the  consequence  of  the  action  of  hemagglutinins).  The  spleen 
often  becomes  considerably  enlarged,  due  in  part  at  least  to  hyperplasia 
and  multiplication  of  the  endothelial  cells  of  the  splenic  pulp — which 
cells  become  phagocytic  and  are  perhaps  otherwise  concerned  in  the 
production  of  immunizing  bodies  (as  in  typhoid  fever,  for  instance); 
in  part  the  enlargement  of  the  spleen  is  due  also  to  the  accumulation 
of  large  numbers  of  degenerated  erythrocytes  (the  consequence  of  the 
action  of  hemolysins).  In  some  cases  degenerative  changes  occur 
in  the  nerves.  In  other  cases  small  hemorrhages  develop  beneath  the 
skin  or  mucous  membranes  or  in  the  tissues,  especially  in  typhus  fever, 
variola,  cerebrospinal  fever,  scarlatina,  pyococcic  infections,  etc.;  in 
some  of  these  cases,  notably  the  pyococcic  infections  (so-called  malig- 
nant endocarditis,  etc.),  the  hemorrhage  often  results  from  rupture 
of  miliary  (so-called  mycotic)  aneurysms,  whereas  in  other  cases  the 
hemorrhage  occurs  in  consequence  of  the  action  of  an  endotheliolysin 
that  destroys  the  cells  of  the  capillaries  and  the  lining  of  the  small 
arterioles,  and  thus  permits  the  extravasation  of  blood.  In  many 
infections,  changes  in  the  composition  of  the  blood  are  conspicuous, 
notable  anemia  and  leukocytosis;  these  may  be  associated  with  changes 
(usually  delay)  in  the  clotting  time  of  the  blood  and  various  ill-under- 
stood alterations  in  the  constitution  of  the  plasma.  The  anemia  is 
due  at  first  to  increased  hemolysis,  but  later  often  to  interference  with 
the  erythroblastic  function  of  the  bone  marrow  (defective  hemogenesis). 
The  leukocytosis  is  an  active  process,  commonly  attributed  to  chemo- 
taxis,  and  the  result  largely  of  proliferation  of  the  leukoblastic  tissues 
of  the  bone  marrow;  it  is  a  beneficial  process,  constituting,  together 
with  the  phagocytic,  antitoxic,  and  bactericidal  properties  of  the  blood, 
the  process  whereby  the  body  becomes  protected  against  or  immune 
to  infections.  Leukocytosis  is  notably  absent  in  typhoid  fever,  malaria, 
measles,  rotheln,  influenza,  mumps,  the  early  stages  of  tuberculosis 
(except  the  meningeal  form),  and  leprosy.  The  cause  of  this  is  not 
well  understood,  but  it  is  attributable,  in  typhoid  fever  at  least,  to 
degenerative  changes  in  the  bone  marrow;  in  other  cases  it  may  be 
due  to  the  absence  from  the  blood  serum  of  a  positively  chemotactic 
substance. 

Pathological  Physiology  of  the  Infections. — ^The  evidence  of  reaction 
on  the  part  of  the  body  to  an  established  infection,  that  is,  the  onset 
of  symptoms,  may  occur  soon  after  the  infection  has  taken  place,  or 
it  may  be  delayed  for  a  variable,  even  long,  time.  It  is  delayed  until 
the  toxins  are  present  in  such  amount  and  virulence  as  to  overcome 


24  INFECTIOUS  DISEASES 

the  neutralizing  or  antagonistic  forces  of  the  body,  to  disturb  the  func- 
tional activity,  and  compromise  the  structural  integrity,  of  the  constituent 
cells.  This  period,  that  is,  the  period  that  intervenes  between  the 
time  the  pathogenic  microorganisms  begin  to  increase  and  multiply 
within  the  living  body  and  the  onset  of  symptoms,  is  known  as  the 
period  of  incubation.  This  varies  considerably  in  duration  in  different 
diseases  and  somewhat  in  different  cases  of  the  same  disease;  it  may 
be  apparently  twelve  hours  or  less  in  some  cases  of  pneumococcic 
infection  of  the  lung  (croupous  pneumonia),  and  as  much  as  two  to  six 
or  more  months  in  hydrophobia.  In  many  infections  this  period  is 
unannounced  by  symptoms;  but  in  some  infections,  notably  typhoid 
fever,  toward  the  end  of  this  period,  concurrently  with  the  diffusion 
throughout  the  body  of  some  toxins  or  the  dissemination  of  the  causa- 
tive bacteria,  certain  more  or  less  ill-defined,  so-called  prodromal  or 
premonitory,  symptoms  become  manifest,  such  as  malaise,  lassitude, 
muscular  weakness,  and  readily  induced  weariness,  general  neuro- 
muscular pains  and  soreness,  headache,  mental  hebetude  or  irritability, 
perhaps  even  slight  rise  of  bodily  temperature,  etc. 

The  onset  of  definite  symptoms,  the  so-called  period  of  invasion, 
may  be  abrupt  (acute)  or  insidious  (subacute  or  chronic).  In  certain 
acute  infections,  such  as  croupous  pneumonia,  malaria,  etc.,  the  period 
of  onset  may  usually  be  determined  with  great  exactitude,  the  invasion 
symptoms  consisting  of  a  more  or  less  severe  chill  and  fever.  Similar, 
but  less  aggravated  phenomena  may  attend  the  onset  of  other  acute 
infections;  in  infants  and  children  the  initial  chill  or  chilliness  is  often 
replaced  by  a  convulsion.  In  infections  of  more  insidious  development, 
such  may  be  the  gradual  increment  of  symptoms  that  it  may  be  almost 
if  not  quite  impossible  to  determine  accurately  the  time  of  onset  of 
the  disease.  In  infections  generally,  of  all  the  symptoms  of  invasion, 
fever  is  the  most  constant  and  most  significant.  Such,  in  point  of  fact, 
is  its  significance  that  in  the  great  majority  of  cases  its  occurrence 
should  be  interpreted  to  mean  infection  or  intoxication;  other  less 
common  causes  comprise  the  action  of  enzymes  such  as  are  liberated 
during  hemolysis  (internal  hemorrhages,  certain  severe  anemic  states, 
burns,  etc.),  the  excessive  action  of  internal  secretions  (thyroid),  grave 
perturbations  of  the  central  nervous  system  associated  with  increased 
heat  production  or  lessened  heat  dissipation,  exposure  to  high  external 
temperature,  and  certain  drugs  (strychnine  poisoning,  etc.). 

Following  upon  the  period  of  invasion,  the  infections  are  characterized 
by  a  more  or  less  prolonged  period  of  fever,  the  so-called  fastigium — 
which  may  last  several  hours,  several  days,  or  several  months  or  more. 
The  type  and  course  of  the  infection  may  be  acute,  subacute,  or  chronic. 
The  acute  infections,  such  as  measles,  scarlatina,  smallpox,  croupous 
pneumonia,  typhoid  fever,  relapsing  fever,  etc.,  are  characterized  by 
a  definite  period  of  incubation,  a  characteristic,  often  abrupt  period 
of  onset,  a  definite  fastigium  (typical  fever  course),  and  often  quite 
characteristic  if  not  pathognomonic  symptoms.     Depending  upon  the 


PATHOLOGICAL  PHYSIOLOGY  OF  THE  INFECTIONS  25 

virulence  of  the  infectious  agent  and  the  resistance  of  the  subject, 
recovery  or  death  eventually  occurs.  In  favorable  cases,  following 
the  fastigium,  defervescence  ensues — the  temperature  falls  either 
suddenly  (crisis)  or  slowly  (lysis),  the  other  symptoms  abate,  and 
convalescence  becomes  established.  The  convalescence,  however, 
may  be  interrupted  by  relapses  or  complications  (often  secondary 
infections),  and  restoration  to  complete  health  may  be  delayed  by 
sequels.  Certain  of  the  acute  infections  are  sometimes  characterized 
by  dominant  intoxication,  marked  mental  depression  or  coma,  slight 
fever  or  even  subnormal  temperature  (that  is,  little  or  no  reaction), 
rapid  and  feeble  pulse,  low  and  falling  blood  pressure,  absence  of 
leukocytosis  in  diseases  in  which  it  ordinarily  occurs,  and  early  death. 
These  cases  are  often  spoken  of  as  hyperacute,  fulminating,  or  malig- 
nant; they  are  sometimes  exemplified  in  smallpox,  cholera,  yellow 
fever,  plague,  pyococcic  (especially  streptococcic)  infections,  cerebro- 
spinal fever,  scarlatina,  malaria,  etc.  The  chronic  infections,  such  as 
tuberculosis,  glanders,  actinomycosis,  etc.,  as  a  rule,  are  characterized 
by  a  variable  period  of  incubation,  although  syphilis  is  a  noteworthy 
exception,  having  a  definite  period  of  incubation;  as  a  rule,  also,  they 
are  insidious  in  onset,  a  distinct  period  of  invasion  often  being  undeter- 
minable; and  their  course  is  protracted.  To  intermediate  cases  the 
term  subacute  is  often  applied;  other  cases,  characterized  by  periods 
of  remission  and  of  relapse  or  exacerbation,  are  spoken  of  as  remittent 
or  recurring.  Finally,  Adami  has  postulated  what  he  describes  as 
subinfection,  a  condition  in  which  pathogenic  and  non-pathogenic 
bacteria,  instead  of  proliferating,  are  destroyed  in  the  various  tissues 
and  organs,  especially  the  liver  and  the  mesenteric  lymph  nodes,  to 
which  they  may  be  carried  by  the  lymph  and  blood  stream.  The  long 
continuation  of  this  process  is  believed  by  Adami  to  lead  ultimately 
to  cell  exhaustion  and  to  be  perhaps  a  factor  in  the  production  of  cirrhosis 
of  the  liver,  some  cases  of  pernicious  anemia,  some  cases  of  chronic 
interstitial  nephritis — an  opinion  that  has  not  yet  found  confirmation. 
The  obtrusive  characteristic  of  the  infections  is  fever;  but  increased 
temperature  is  only  one  feature  of  the  febrile  state.  Although  under 
the  influence  of  bacterial  intoxication  the  thermogenic  regulating 
centres  are  much  disturbed,  the  increased  temperature  is  due  largely, 
if  not  wholly,  to  increased  heat  production,  which  in  turn  results  from 
augmented  tissue  katabolism  and  oxidation;  that  is,  under  the  influence 
of  bacterial  toxins,  and  independently  of  the  amount  and  character 
of  the  food,  tissue  destruction  is  greater  than  tissue  formation;  the 
tissue  destruction,  however,  may  be  somewhat  controlled  by  appropriate 
food.  Adami  looks  upon  fever  as  the  process  of  adaptation  to  such 
agencies  as  can  be  neutralized  by  the  development  of  antibodies.  Since 
it  represents  the  reaction  of  the  body  to  the  infection,  and  in  an  other- 
wise toxic  case  is  to  some  extent  a  measure  of  that  reaction,  it  is  by  no 
means  an  unmixed  evil;  it  shows  that  the  body  is  coping  better  with 
the   infection   than   if  fever  did  not  occur.     Although   hyperthermia, 


26  INFECTIOUS  DISEASES 

especially  if  prolonged,  is  of  itself  dangerous  to  life,  the  toxic  apyretic 
cases,  particularly  cases,  in  which  the  manifestations  of  intoxication 
increase  while  the  temperature  falls,  are  really  serious  and  commonly 
terminate  fatally. 

As  already  stated,  the  fever  of  invasion  is  often  accompanied  by  a 
more  or  less  severe  chill;  this  is  the  more  likely  to  occur  if  the  initial 
(pyrogenetic)  stage  of  the  fever  is  short — from  one-half  to  two  hours; 
in  other  cases  there  may  be  only  chilliness,  which  may  last  for  some 
time  or  be  repeated.  The  chill  is  a  nervous  manifestation,  characterized 
by  subjective  sensations  of  coldness,  chattering  of  the  teeth,  fibrillary 
twitchings  of  the  muscles,  and  pallor  and  lividity  of  the  face  and  ex- 
tremities. Although  the  patient  feels  cold  and  complains  thereof, 
the  internal  temperature  of  the  body  is  increased.  The  condition  is 
attributable  to  contraction  of  the  peripheral  bloodvessels  under  the 
influence  of  vasomotor  stimulation,  in  consequence  of  which  the  surface 
of  the  body  is  ill-supplied  with  blood,  while  the  internal  organs  are 
congested;  the  fibrillary  twitchings  and  the  increased  tone  (rigor)  of 
the  muscles  are  doubtless  in  part  responsible  for  the  augmented  heat 
production. 

In  addition,  the  febrile  state  is  characterized  by  other  nervous 
manifestations,  as  well  as  disturbances  of  the  circulatory,  respiratory, 
digestive,  and  urinary  systems,  and  disorders  of  general  metabolism. 
The  nervous  manifestations  may  be  irritative  or  depressive :  the  irritative, 
which  usually  precede  the  depressive,  consist  of  general  neuromuscular 
pains  and  soreness,  headache,  mental  irritability,  intolerance  of  light 
and  noises,  insomnia,  active  delirium,  etc.;  the  depressive  consist  of 
mental  hebetude,  apathy,  inattention  to  surroundings,  retention  of  urine 
or  involuntary  evacuation  of  the  bladder  and  rectum,  muttering  delirium, 
stupor,  coma,  etc.  These  are  attributable  to  a  direct  action  of  toxins 
on  the  central  nervous  system,  which  at  first  is  irritated  and  finally 
exhausted.  In  some  cases  nervous  symptoms  are  unusually  dominant 
and  give  rise  to  so-called  cerebral  types  of  several  infections;  these  very 
much  simulate  meningitis,  and  constitute  the  so-called  meningism  of 
the  French.  In  other  cases,  such  as  tetanus,  hydrophobia,  epidemic 
poliomyelitis,  etc.,  the  toxin  (or  virus)  possesses  a  special  affinity  for 
the  nervous  system,  and  may  reach  the  central  nervous  organs  by  way 
of  the  peripheral  nerves. 

Rapidity  of  the  cardiac  action  and  of  the  pulse  is  an  almost  constant 
concomitant  of  the  febrile  state;  as  a  rule,  each  degree  of  added  tem- 
perature corresponds  to  about  ten  added  cardiac  beats  per  minute, 
but  there  are  exceptions:  in  typhoid  fever,  for  instance,  the  pulse  is 
commonly  disproportionately  infrequent,  in  scarlatina  it  is  character- 
istically disproportionately  rapid,  and  in  the  event  of  stimulation  of  the 
pneumogastric  nerve  (as  in  meningitis),  it  may  be  very  infrequent.  In 
addition  to  being  rapid,  the  pulse  may  be  full  and  bounding,  with  normal 
or  perhaps  increased  blood  pressure  (in  sthenic  states);  or  weak,  easily 
compressible,  or   thready,   with  lowered   blood   pressure   (in   asthenic 


PATHOLOGICAL  PHYSIOLOGY  OF  THE  INFECTIONS  27 

states).  Increasing  rate  and  weakness  are  of  bad  prognostic  omen, 
whereas  decreasing  rate  and  increasing  strength  render  the  outlook 
hopeful.  These  changes  are  the  result  of  various  factors:  perhaps 
early  there  is  toxic  stimulation  of  the  accelerator  nerves  and  increased 
excitability  of  the  heart,  and  consequent  increased  pulse  rate;  later 
toxic  degeneration  of  the  myocardium  occurs  and  leads  to  depression 
of  contractility  and  tonicity  and  more  or  less  ineffectual  systoles;  toxic 
degeneration  of  the  pneumogastric  nerves  may  be  answerable  for  some 
of  the  sudden  deaths  that  occur  during  the  course  of  or  in  convalescence 
from  diphtheria,  influenza,  etc.;  and  toxic  paralysis  of  the  vasomotors 
is  responsible  for  the  lowered  blood  pressure  and  the  common  capillary 
stasis,  especially  of  the  fingers,  toes,  nose,  ears,  etc. 

Furthermore,  the  respiratory  rate  and  the  respiratory  exchange  of 
gases  become  increased.  The  increased  respirations  are  due  to  a  direct 
action  of  the  toxins  and  the  augmented  temperature  on  the  respiratory 
centres  and  to  surcharging  of  the  blood  with  carbon  dioxide;  the  in- 
creased gaseous  exchange  in  the  lungs  is  a  direct  consequence  of  the 
Increased  metabolism,  of  the  increased  formation  of  carbon  dioxide, 
and  the  necessity  for  more  oxygen.  The  increased  respirations  serve 
in  a  measure  to  reduce  the  bodily  temperature,  some  of  which  is  dis- 
sipated in  the  process  of  warming  the  increased  amount  of  air  inhaled. 
The  chief  digestive  disturbances  consist  of  anorexia,  dry  mouth,  thirst, 
lessening  of  the  digestive  juices,  and  often  constipation;  the  gastric 
juice,  as  a  rule,  is  lessened  in  amount  and  reduced  in  acidity;  the  bile 
becomes  inspissated  and  is  perhaps  otherwise  altered;  the  intestinal 
juices  are  reduced  in  amount,  which  together  with  diminished  peristalsis 
is  answerable  for  the  constipation  of  some  cases.  The  urine  becomes 
reduced  in  amount,  concentrated,  of  heightened  color,  increased  acidity, 
increased  specific  gravity,  and  increased  toxicity;  it  contains  an  increased 
amount  of  nitrogenous  substances  (urea,  uric  acid,  kreatinine,  etc.) 
and  of  potassium,  magnesium,  and  calcium  salts,  but  sometimes 
there  is  a  decrease  of  the  chlorides;  there  is  often  also  a  small  amount 
of  albumin,  and  sometimes  hyaline  and  other  casts;  in  the  event  of 
intestinal  putrefaction,  decomposition  products,  such  as  indol,  skatol, 
and  other  aromatic  substances,  may  be  encountered.  The  significant 
change  from  the  normal  is  the  great  increase  in  the  nitrogenous  excretion, 
which  may  reach  twice  or  thrice  that  of  a  normal  person  on  a  like  diet; 
this  is  the  result  of  the  augmented  katabolism  affecting  especially  the 
proteins  of  the  body.  One  evidence  of  this  is  seen  in  the  emaciation 
of  the  infected  subject — at  first  the  panniculus  adiposus  disappears, 
but  the  muscles  soon  decrease  in  size,  lose  their  tone,  and  become  soft, 
flabby,  and  readily  exhausted. 

The  foregoing  statements  in  reference  to  the  bacterial  infections  apply 
with  equal  force,  although  in  somewhat  modified  form,  to  the  non- 
bacterial fungus  infections  and  the  zooparasitic  infections.  Some  of 
the  protozoan  infections,  such  as  malaria,  syphilis,  relapsing  fever, 
trypanosomiasis,  etc.,  exhibit  many  analogies  with  bacterial  infections — 


28  INFECTIOUS  DISEASES 

the  fever,  toxemia,  hemolysis,  disturbances  of  metabolism,  etc.  Some 
of  the  metazoan  infections  also  seem  to  be  associated  with  the  produc- 
tion of  a  hemolytic  and  perhaps  other  poisons,  and  the  metazoa 
often  serve  also  as  hosts  carrying  pathogenic  bacteria  into  the  human 
subject.  Many  questions  concerning  the  zooparasitic  infections,  how- 
ever, await  elucidation,  not  only  those  pertaining  to  etiological  factoi-s 
and  the  modes  of  transmission,  but  also  those  relating  to  natural  and 
acquired  immunity. 

Diagnosis. — ^Many  of  the  infections  may  be  recognized  with  certainty, 
others  with  relative  certainty,  by  means  of  their  clinical  manifestations — 
which  are  discussed  under  the  respective  headings.  In  addition,  the 
progress  of  medical  science  during  recent  years  has  rendered  available 
several  more  or  less  specific  diagnostic  methods.  Many  infections 
of  known  etiology  may  be  diagnosticated  without  doubt  by  isolating 
from  the  patient  the  specific  causative  microorganism.  This  may  be 
found  on  or  in  more  or  less  superficial  lesions  of  the  skin  or  accessible 
mucous  membranes,  in  the  blood,  in  the  cerebrospinal  fluid,  in  fluid 
removed  by  puncture  from  the  serous  sacs,  in  the  organs  and  tissues 
of  the  body,  in  discharges,  etc. ;  and  the  microorganisms  may  be  studied 
in  coverslip  preparations  or  by  cultural  methods.  As  already  stated, 
the  agglutinins  are  the  active  factor  in  causing  agglutination  of  bacteria, 
a  phenomenon  utilized  in  the  Gruber-Widal  reaction — the  agglutination 
or  clumping  of  microorganisms  when  added,  in  dilutions  of  1  to  50 
to  1  to  1000  or  more,  to  blood  serum  containing  specific  agglutinins. 
This  is  an  important  diagnostic  test  in  typhoid  fever,  paratyphoid  fever, 
relapsing  fever,  Malta  fever,  bacillary  dysentery,  cholera,  plague, 
glanders,  tuberculosis,  etc.  The  presence  of  bound  or  unbound  com- 
plement is  utilized  as  a  basis  of  the  Wassermann  complement-binding 
(or  deviation-of-the-complement)  test  in  the  diagnosis  of  s^^hilis  and 
so-called  parasyphilitic  disorders,  like  tabes  dorsalis  and  paretic  de- 
mentia; its  use  has  been  suggested  also  in  typhoid  fever,  meningo- 
coccic  and  gonococcic  infections,  trypanosomiasis,  echinococcic  disease, 
carcinoma,  etc.  The  reaction,  which  is  based  upon  original  observa- 
tions of  Bordet  and  Gengou,  requires  for  its  successful  carrying  out 
much  experience  and  laboratory  facilities.  In  brief,  it  consists  of  adding 
to  the  blood  serum  of  a  patient  suspected  of  being  syphilitic  a  watery 
extract  of  a  sj^hilitic  (usually  foetal)  liver  (or  other  organ  containing 
Treponema  pallidum);  if  the  patient  is  syphilitic,  the  blood  serum 
contains  syphilitic  antibodies  or  amboceptors  and  the  complement  is 
bound.  If  this  mixture  be  now  added  to  sheep's  erythrocytes  and  the 
corresponding  amboceptors,  hemolysis  does  not  occur — the  available 
complement  (necessary  to  complete  the  hemolysis)  being  already 
bound.  Recently  it  has  been  found  that  extracts  of  normal  liver, 
sodium  glycocholate,  lecithin,  and  other  lipoids  may  be  utilized 
instead  of  the  original  antigen  (syphilitic  liver);  and  more  recently 
Noguchi  has  modified  the  test  by  substituting  an  antihuman  for  the 
original    antisheep   hemolytic    system,    and    by    utilizing    test    papers 


PROPHYLAXIS  OF  THE  INFECTIONS  29 

saturated  with  antigen,  amboceptor,  and  complement.  Finally,  it  has 
been  found  that  under  the  influence  of  bacterial  toxins  and  other  antigens, 
certain  animals  and  human  subjects  develop  a  specific  hypersensitive- 
ness  to  the  antigen  in  question  (anaphylaxis),  so  that  a  second  injection 
of  the  antigen  may  bring  about  serious  and  sometimes  fatal  results, 
although  the  two  doses  combined  were  less  than  that  ordinarily  provoca- 
tive of  toxic  results.  Such  a  phenomenon  is  sometimes  observed  in 
human  subjects  after  the  injection  of  diphtheria  and  other  antitoxins, 
the  serum  and  not  the  antitoxin  as  such  being  the  active  factor  (serum 
disease  or  fatality).  In  tuberculosis,  glanders,  and  other  infections 
the  tissues  also  become  sensitized  to  the  toxin  in  question,  so  that  when 
an  extra  amount  is  added  they  react  variously;  this  is  the  basis  of  the 
various  tuberculin  reactions,  the  mallein  reaction,  etc. 

Prophylaxis. — The  prevention  of  the  infections  is  no  less  important 
than  their  cure,  and  since  each  case  presupposes  an  antecedent  case, 
efforts  should  be  made  to  throttle  the  disease  at  its  source.  This,  the 
individual  patient,  is  the  practising  physician's  chief  concern.  The 
patient  should  be  isolated.  So  imperative  is  this  in  infections,  such 
as  smallpox,  scarlatina,  diphtheria,  typhus  fever,  yellow  fever,  cholera, 
plague,  etc.,  that  isolation  and  supervision  is  one  of  the  readily  conceded 
functions  of  the  health  authorities,  is  ordered  by  law,  and  in  the  best 
regulated  communities  is  effected  in  special  hospitals  provided  for  the 
purpose.  It  is  equally  desirable  that  isolation  should  be  practised  in 
other  infections,  which  if  they  do  not  create  the  communal  consterna- 
tion that  pertain  to  those  already  mentioned,  still  have  a  greater  mor- 
bidity and  often  a  larger  death  toll — that  is,  typhoid  fever,  measles, 
rubella,  pertussis,  cerebrospinal  fever,  puerperal  fever,  pneumonia, 
tuberculosis,  gonococcic  infection,  syphilis,  etc.  If  treated  at  his  home, 
the  patient  should  be  placed  in  a  large,  clean,  quiet  room,  provided 
with  an  abundance  of  sunlight  and  fresh  air,  and  adequately  protected 
against  flies,  mosquitoes,  and  other  insects;  all  unnecessary  furniture, 
carpets,  hangings,  pictures,  etc.,  should  be  removed;  and  a  sheet,  wet 
with  carbolic  acid,  mercuric  bichloride,  or  formalin,  may  be  hung  before 
the  door,  if  for  no  better  purpose  than  to  warn  away  the  inquisitive. 
In  the  readily  transmissible  infections  (diphtheria,  scarlatina,  small- 
pox, etc.)  the  patient  should  be  provided  with  at  least  one,  preferably 
two,  nurses  or  attendants;  all  other  persons  should  be  rigidly  excluded 
from  the  sick  room.  The  nurses,  as  well  as  the  physician,  prior  to 
entering  the  sick  room,  should  don  a  gown  that  entirely  envelops  the 
body  and  should  cover  the  head ;  and  on  leaving  the  room  and  removing 
the  gown,  they  should  wash  the  exposed  parts  of  the  body  (hands  and 
face).  The  nurses  should  also  wash  their  hands  after  touching  or 
handling  the  patient;  or  they  may  protect  themselves  by  w'earing  rubber 
gloves.  Similar  precautions  should  be  adopted  also  in  the  less  readily 
transmitted  infections,  notably  typhoid  fever,  tuberculosis,  etc. 

In  all  cases  of  infection,  the  patient's  personal  linen,  bed-linen, 
dishes,    knives,    forks,   spoons,    etc.,   should   under    no   circumstances 


30  INFECTIOUS  DISEASES 

be  placed  in  contact  with  those  used  by  other  members  of  the  house- 
hold; nor  should  the  attendants  upon  the  patient  prepare  food  for 
other  members  of  the  family.  All  dishes  and  other  utensils  used 
by  the  patient  (such  as  the  bed-pan,  urinal,  etc.),  should  be  dis- 
infected after  use,  by  boiling  or  the  use  of  a  5  per  cent,  carbolic 
acid  solution.  All  discharges  from  the  patient,  such  as  from  the 
mouth,  nose,  or  ear,  the  urine,  feces,  sputum,  vomitus,  etc.,  should 
be  destroyed:  if  possible,  by  incineration  and  complete  destruction,  or, 
when  this  is  not  available,  by  the  use  of  milk  of  lime,  carbolic  acid 
(5  per  cent.),  or  mercuric  bichloride  (1  to  500  or  1  to  1000).  The 
milk  of  lime  must  be  freshly  prepared  by  adding  to  a  lump  of  quicklime 
about  half  its  volume  of  water;  the  resulting  hydrate  should  be  kept 
sealed,  and  as  required  one  part  of  it  should  be  added  to  four  to  six 
parts  of  water.  Whichever  disinfecting  solution  is  used  should  be 
added  to  the  discharge  in  the  proportion  of  two  to  three  volumes  to  one"^ 
thoroughly  mixed,  and  allowed  to  act  for  two  to  six  hours  before  being 
emptied  into  the  closet.  Throughout  the  course  of  the  infection,  the 
patient's  personal  and  bed-linen,  etc.,  should  be  put  directly  from  the 
bed  into  a  large  sheet  and  then  into  carbolic  acid  (5  per  cent.),  or 
mercuric  bichloride  (1  to  500);  thence  it  should  be  removed  to  a  suitable 
place  and  boiled  for  at  least  one  hour. 

After  the  patient  has  recovered,  he  may  be  given  a  bichloride  bath 
(1  to  2000),  and  his  skin  may  be  anointed  with  olive  oil;  he  should 
then  be  removed  to  another  room,  previously  well  aired,  and  fresh  linen 
should  be  provided.  Should  death  occur,  the  body  should  be  enveloped 
in  several  sheets  or  other  cloths  wet  with  carbolic  acid  (5  per  cent.) 
or  mercuric  bichloride  (1  to  500),  and  as  soon  as  possible  placed  in  a 
coffin  and  hermetically  sealed.  After  convalescence  (or  death)  the 
room  and  its  contents  must  be  thoroughly  disinfected.  The  preferable 
method  for  the  contents  is  by  incineration  and  complete  destruction; 
this  is  desirable  especially  for  old  mattresses,  carpets,  rugs,  hangings, 
and  other  articles  of  little  value;  articles  of  value  may  be  subjected  to 
the  action  of  superheated  steam  (steam  under  pressure),  or  boiling 
water,  or  chemicals,  such  as  carbolic  acid,  mercuric  bichloride,  or 
formaldehyde.  The  room  itself  should  be  hermetically  sealed  and 
subjected  to  the  action  of  formaldehyde  gas,  which  may  be  generated 
in  special  generators,  or  by  the  addition  of  potassium  permanganate 
to  the  official  formalin,  in  the  proportion  of  8  ounces  (250  grams)  of 
the  permanganate  to  one  pint  (500  c.c.)  of  the  formalin  to  each  1600 
cubic  feet  of  air  space.  The  room  should  not  be  opened  until  after 
the  lapse  of  twelve  to  twenty-four  hours.  Thereupon  the  floor  and 
other  woodwork,  etc.,  should  be  scrubbed  with  hot  water  and  soap, 
and  then  washed  with  mercuric  bichloride  (1  to  500) — which  some 
time  after  it  has  dried  should  itself  be  washed  off.  The  room  then 
should  be  exposed  for  a  day  or  two  to  a  vigorous  current  of  fresh  air 
and  as  much  sunlight  as  possible.  New  wall  paper  should  be  sub- 
stituted for  the  old. 


TREATMENT  OF  THE  INFECTIONS  31 

In  addition  to  the  aforementioned  measures,  which  are  designed  to 
prevent  the  spread  of  infection,  there  are  other  important  prophylactic 
procedures.  These  comprise,  particularly,  a  pure,  non-infected  water 
supply,  which  is  especially  important  as  regards  typhoid  fever,  dysen- 
tery, cholera,  etc.  The  water  should  be  taken  from  a  source  as  pure  as 
possible,  and  in  the  event  of  even  the  slightest  doubt,  should  be  filtered 
(chemical  disinfection  does  not  seem  to  be  as  efficacious  as  filtration, 
and  is  otherwise  objectionable).  During  the  prevalence  of  an  epidemic 
all  the  drinking  water  should  be  boiled,  and  only  boiled  water  should 
be  used  for  washing  the  teeth,  as  well  as  foodstuffs,  like  celery,  lettuce, 
etc.  Special  care  must  be  taken  to  see  that  other  articles  of  diet  are 
not  contaminated;  such  as  milk  (diluted  with  infected  water  or  handled 
in  dairies  where  an  infection  prevails);  oysters  and  other  shellfish 
grown  in  polluted  streams;  vegetables  grown  in  infected  ditches  or 
watered  or  washed  with  infected  water;  meats  from  diseased  animals, 
etc.  These  if  eaten  at  all  must  be  thoroughly  cooked.  Attention  must 
be  paid  to  the  existence  of  chronic  "carriers,"  who  are  often  responsible 
for  local  or  widespread  epidemics  of  typhoid  fever,  dysentery,  etc.,  as 
well  to  the  slight  sore  throat  (diphtheria,  scarlatina)  and  the  persisting 
nasal  and  aural  discharges  that  often  follow  diphtheria,  scarlatina,  etc. 
In  time  of  war  or  during  peaceful  military  encampments,  additional 
sanitary  measures  should  be  undertaken,  especially  the  proper  disposal 
of  refuse,  urine,  and  feces,  the  protection  of  latrines  and  garbage  cans 
from  flies  and  other  insects,  etc.  An  efficient  prophylaxis  of  the  large 
and  increasing  number  of  ill-understood  infections  in  the  tropical  and 
subtropical  regions,  some  of  demonstrated  protozoan  origin  and  many 
known  to  be  transmitted  by  various  insects,  is  to  be  expected  from  a 
careful  study  of  the  life  history  of  the  infection-carrying  insects,  and 
the  adopting  of  preventive  measures  in  accordance  with  the  discoverable 
facts.  Finally,  among  the  prophylactic  measures,  one  must  mention 
preventive  inoculations,  which  are  resorted  to  with  complete  success 
in  smallpox  (vaccinia),  and  have  been  used  with  encouraging  results  in 
hydrophobia,  typhoid  fever,  cholera,  plague,  anthrax  in  the  lower 
animals,  etc. 

Treatment. — Since  the  specific  nature  of  many  infections  has  been 
demonstrated,  scientists  have  labored  to  produce  specific  remedies 
that  shall,  in  some  measure,  at  least,  reproduce  the  normal  immunizing — 
antitoxic,  bacteriolytic,  and  phagocytic — processes  of  the  body.  Some 
are  available  and  of  unquestionable  utility.  Diphtheria  antitoxin,  the 
first  discovered,  has  virtually  revolutionized  the  treatment  of  diph- 
theria, and  may  be  looked  upon  as  a  specific,  certain  to  cure  if  resorted 
to  early  in  the  course  of  the  infection.  The  hope  born  of  this  success 
has  not  found  fulfilment  as  regards  many  of  the  other  infections — 
because  antitoxin  is  efficacious  only  if  resorted  to  before  the  toxin  has 
formed  a  firm  union  with  or  destroyed  the  tissues,  and  because  many  of 
the  bacteria  produce  not  an  extracellular  toxin,  but  an  intracellular, 
so-called  endotoxin,  which  does  not  provoke  the  formation  of  an  anti- 


32  BACTERIAL  INFECTIONS 

toxin,  although  it  may  lead  to  the  formation  of  a  bacteriolytic  sub- 
stance. The  tetanus  antitoxin,  for  instance,  is  usually  inefficacious, 
because  the  development  of  symptoms  is  significant  of  a  firm,  almost 
indissoluble  union  between  the  toxin  and  the  nervous  tissues.  Success 
has  attended  the  prophylactic  use  of  this  tetanus  antitoxin  in  cases, 
such  as  Fourth-of-July  wounds,  known  to  be  especially  likely  to  be 
followed  by  tetanus.  The  use  of  pneumococcic,  staphylococcic,  strep- 
tococcic, and  plague  antitoxin,  as  a  rule,  has  not  been  followed  by 
results  better  than  those  which  attend  other  forms  of  treatment,  although 
some  notable  successes  have  been  achieved.  Encouraging  results  have 
followed  the  use  of  Flexner's  antimeningococcic  serum.  The  use  of 
bacteriolytic  serums  is  not  to  be  unreservedly  commended,  since  the 
solution  of  bacteria  in  the  tissues  is  not  free  from  danger.  Recently 
bacterins  (bacterial  vaccines;  suspensions  in  physiological  saline  solution 
of  killed  bacteria)  have  been  used  with  considerable  success,  especially 
in  staphylococcic,  streptococcic,  pneumococcic,  gonococcic,  tuberculous, 
dysenteric,  some  typhoid-colon  infections,  Malta  fever,  etc.  These  bac- 
terins act  by  facilitating  or  augmenting  an  active  immunity,  and  while 
they  doubtless  favor  the  production  of  several  immune  substances,  their 
chief  action  perhaps  is  to  stimulate  the  production  of  specific  opsonins, 
and  thus  to  facilitate  phagocytosis.  Wright  believes  that  the  adminis- 
tration of  bacterins  should  be  controlled  by  estimations  of  the  opsonic 
index  (the  opsonic  power  of  a  patient's  blood,  as  compared  with  that  of 
a  healthy  person,  in  respect  to  a  given  microorganism) ;  this  in  practice, 
however,  has  not  been  found  necessary.  Autogenous  vaccines  are  much 
more  efficacious  than  stock  vaccines.  Recently  also  Hiss,  acting  upon 
the  hypothesis  that  the  activity  of  the  phagocytes  in  the  processes  of 
immunity  is  due,  in  part  at  least,  to  the  presence  of  an  intracellular 
antitoxin  (endo-antitoxin),  has  suggested  the  use  of  aqueous  extracts  of 
washed  dead  leukocytes  in  staphylococcic,  streptococcic,  pneumococcic, 
meningococcic,  and  other  infections.  Encouraging  reports  of  the  effi- 
cacy of  the  treatment  have  been  made.  But  all  methods  of  specific 
therapy  are  still  on  trial;  the  final  pronouncement  regarding  their 
value  is  reserved  for  the  future. 


BACTEEIAL  INFECTIONS. 

TYPHOID  FEVER. 

(Enteric  Fever;  Abdominal  Typhus.) 

Typhoid  fever  is  an  acute,  specific,  infectious  disease  caused  by 
Bacillus  typhosus  (Eberth-Gaffky) ;  it  is  a  true  bacteremia,  characterized 
anatomically  by  hyperplasia  and  necrosis  of  the  lymphoid  tissues  of  the 
body,  especially  of  the  intestinal  tract,  and  clinically,  by  slow  onset, 
continued  fever  of  characteristic  type,  enlargement  of  the  spleen,  a 


TYPHOID  FEVER  33 

characteristic  roseolous  rash,  a  specific  serum  reaction,  the  so-called 
typhoid  state,  and  a  tendency  to  relapse  and  to  the  occurrence  of 
certain  complications,  notably  intestinal  hemorrhage  and  perforation. 

Etiology. — While  typhoid  fever  occurs  at  all  ages,  even  in  infancy 
and  in  old  age,  it  is  especially  frequent  between  the  ages  of  fifteen  and 
thirty  years ;  but  typhoid  infection  may  occur  even  in  utero.  It  is  ecjually 
common  in  both  sexes,  and  aftects  persons  in  all  stations  of  life.  It 
occurs  in  all  parts  of  the  world,  but  is  especially  prevalent  in  the  temperate 
and  subtropical  zones.  It  is  endemic  in  most  large  cities  and  frequently 
prevails  epidemically,  especially  in  the  autumn  and  early  winter — more 
commonly  after  a  dry,  hot  summer  (whence  the  term  autumnal  fever) ;  but 
in  some  localities  the  disease  is  quite  frequent  in  the  spring,  concurrent 
with  the  thaws  and  floods.  Newcomers  in  infected  localities  are  espe- 
cially susceptible,  more  particularly  those  who  move  from  the  country 
to  the  city.  Bad  sanitary  arrangements,  familial  and  municipal,  such 
as  defective  drainage,  contaminated  water  supply,  poor  ventilation, 
the  accumulation  of  filth,  etc.,  act  as  predisposing  factors — favoring  the 
development  of  the  typhoid  bacillus  and  reducing  the  vitality  of  the 
individual.  Pettenkofer  attributed  the  development  of  the  disease  to 
the  condition  of  the  "ground  soil,"  believing  that  a  low  level  of  the 
standing  water  favors  the  occurrence  of  the  disease.  One  attack  usually 
confers  more  or  less  absolute  immunity,  but  recurrences  are  by  no  means 
unknown.  Some  persons  seem  to  possess  a  natural  immunity.  The 
immunity  of  old  residents  in  infected  localities,  however,  is  frequently 
due  to  their  having  had  the  disease  in  early  life — when  the  symptoms, 
as  a  rule,  are  mild  and  the  mortality  low. 

The  exciting  cause  of  the  disease  is  Bacillus  typhosus.  Infection 
is  almost  exclusively  transmitted  by  infected  food  or  infected  drink; 
sometimes  by  direct  contact,  by  a  third  person,  by  the  air,  by  fomites, 
or  by  infected  animals.  Every  case  of  the  disease  thus  presupposes 
the  existence  of  some  previous  case,  that  directly  or  indirectly  acts  as 
a  source  of  infection;  niany  widespread  and  fatal  epidemics  have  been 
traced  to  a  single  case.  Infection  is  commonly  acquired  by  way  of  the 
gastro-intestinal  tract;  rarely  perhaps  by  way  of  the  respiratory  tract. 
In  the  usual,  that  is,  the  gastro-intestinal  cases,  the  infectious  atrium 
has  not  been  definitely  determined,  the  ileum,  the  upper  part  of  the 
intestine,  the  stomach,  and  the  tonsils  being  variously  looked  upon  as 
the  portal  of  entry  of  the  l)acillus.  For  obvious  and  good  reasons  the 
ileum  is  generally  believed  to  be  the  portal  of  entry,  but  as  opposed  to 
the  correctness  of  this  view  one  may  perhaps  adduce  the  early  bac- 
teremia (as  early  as  the  fourth  day)  when  changes  in  the  lymphoifl 
follicles  of  the  ileum  are  slight,  and  the  early  disappearance  of  bacilli 
from  the  feces:  they  are  believed  not  to  thrive  well  in  the  intestinal 
contents  and  those  present  not  improbably  come  from  the  gall-bladder 
and  the  bile  into  which  they  are  promptly  excreted  from  the  blood. 
Infection  by  way  of  the  gastro-intestinal  tract  results  from  the  swallow- 
ing of  infected  food  or  drink,  especially  water,  milk,  oysters,  and  the 
3 


34  BACTERIAL  INFECTIONS 

like.  The  drinking  water  usually  becomes  contaminated  by  soakage  of 
infected  sewage,  feces,  or  urine  into  wells,  cisterns,  springs,  reservoirs, 
rivers,  etc.  Milk  is  usually  contaminated  by  being  diluted  with  infected 
water,  or  by  being  put  into  utensils  washed  with  infected  water;  or  it 
becomes  infected  from  the  unclean  hands  of  dairy  attendants  or  other 
persons.  Derivatives  of  milk,  such  as  cream,  ice  cream,  butter,  etc.,  may 
also  serve  as  sources  of  infection,  as  well  as  articles  of  food  that  have 
been  washed  with  contaminated  water,  or  that  may  be  eaten  raw,  such 
as  oysters  fattened  in  polluted  streams,  and  lettuce,  celery,  etc.,  grown  in 
contaminated  ditches  or  watered  with  contaminated  water.  Food  may 
also  become  infected  by  flies  and  other  insects,  to  whose  feet  the  bacillus 
readily  adheres  or  whose  feces  may  contain  the  specific  germ.  This 
occurs  especially  in  rural  districts,  the  family  privy  vault  often  being 
the  source  of  infection ;  in  warm  climates ;  and  during  army  movements, 
the  flies  conveying  the  bacillus  directly  from  latrines  to  the  kitchen  or 
mess  table. 

Direct  transmission  from  the  sick  to  the  well  sometimes  occurs  (one- 
fourth  of  the  cases  Conradi),  and  is  apparently  the  only  cause  that  can 
be  assigned  for  some  cases  of  the  disease  occurring  in  nurses,  attend- 
ants, etc.  The  emanations  from  the  patient  are  not  necessarily  infective; 
but  the  stools,  urine,  etc.,  are  not  properly  disinfected,  and  infect  the 
bed-clothing,  the  patient's  personal  linen,  etc.,  and  these  being  incau- 
tiously handled,  serve  as  the  indirect  source  of  infection.  A  number  of 
cases,  even  restricted  epidemics,  have  recently  been  traced  to  so-called 
"carriers,"  subjects  of  past  typhoid  fever,  whose  feces  may  contain  the 
typhoid  bacillus  continuously  or  intermittently  (chronic  or  intermittent 
carriers).  The  feces  become  contaminated  from  the  gall-bladder,  which 
may  remain  a  permanent  habitat  of  the  bacillus. 

Infection  by  way  of  the  respiratory  tract  is  relatively  uncommon.  That 
it  is  possible  cannot  be  denied  (some  cases  of  apparently  primary  typhoid 
pneumonitis).  However,  bacilli  in  the  air  being  inhaled  are  usually 
arrested  in  the  pharynx  and  eventually  gain  the  gastro-intestinal  tract — 
whence  infection  occurs,  as  is  usual.  It  is  possible  that  in  rare  instances 
infection  may  occur  through  the  tonsil,  and  the  blood  thus  become 
primarily  infected  (certain  cases  of  typhoid  fever  without  intestinal 
lesions?). 

Pathology. — The  characteristic  macroscopic  lesions  of  typhoid  fever 
involve  the  solitary  and  agminate  lymph  follicles  of  the  intestine,  the 
mesenteric  and  other  lymph  nodes,  and  the  spleen.  The  typhoid  bacilli 
having  reached  the  intestine  doubtless  invade  the  lymphoid  tissues,  the  soli- 
tary and  agminate  follicles,  thence  the  mesenteric  lymph  nodes,  and  ulti- 
mately become  dispersed  through  the  lymphatic  and  the  blood  circulation 
and  all  the  organs  of  the  body.  The  changes  in  the  lymph  follicles  of  the 
intestine  are  commonly  said  to  exhibit  four  stages — infiltration,  necrosis, 
ulceration,  and  cicatrization — ^which  correspond  approximately  to  the 
four  weeks  of  the  disease,  but  approximately  only,  since  the  dift'erent 
processes  may  be  shortened  or  markedly  prolonged,  and  in  some  cases 


TYPHOID  FEVER  35 

the  lesions  may  not  proceed  beyond  infiltration,  resolution  occurring 
soon.  At  the  end  of  the  first  week,  Peyer's  patches  are  swollen,  hyper- 
emic,  and  the  seat  of  endothelial  and  lymphoid  proliferation.  They 
appear  as  flat,  raised  patches,  of  pinkish-gray  color,  somewhat  soft  in 
consistency,  and  with  a  smooth  or  rugous  surface.  During  the  second 
week  more  or  less  complete  necrosis  of  the  solitary  and  agminate  follicles 
takes  place — yellowish-green  and  greenish-brown  sloughs  (stained  with 
bile)  being  formed.  During  the  third  week,  by  a  process  of  ulcera- 
tion, the  slough  is  gradually  separated  and  a  more  or  less  characteristic 
ulcer  results.  These  ulcers  are  ovoid  in  shape  (Peyer's  patches),  their 
long  axis  being  in  the  direction  of  the  long  axis  of  the  bowel;  roundish 
ulcers  (solitary  follicles)  are  also  quite  frequently  seen.  The  edge  of  the 
ulcer  is  undermined,  its  floor  is  smooth  and  made  up  of  the  muscular 
coat  of  the  intestine  or  of  the  peritoneum.  In  some  cases  the  latter 
is  involved  in  the  necrotic  process  and  eventually  becomes  perforated. 
During  the  fourth  week  cicatrization  ensues;  it  may  be  complete  within 
a  week  or  ten  days,  or  it  may  be  unduly  protracted  and  become  chronic. 
Often  side  by  side  one  sees  lesions  in  different  stages  of  progress.  Some- 
times the  cicatrices  are  visible  for  years^ — as  a  thinning  of  the  mucous 
membrane,  absence  of  the  intestinal  villi,  and  the  presence  of  pigment. 

These  lesions  while  most  common  in  the  lymphoid  tissues  of  the 
intestine,  especially  of  the  lower  part  of  the  ileum,  occur  throughout  the 
body.  The  incidence  of  occurrence  in  different  parts  of  the  body  is  well 
exemplified  by  the  following  table,  compiled  by  Baer,  which  gives  in 
percentages  the  results  of  an  analysis  of  the  sites  of  ulcerations  in  over 
1400  typhoid-fever  necropsies :  Small  intestine  (any  part),  97.5;  ileum, 
89;  ileum  alone,  53.3;  ileum  (lower  half),  36.8;  large  intestine,  33.3; 
cecum,  30.3;  colon  (not  specific),  29.1 ;  larynx,  19.9;  ascending  colon,  10.3; 
sigmoid  flexure,  6.9;  ileocecal  valve,  6.7;  jejunum,  5.9;  large  intestine, 
alone,  5.6;  transverse  colon,  4.5;  a'sophagus,4.5;  descending  colon,  2.6; 
vermiform  appendix,  2.5;  rectum,  2.4;  pharynx,  2.2;  cases  without  ulcera- 
tion, but  proved  bacteriologically,  2.2;  stomach,  1.98;  Meckel's  diver- 
ticulum, 1.1;  trachea,  0.38;  duodenum,  0.3;  common  bile  duct,  0.23.  In 
some  cases  the  intestinal  lesions  are  widespread  and  extensive;  in  other 
cases  they  are  so  slight  as  to  be  scarcely  detectable;  in  some  cases  they 
are  altogether  absent — typhoid  fever  without  intestinal  lesions  (typhoid 
bacteremia  or  septicemia). 

The  mesenteric  lymph  nodes,  especially  those  corresponding  to  the 
portion  of  intestine  aftected,  become  hyperemic  and  swollen,  largely 
in  consequence  of  endothelial  and  lymphoid  proliferation.  Generally 
resolution  takes  place,  but  occasionally  they  V)ecome  softened  and 
necrotic,  and  may  rupture  into  the  peritoneum,  causing  peritonitis, 
or  they  may  become  caseous,  calcareous,  or  atrophic.  The  lymph 
nodes  throughout  the  body  sometimes  are  swollen,  and  the  superficial 
nodes  may  be  palpable.  The  spleen  becomes  markedly  enlarged 
(two  or  three  times  its  normal  size),  its  capsule  tense,  the  pulp  dark, 
reddish  brown  in  color,  and  almost  diffluent,  and  the  Malpighian  bodies 


36  BACTERIAL  INFECTIONS 

prominent.     Usually  it  returns  to  its  normal  condition,  but  infarction 
and  abscess  formation  may  ensue. 

Our  knowledge  of  the  nature  of  the  foregoing  lesions  has  been  much 
enhanced  by  the  studies  of  Mallory,  who  states  that  the  essential  lesion 
in  typhoid  fever  is  a  diffuse  proliferation  of  the  endothelial  cells  giving 
rise  to  large  epitheloid  cells  characterized  by  the  possession  of  marked 
phagocytic  properties,  and  that  while  this  proliferation  is  most  marked 
in  the  lymphoid  tissue  of  the  intestine,  the  mesenteric  lymph  nodes, 
the  spleen,  the  bone  marrow,  and  the  liver,  it  may  be  found  also  to  a 
varying  extent  in  all  the  lymphatic  vessels  of  the  body,  as,  for  instance, 
the  lymphatics  of  the  heart,  lungs,  testicles,  pia-arachnoid,  etc.     The 
cause   of   these  proliferative  changes   is   a  mild,  diffusible    toxin  (an 
endotoxin,    liberated    upon    disintegration    of     the    typhoid     bacilli) 
which  circulates  in  the  lymphatic  and  the  blood  stream.     The  swell- 
ing  of   the  lymphoid   nodes   of    the  intestine,  the  mesenteric   nodes, 
and  the  spleen  is  due  almost  entirely  to  these  phagocytic  cells,  and 
the  necrosis  is  purely  accidental,  resulting  from  occlusion  of  the  veins 
and  capillaries  by  fibrinous   thrombi  the   consequence   of    degenera- 
tion of  phagocytic  cells  beneath  the  lining  endothelium  of  the  vessels. 
These  phagocytic  cells  enter  the  general  circulation,  passing  through 
the  liver  and  the  lungs,  on  the  one  hand,  and  through  the  thoracic  duct, 
on  the  other.     Focal  collections  of  these  cells  are  found  in  different 
organs,  the  liver,  the  kidneys,  the  heart,  the  testicles,  where  they  obstruct 
either  the  capillaries,  the  veins,  or  the  lymphatics.     Certain  noteworthy 
changes  occur  in  the  bone  marrow,  as  has  recently  been  pointed  out  by 
Longcope:  lymphoid  proliferation,  large  phagocytes,  foci  of  necrosis, 
more  or  less  hyperplasia  of  the  blood-forming  cells,  and,  in  the  fatal  cases, 
diffuse  degenerative  changes  of  the  blood-forming  cells,  associated  with 
marked  oedema  and  congestion.     Longcope  suggests  that  these  changes 
may  be  in  some  way  related  to,  and  perhaps  responsible  for,  the  leuko- 
penia of  typhoid  fever. 

In  addition  to  the  foregoing  essential  and  characteristic  lesions  of 
typhoid  fever,  others  often  occur — the  result  of  long-continued  fever 
and  toxemia  and  of  secondary  infection  with  pyococci — such  as  paren- 
chymatous degeneration  of  the  liver,  kidneys,  heart,  voluntary  muscles 
(Zenker's  degeneration,  especially  of  the  abdominal  muscles  and  the 
adductors  of  the  thigh),  etc.  A  mild  grade  of  interstitial  hepatitis  some- 
times develops;  the  so-called  lyrnphomatous  or  acute  interstitial  non- 
suppurative nephritis  may  occur;  the  gall-bladder  may  become  inflamed, 
ulcerated,  and  even  perforated  (usually  infection  by  way  of  the  portal 
circulation);  laryngeal  ulceration  may  progress  to  and  cause  ulceration 
of  the  cartilages'^  and  perichondritis;  hypostatic  congestion  of  the  lungs, 
and  lobular  or  lobar  pneumonia  or  pleuritis  may  supervene;  cystitis  and 
pyelitis,  due  to  typhoid  bacilluria,  may  arise;  and  thrombosis,  especially 
of  the  veins  of  the  lower  extremity,  said  by  Mallory  to  be  due  to  the 
same  sort  of  lesions  that  cause  occlusion  of  the  vessels  in  the  intestine, 
may  occur.     In  addition,  abscesses  in  different  parts  of  the  body,  peri- 


TYPHOID  FEVER  37 

ostitis,  peripheral  neuritis,  meningitis,  orchitis,  parotitis,  etc.,  have  been 
observed.  These,  though  often  the  consequence  of  mixed  infection  with 
pyococci,  are  sometimes  due  to  the  typhoid  bacillus  alone,  and,  as  for 
instance  in  periostitis,  they  may  remain  dormant  for  a  long  time^months 
and  years. 

In  the  living  subject  the  typhoid  bacilli  may  be  found  in  the  stools, 
especially  from  the  end  of  the  first  to  the  middle  of  the  third  week,  during 
some  relapses,  and  sometimes  for  months  or  years  after  an  attack  of 
typhoid  fever  (so-called  typhoid  carriers);  in  the  urine,  especially  in  cases 
of  albuminuria,  sometimes  for  long  periods,  even  months,  after  con- 
valescence; in  the  gall-bladder,  during  and  for  months  or  years  after 
an  attack  of  typhoid  fever  (the  usual  habitat  of  the  organisms  in  the 
chronic  typhoid  carriers);  in  the  blood  from  the  spleen,  the  rose  spots, 
and  the  peripheral  circulation;  sometimes  in  the  sputum;  in  the  cerebro- 
spinal fluid  in  the  event  of  certain  complications,  etc.  In  many  of  the 
complications  and  sequels,  especially  in  post-typhoidal  abscesses  of  the 
bones,  subcutaneous  tissues,  etc.,  the  bacilli  may  also  be  found,  but 
they  are  usually  associated  with  different  pyococci.  After  death  the 
typhoid  bacilli  have  been  found  in  the  intestine,  Peyer's  patches,  mesen- 
teric lymph  nodes,  spleen,  liver,  kidneys,  meninges,  myocardium,  bone 
marrow,  blood,  lymph,  and  divers  complicating  lesions. 

Symptoms. — The  period  of  incubation  varies,  as  a  rule,  between  ten 
and  fourteen  days,  but  it  may  be  as  short  as  five,  or  as  long  as  twenty- 
one  or  more  days.  Occasionally  this  period  is  unannounced  by  symp- 
toms. Usually,  however,  there  are  prodromes,  such  as  malaise  that 
increases  with  the  onset  of  the  febrile  stage,  headache,  insomnia,  anorexia, 
sometimes  diarrhoea,  and,  especially  in  children,  vomiting.  In  most 
cases  the  onset  of  the  disease  is  insidious,  the  patient  complaining  of 
gradually  increasing  malaise,  disinclination  to  exertion,  headache,  neuro- 
muscular pains  in  the  back  and  limbs,  anorexia,  epistaxis,  possibly 
chilly  sensations  and  feverishness ;  finally,  he  takes  to  bed — from  which 
day  we  date,  though  often  incorrectly,  the  onset  of  the  disease.  Occa- 
sionally the  onset  is  sudden  and  manifested  by  severe  headache,  pains  in 
the  back  and  legs,  chills  that  may  be  repeated,  marked  prostration,  etc. 

During  the  first  week  the  symptoms  mentioned  become  aggravated; 
the  temperature  rises  in  a  characteristic  step-ladder  manner;  the  tongue, 
though  it  remains  moist,  becomes  furred;  the  pulse  becomes  increased  in 
frequency  (90  to  100);  there  is  thirst;  the  abdomen  becomes  distended  and 
tender  on  pressure;  though  there  may  be  diarrhoea,  constipation  is  the 
more  likely;  and  there  may  be  slight  cough  due  to  broncliitis. 

At  the  end  of  the  first  week,  sometimes  by  the  fourth  or  fifth  day,  the 
fastigium  is  reached.  All  of  the  symptoms  become  aggravated;  tlie 
temperature  reaches  its  highest  point  (usually  103°  to  104°  F.),  and 
it  remains  high,  the  daily  remissions  being  less  than  during  the  first 
week;  the  pulse  becomes  accelerated,  90  to  110,  and  dicrotic  (an  early 
feature) ;  the  headache  gives  way  to  mental  hebetude  and  later  to  delirium, 
especially  at  night;  the  patient  is  often  quite  deaf;  and  the  typhoid  state 


38  BACTERIAL  INFECTIONS 

frequently  supervenes.  The  skin  is  usually  hot  and  diy,  but  frequent 
attacks  of  profuse  perspiration,  followed  by  sudamina,  may  occur. 
About  the  eighth  day  of  the  disease  a  number  of  rose-colored  spots, 
that  are  quite  pathognomonic,  appear  on  the  abdomen,  the  chest,  and 
frequently  elsewhere,  especially  on  the  back.  The  spleen  is  enlarged,  dis- 
tinctly palpable,  and  somewhat  tender.  The  tongue  becomes  dry  and 
later  fissured,  and  sordes  may  form  on  the  teeth  and  gums.  The  abdo- 
men may  become  markedly  distended,  gurgling  in  the  right  iliac  fossa 
may  develop,  and  the  constipation  may  give  way  to  diarrhoea.  The 
stools  are  of  a  pale  yellow^  (pea-soup)  color  and  highly  malodorous 
(characteristic  t}-phoid  stool).  The  fastigium  usually  lasts  from  ten 
days  to  two  weeks. 

Toward  the  end  of  the  fastigium,  that  is,  in  the  third  week,  the  typhoid 
state  becomes  more  pronounced,  and  the  pulse  more  rapid,  110  to  130 
or  more;  the  temperature,  previously  continuous,  becomes  remittent, 
and  usually  somewhat  lower  than  during  the  second  week;  and  any  of 
the  many  complications  may  arise.  In  favorable  cases  at  about  the 
twenty-first  day  of  the  disease  (the  commencement  of  the  fourth  week) 
the  stage  of  decline  or  defervescence  sets  in.  The  fever  lessens  and 
finally  becomes  intermittent  with  less  and  less  diurnal  variations;  the 
local  and  general  s}Tiiptoms  abate ;  and  convalescence  ensues. 

From  the  foregoing,  which  represents  in  outline  the  course  of  an 
ordinary  or  average  case  of  t}^hoid  fever,  there  are  many  departures;  the 
symptoms  vary  much  with  the  virulence  of  the  infecting  microorganisms, 
the  resistance  of  the  individual,  and  the  presence  or  absence  of  compli- 
cations and  secondary  infections — due  usually  to  pyogenic  cocci. 

The  Fever. — In  the  majority  of  cases,  during  the  first  four  or  five 
days  of  the  disease,  a  daily  increase  of  temperature  of  1.5°  to  2°  F., 
and  a  morning  remission  of  from  1°  to  1.5°  F.,  occur — producing  what 
is  spoken  of  as  the  step-ladder  or  zig-zag  course  of  the  fever  (Fig.  1), 
The  temperature  usually  reaches  its  maximum  on  the  fourth,  fifth,  or 
sixth  day.  Then  follow^s  the  fastigium,  which  lasts  usually  from  ten  to 
fourteen  days,  and  during  which  the  temperature  is  more  uniform  and 
of  the  continuous  type,  the  morning  temperature  being  102°  to  103°  F., 
and  the  evening  from  103°  to  104°  F.,  or  higher.  In  ordinary  eases 
toward  the  end  of  the  fastigium  (thirteenth  to  sixteenth  day)  the  tem- 
perature becomes  remittent,  and  the  evening  rise  shows  some  tendency 
to  be  less  marked.  At  the  end  of  the  fastigium  (sixteenth  to  twenty- 
first  day)  the  temperature  is  usually  intermittent ;  the  morning  temperature 
approaching  if  not  quite  reaching  the  normal,  and  the  evening  tem- 
perature being  101°  to  101.5°  or  102°  F.  Gradually  the  evening 
temperature  also  becomes  normal.  In  cases  of  moderate  severity 
the  temperature  may  begin  to  decline  at  the  end  of  the  second  week 
and  soon  reach  normal;  in  severe  cases  it  may  remain  high  (104°  to 
105°  F.)  in  the  evening  throughout  the  third  week,  even  into  the  fourth 
week,  and  then  gradually  decline.  Defervescence  occurs  usually  by 
lysis,  rarely  by  slow  crisis. 


TYPHOID  FEVER 


39 


Variations  in  the  course  of  the  temperature,  however,  are  quite 
common.  Thus,  the  early  step-ladder  rise  may  be  missed.  During 
the  greater  part  of  the  fastigium  the  temperature  may  be  105°  to 
106°  F.  or  more  (hyperpyrexia).  Even  higher  temperatures  are 
occasionally  met  with— 107°,  109°,  110°  F.,  especially  in  the  event 
of  certain  complications,  such  as  pneumonia,  septic  manifestations, 
pyococcic  infections,  etc.  Again,  the  fever  may  be  unduly  protracted, 
continuing  four,  five,  six,  or  more  weeks — usually  the  consequence  of 
certain  inflammatory  complications  (secondary  infections),  such  as 
suppurating  mesenteric  lymph  nodes,  or  sluggish  intestinal  ulcers,  post- 
typhoidal    anemia,    intestinal    auto-intoxication,    etc.     Sometimes    the 


Fig.  1 


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F. 
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DAY  OF 

1       2 

3 

4 

5 

6 

7 

8 

9 

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12 

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14 

15 

16 

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18 

19 

20 

21 

PULSE 

90  TO  120-DICROTIC  PULSE 

J^ 

A\y 

'h^ 

BLOOD   EXAM.    WIDAL  REACT.      ABSFNCE  OF  LEUCOCYTOSIS 
ANAEMIA    REDUCTION  OF  R.  B.C.      GREATER  REDUCTION  OF  H/tMAGLOBIN. 


The  temperature  curve  and  the  chief  symptoms  in  typhoid  fever.    (Musser.) 

temperature  is  distinctly  intermittent  throughout  the  course  of  the 
disease,  even  in  the  absence  of  complicating  malaria.  In  other  cases  the 
fever  may  be  slight  throughout  the  entire  course,  or  the  temperature  may 
be  scarcely  above  normal  (apyrexial  form),  or  even  subnormal.  It  is 
quite  often  subnormal  during  convalescence. 

Sudden  temporary  falls  of  temperature  are  sometimes  met.  They 
are  due  to:  (1)  Intestinal  hemorrhage;  (2)  intestinal  perforation;  (3) 
cardiac  failure  or  vasomotor  collapse;  (4)  abortion  or  premature  lal)or; 
(5)  the  use  of  coal-tar  products;  (6)  ill-understood  nervous  factors;  and 
(7)  they  sometimes  occur  without  obvious  cause. 

Post-typhoidal  elevations  of  temperature  (recrudescences)  are  quite 
common.     They  sometimes  occur  during  the  period  of  defervescence, 


40  BACTERIAL  INFECTIONS 

but  more  frequently  during  convalescence — after  the  morning  and 
evening  temperatures  have  been  normal  for  several  days.  The  recrudes- 
cence often  occurs  rather  suddenly,  the  temperature  may  reach  a 
high  grade  (103°  to  105°  F.),  but  usually  it  subsides  within  three  or  four 
days,  although  it  may  last  a  week.  Such  recrudescences  are  attrib- 
utable to  dietetic  errors,  constipation  (auto-intoxication),  emotion  and 
excitement  attending  the  visits  of  too  solicitous  friends,  etc.  If  pro- 
tracted the  fever  is  significant  of  some  complication,  or  of  anemia,  or 
it  may  be  what  has  been  aptly  termed  "bed  fever" — due  to  low  diet 
and  too  prolonged  stay  in  bed. 

Chills,  according  to  Osier,  occur  (a)  sometimes  with  the  fever  of  onset; 
(b)  occasionally  at  intervals  throughout  the  course  of  the  disease,  and 
followed  by  sweats  (so-called  sudoral  form);  (c)  with  the  advent  of 
complications,  pleurisy,  pneumonia,  otitis  media,  periostitis,  etc.;  (d) 
with  active  antipyretic  treatment  by  the  coal-tar  products-;  (e)  occasion- 
ally during  the  period  of  defervescence  without  relation  to  any  complica- 
tion or  sequel,  probably  due  to  septic  infection;  (J)  according  to  Herring- 
ham,  chills  may  result  from  constipation;  there  are  some  cases  in  which 
during  the  latter  half  of  the  disease  chills  recur  with  great  severity. 

Skin. — In  from  75  to  85  per  cent,  of  all  cases  a  characteristic  roseolous 
rash  appears  on  the  body  on  from  the  seventh  to  the  ninth  day;  rarely 
it  may  be  delayed  to  the  twelfth  day.  It  consists  of  isolated,  circular, 
slightly  elevated  macules  or  maculo-papules,  from  2  to  4  mm.  in  diameter. 
They  are  found  almost  always  on  the  trunk,  especially  on  the  abdomen 
and  the  lower  chest ;  but  their  absence  should  not  be  certified  to  until  the 
back  has  been  thoroughly  examined.  Sometimes  they  are  present  on 
the  arms  and  the  legs,  and  the  face;  occasionally  in  large  numbers.  They 
disappear  upon  pressure  and  reappear  immediately  the  pressure  is 
removed.  Usually  they  come  out  in  successive  crops,  each  crop  con- 
sisting, as  a  rule,  of  from  six  to  a  dozen  or  more  spots.  Each  spot  lasts 
about  four  or  five  days,  so  that  fading  spots  are  seen  side  by  side  with 
others  of  a  newer  crop.  They  continue  to  appear  until  the  end  of  the 
second  week;  sometimes  even  in  the  third  week,  and  occasionally  during 
convalescence;  and  they  are  not  infrequently  observed  during  a  true 
relapse.  In  some  cases  they  are  entirely  absent;  in  other  cases  they 
are  numerous  and  cover  the  entire  body.  When  numerous  they  are 
usually  darker  than  when  fewer;  occasionally  they  are  hemorrhagic. 
A  fine,  furfuraceous  desquamation  is  not  infrequent;  occasionally  the 
desquamation  is  flaky. 

Other  eruptions  are  often  encountered.  Thus  sudamina  and  miliaria 
are  common,  especially  during  the  second  and  the  third  weeks;  they 
are  usually  associated  with  profuse  perspiration  and  not  infrequently 
with  chills — sudoral  typhoid,  of  the  French.  A  diffuse  scarlatiniform 
erythematous  rash  (in  some  cases  undoubtedly  a  drug  eruption)  has 
sometimes  been  observed,  especially  during  the  first  week.  ]\Iorb ill i form 
rashes,  urticaria,  and  herpes  are  occasionally  seen.  Rarely  one  en- 
counters, especially  on  the  abdomen,  small   bluish  spots   that  do  not 


TYPHOID  FEVER  41 

disappear  on  pressure  (maculae  cerulese,  laches  hleuatres  of  Trousseau, 
or  peliomas) ;  they  have  been  attributed  to,  but  are  probably  not  always 
due  to,  pediculi.  Again,  petechiiie  and  purpuric  spots  occur,  especially 
in  debilitated  subjects;  and  rarely  even  extensive  gangrenous  dermatitis 
(due,  doubtless,  to  infection  of  the  skin),  of  which  I  have  seen  a 
number  of  cases.  More  or  less  extensive  furunculosis  is  not  uncommon. 
Bed  sores  are  not  so  common  as  formerly — due  to  improved  nursing; 
but  they  may  occur  in  debilitated  subjects,  especially  if  the  disease  be 
protracted.  Loss  of  the  hair  and  cessation  of  the  growth  of  the  nails  are 
not  uncommon.  QEdema  of  the  skin  and  subcutaneous  tissues  may 
result  from  venous  thrombosis,  anemia,  or  nephritis. 

Digestive  System. — The  tongue  is  usually  coated  throughout  the 
course  of  the  disease;  at  first  moist,  it  soon  becomes  dry,  swollen,  brown, 
and  fissured.  I  have  seen  severe  acute  glossitis.  The  gums  are  not 
infrequently  covered  with  sordes  (epithelial  debris,  food  particles, 
bacteria,  etc.).  Stomatitis  progressing  to  hemorrhage  and  ulceration 
may  ensue.  Parotitis,  unilateral  or  bilateral,  and  due  to  extension  of 
infection  along  Stenson's  duct  or  rarely  to  metastatic  pyogenic  infection, 
is  occasionally  observed.  Extension  of  infection  along  the  Eustachian 
tube  may  result  in  suppurative  median  otitis.  Cancrum  oris  is  rare; 
I  have  seen  a  case  from  which  the  diphtheria  bacillus  was  isolated. 
Sore  throat  is  sometimes  complained  of;  the  tonsils  may  be  swollen 
and  congested,  and  present  whitish  spots  of  lacunar  or  other  inflamma- 
tion which  may  proceed  to  ulceration  (tonsillar  typhoid).  Catarrhal 
and  ulcerative  pharyngitis  and  oesophagitis  are  by  no  means  infrequent, 
and  may  be  followed  by  stenosis.  Anorexia  is  the  rule.  Nausea  and 
vomiting  are  unusual,  although  they  may  be  present  at  the  outset,  and 
have  been  known  to  recur  about  the  third  week  or  to  continue  throughout 
the  course  of  the  disease,  and  to  contribute  to  the  fatal  issue.  The 
gastric  juice  is  deficient  in  amount,  and  hydrochloric  acid  is  usually 
much  diminished  or  absent.  While  diarrhoea  may  be  present  at  the 
beginning  and  continue  throughout  the  course  of  the  disease,  constipa- 
tion is  the  rule  at  the  onset  and  not  infrequently  persists.  Usually, 
however,  at  about  the  end  of  the  second  week,  if  not  earlier,  diarrhoea 
(four  to  ten  or  more  stools  in  the  twenty-four  hours)  appears;  but  even 
marked  constipation  may  be  present  with  even  extensive  ulceration  of  the 
ileum.  The  diarrhoeic  stools  are  quite  characteristic:  of  the  color  and 
consistency  of  pea-soup,  alkaline,  and  very  malodorous;  usually  they 
separate  on  standing  into  an  upper  turbid  liquid  layer,  and  a  lower  thick 
sedimentary  layer,  consisting  of  partly  digested  food,  desquamated, 
epithelial  cells,  necrotic-tissue  elements,  blood  corpuscles,  granular  debris, 
triple  phosphate  crystals,  and  numerous  bacteria.  Cultures  may  reveal 
the  typhoid  bacillus. 

Tympanites  is  common,  but  rarely  nowadays  so  marked  as  to  be 
grave.  When  marked,  by  interfering  with  the  action  of  the  diaphragm, 
it  occasions  dyspnoea,  and  may  embarrass  the  heart,  and  also  favor 
intestinal  perforation.     Gurgling  and  pain  on  pressure  may  be  found 


42  BACTERIAL  INFECTIONS 

in  the  right  iliac  fossa.  Spontaneous  pain  in  the  abdomen  is  present  in 
about  one-third  of  the  patients,  and  contrary  to  former  opinions  accord- 
ing to  which  it  was  believed  always  to  indicate  or  suggest  perforation 
and  peritonitis,  it  may  be  due  to  a  wide  variety  of  diseased  conditions : 
it  is  not  infrequently  due  to  extra-abdominal  conditions,  such  as  pleurisy 
or  pneumonia,  or  even  femoral  phlebitis ;  it  is  a  not  infrequent  concomi- 
tant of  an  enlarged  spleen,  of  a  distended  urinary  bladder,  of  severe 
diarrhoea  or  marked  constipation,  and  sometimes  it  attends  intestinal 
hemorrhage.  Usually,  however,  it  suggests  serious  complications,  of 
which  the  most  important  are  intestinal  perforation,  appendicitis,  and 
cholecystitis. 

Intestinal  hemorrhage  occurs  in  from  3  to  7  per  cent,  of  the  cases. 
It  is  rarer  in  children.  It  may  occur  at  the  end  of  the  first  week,  when  it 
is  usually  slight  and  due  to  marked  congestion;  usually  it  occurs  toward 
the  end  of  the  second  week,  or  during  the  third  week,  or  later.  The 
hemorrhage  may  occur  once  or  repeatedly;  and  the  amount  of  blood 
lost  may  be  so  slight  as  almost  if  not  quite  to  elude  detection,  or  so  extreme 
as  to  lead  immediately  to  a  fatal  termination  (a  rather  unusual  event). 
Slight  hemorrhages  are  unattended  by  subjective  symptoms;  large 
hemorrhages  are  indicated  by  sudden  and  rapid  fall  of  the  temperature 
(2°  to  8°  F.),  pallor,  a  sensation  of  faintness,  a  rapid  and  small  pulse, 
low  and  falling  blood  pressure,  extreme  prostration,  and  visible  blood 
in  the  stools  (though  even  death  may  occur  without  the  discharge  of 
blood  from  the  bowel).  Clinically,  a  single,  even  rather  large,  hemor- 
rhage is  not  necessarily  a  serious  phenomenon,  since  patients  often 
improve  after  a  hemorrhage,  especially  when  it  occurs  early;  but 
repeated  hemorrhages  are  likely  to  lead  to  a  fatal  termination. 

Perforation  occurs  in  from  3  to  4  per  cent,  of  the  cases,  and  is  re- 
sponsible for  one-fourth  or  more  of  the  deaths.  It  bears  no  direct 
relationship  to  the  severity  of  the  infection,  since  it  is  not  infrequent  in 
mild  cases,  although  most  common  in  the  severer  infections,  especially 
those  attended  by  tympanites  and  hemorrhage.  It  is  more  common  in 
males  than  in  females,  and  is  rare  in  children.  Although  it  may  occur 
at  any  time  during  the  course  of  the  disease,  even  during  the  first  week 
as  well  as  very  late  during  protracted  convalescence  or  relapses,  at  least 
one-half  of  the  cases  occur  during  the  second  and  the  third  weeks  (most 
commonly  in  the  third  week).  The  perforation  involves  the  ileum  in 
88  per  cent,  of  the  cases,  the  colon  in  4.7  per  cent.,  and  the  vermiform 
appendix  in  4.7  per  cent.  (Scott). 

The  symptoms  of  the  perforation  are  those  of  the  rupture  (which  rarely 
occurs  almost  if  not  quite  unannounced)  and  those  of  the  consecutive 
peritonitis  (which  I  have  several  times  seen  at  necropsy  without  note- 
worthy clinical  signs).  The  most  important  symptom  of  the  perfora- 
tion is  pain  (scarcely  missed  unless  the  patient  is  comatose),  wliich 
usually  comes  on  suddenly,  is  sharp  and  paroxysmal  in  character,  com- 
monly situated  in  the  right  lower  abdominal  quadrant,  and  not  infre- 
quently increases  in  severity  for  some  time.     Concurrent  with  the  pain 


TYPHOID  FEVER  43 

there  are  often  the  usual  evidences  of  collapse  (fall  of  the  temperature 
often  to  or  below  the  normal,  increased  frequency  and  smallness  of  the 
pulse,  vomiting,  pallor,  perspiration,  etc.),  and  subsequently  the  ordinary 
manifestations  of  peritonitis.  These  comprise  local  pain,  tenderness,  and 
rigidity  of  the  abdominal  muscles,  and,  as  a  rule,  increasing  abdominal 
distention  and  limitation  of  the  respiratory  movements.  Replacement  of 
the  liver  flatness  by  tympany  is  of  value  only  when  it  develops  rapidly 
and  is  present  in  a  flat  or  slightly  distended  abdomen,  and  when  by 
changing  the  posture  of  the  patient  flatness  and  tympany  alternate; 
even  marked  tympany  may  be  due  merely  to  intestinal  distention. 
Peritoneal  exudate  may  occasion  dulness  in  the  flanks,  which  may  shift 
its  position  with  change  in  the  posture  of  the  patient,  and  may  even  be 
recognizable  by  rectal  examination.  Auscultation  may  reveal  peri- 
toneal frictions,  sometimes  within  a  few  hours;  later  there  may  be  an 
entire  absence  of  peristaltic  sounds  and  movements.  The  general 
signs  of  peritonitis  are  often  relatively  inconspicuous  as  contrasted  with 
the  local  signs.  As  a  rule,  however,  the  Hippocratic  facies,  pallid,  dusky, 
pinched,  and  clammy,  is  present;  the  temperature  soon  rises  (after  the 
initial  fall)  and  becomes  intermittent;  the  pulse-rate  and  the  respiration- 
rate  become  increased;  and  hiccough  and  vomiting  sometimes  develop. 
Leukocytosis  is  a  valuable,  though  inconstant,  sign. 

Peritonitis  may  be  due  also  to  infection  passing  through  an  ulcer 
that  has  not  perforated;  to  gangrene  of  the  intestine;  to  softening  and 
rupture  of  a  mesenteric  or  retroperitoneal  lymph  node;  to  splenic 
infarction  and  abscess;  to  a  twisted  and  necrotic  Meckel's  diverticulum; 
to  cholecystitis,  appendicitis,  salpingitis,  etc.  The  swollen  mesenteric 
lymph  nodes  are  sometimes  palpable  through  the  abdominal  wall. 

The  liver  is  often  enlarged  from  cloudy  swelling,  and  is  occasionally 
somewhat  tender.  Jaundice  is  occasionally  observed;  it  may  be  a  toxic 
process  or  due  to  cholangitis  and  obstruction.  Cholecystitis  is  quite 
common,  and  may  occur  during  the  course  of  the  disease  or  during 
convalescence — when  the  local  signs  being  in  abeyance  the  condition  is 
not  infrequently  thought  to  be  a  "relapse."  The  symptoms,  as  a  rule, 
however,  consist  of  local  pain,  tenderness,  and  muscular  rigidity,  and 
a  palpably  enlarged  gall-bladder;  vomiting  sometimes  occurs  at  the 
onset;  jaundice  is  inconstant.  Perforation  of  the  gall-bladder  is  re- 
vealed by  pain,  fall  of  temperature,  collapse,  and  consecutive  peritonitis. 
Typhoid  bacilli  are  often  found  in  the  gall-bladder  after  death  in  the 
absence  of  local  disease,  and  it  is  to  such  latent  biliary  infection  that 
many  of  the  cases  of  true  relapse  are  attril)utable.  Cholelithiasis  not 
infrequently  follows  typhoid  fever,  and  from  the  gallstones  tiie  typhoid 
bacilli  have  been  cultivated.  I  have  observed  several  cases  of  primary 
typhoid  cholecystitis  (recovery  of  the  typhoid  bacillus)  without  other 
evidences  of  typhoid  infection.  Suppurative  cholangitis,  suppurative 
pylephlebitis,  and  liver  abscess  have  occasionally  been  observed. 

Respiratory  System. — Epistaxis  is  a  sigin"flcant  symptom  of  the  <>!wly 
stages  of  typhoid  fever,  and  occurs  usually  at  the  end  of  the  first  ami  the 


44  BACTERIAL  INFECTIONS 

beginning  of  the  second  week.  A  simple  laryngitis  is  not  very  uneomnion. 
(Edema,  ulceration,  perichondritis,  and  paralysis  of  the  larjmx  are 
quite  rare.  Bronchitis  is  a  part  of  the  disease,  and  one  of  the  early 
manifestations.  It  is  usually  slight  or  moderate  in  degree  only,  and 
revealed  by  cough,  slight  expectoration,  harsh  vesicular  breath  sounds, 
and  a  few  sibilant  and  fine  bubbling  rales.  Rarely  the  finer  tubes  are 
involved — whence  bronchopneumonia  may  supervene.  Bronchopneu- 
monia may  also  follow  oedema  and  congestion  of  the  lungs,  which  are  by 
no  means  uncommon  during  the  second  and  third  weeks ;  during  the  same 
periods,  when  the  patient  is  more  or  less  stuporous,  an  aspiration  pneu- 
monia is  not  infrequent.  True  croupous  pneumonia  may  also  occur  during 
the  later  half  of  the  disease,  and  is  a  serious  complication.  Occasion- 
ally it  is  an  initial  manifestation — pneumotyphoid  (pneumonia  due  to  the 
typhoid  bacillus,  with  t^-phoid  bacilli  in  the  sputum);  in  this  event  the 
early  signs  are  those  of  pneumonia,  the  intestinal  and  other  manifesta- 
tions of  t}^hoid  fever  only  developing  later.  Pulmonary  abscess  or 
gangrene  and  pneumothorax  are  rare  sequels.  Pleurisy  may  be  primary 
or  secondary:  secondary  to  any  of  the  aforementioned  pulmonary 
conditions;  primary  and  due  to  direct  infection  with  the  typhoid  bacillus 
— ^pleurotyphoid.  Occurring  early,  the  lesions  are  usually  dry  or  serous, 
later  often  purulent.  The  bronchial  l}Tnph  nodes  have  been  known  to 
soften  and  suppurate. 

Circulatory  System. — ^The  pulse  is  usually  increased  in  frequency, 
though  not  proportionately  to  the  fever.  During  the  first  week  it  is 
less  than  100,  as  a  rule;  in  the  second  week  it  commonly  fluctuates 
below  110  and  becomes  dicrotic  (an  early  and  quite  characteristic  feature). 
With  the  progress  of  the  disease  the  evidences  of  vasomotor  paresis 
become  manifest — low  blood  pressure,  increased  frequency  of  the  pulse 
(130  or  more  sometimes),  which  often  becomes  running  or  thready, 
capillary  stasis  (coldness  and  lividity  of  the  extremities),  overfilling  of 
the  splanchnic  vessels,  anemia  of  the  cerebral  vessels,  and  sometimes 
vasomotor  collapse.  As  convalescence  sets  in  vasomotor  tone  is  restored, 
and  the  pulse  becomes  slower,  fuller,  and  stronger;  during  convalescence 
the  pulse  is  often  unusually  slow  (a  characteristic  feature).  Changes 
in  the  heart  muscle  (parenchymatous  degeneration,  and  acute  interstitial 
myocarditis)  are  common.  Often  the  only  noteworthy  clinical  manifesta- 
tion is  feebleness  of  the  first  sound  of  the  heart.  When  more  marked, 
however,  there  is  not  infrequently  gallop  rhythm,  or  embryocardia, 
or  dilatation  of  the  heart  (systolic  murmur,  increase  of  the  dulness,  etc.). 
Endocarditis  and  pericarditis  are  uncommon,  but  not  unknown. 

Venous  thrombosis,  especially  of  the  lower  extremity  (femoral,  pop- 
liteal, saphenous,  or  superficial  veins),  is  not  infrequent,  particularly 
during  convalescence.  It  may  be  due  to  thrombophlebitis  (in  which 
event  the  typhoid  bacillus  may  be  cultivated  from  the  vein  and  the 
clot),  or  to  cardiac  weakness  and  slowing  of  the  circulation;  the 
more  common  occurrence  of  the  thrombosis  in  tlie  left  leg  may  be 
due  to  the  pressure  exerted  by  the  right  iliac  artery  crossing  the  left 


TYPHOID  FEVER  45 

iliac  vein,  as  well  as  to  congenital  adhesions,  which  are  ten  times  as 
common  in  the  left  as  in  the  right  iliac  vein.  The  thrombosis  is 
evidenced  by  swelling  and  oedema  of  the  leg,  and  by  pain  and  tender- 
ness along  the  course  of  the  involved  vein.  The  process  usually  subsides 
without  ill  effects,  but  it  may  require  a  long  time,  and  embolism  of  the 
pulmonary  artery,  ensuing  on  dislodgement  of  the  thrombus,  has  been 
known  to  result  in  death.  Infarcts  of  the  internal  organs  are  not  very 
uncommon,  and  may  result  from  arterial  thrombosis  or  embolism. 
Gangrene  sometimes  results  from  occlusion  of  one  of  the  larger  arteries, 
and  a  number  of  cases  of  more  or  less  local  (though  sometimes  wide- 
spread) gangrene  unrelated  to  definite  vascular  distribution  have 
been  reported;  they  are  probably  due  to  secondary  infisction  of  the  skin 
(gangrenous  dermatitis).     Heart  clot  is  rather  unusual. 

Blood  and  Hemopoietic  System. — Leukopenia  is  present  through- 
out the  disease,  except  in  the  event  of  complications,  although  a  temporary 
increase  in  the  leukocytes  in  the  peripheral  circulation  is  not  infrequently 
produced  by  the  cold  baths.  With  the  leukopenia  there  is  a  dispro- 
portionate increase  of  the  large  mononuclear  leukocytes  and  a  reduction 
of  the  polynuclear  neutrophiles  (to  60  per  cent,  or  less).  An  increase 
of  the  polynuclear  neutrophiles  is  often  an  early  manifestation  of  in- 
flammatory complications  (perforation,  cholecystitis,  etc.)  and  may 
be  present  with  little  or  no  increase  in  the  total  number  of  leukocytes. 
The  blood  serum  agglutinates  the  typhoid  bacillus  (Gruber-Widal 
reaction).  During  the  later  half  of  the  disease  a  rather  well-marked 
anemia  usually  develops;  during  convalescence  this  may  assume  a  high 
grade  and  constitute  a  serious  feature  (post-typhoidal  anemia).  The 
spleen  is  enlarged  and  palpable  in  at  least  three-fourths  of  the 
cases.  It  may  extend  two,  three,  or  more  finger  breadths  beyond  the 
free  margin  of  the  ribs,  and  it  is  not  infrequently  quite  tender.  The 
enlargement  is  sometimes  missed  in  elderly  subjects  and  in  the  event  of 
perisplenitis.  I  have  seen  infarction  and  abscess  of  the  spleen ;  rupture 
has  been  reported.  The  superficial  lymph  nodes  throughout  the  body 
are  sometimes  palpably  enlarged. 

Nervous  System. — Persistent  headache  (usually  temporal  and 
occipital)  is  a  prominent  and  significant  symptom  of  the  first  week,  and 
is  often  associated  with  severe  pains  and  aching  in  the  back  and  legs. 
During  this  period  also  restlessness  and  insomnia  are  likely  to  be  present, 
and  are  often  distressing.  Sometimes  the  patient  is  quite  deaf.  The 
pupils  are  usually  markedly  dilated.  Gradually,  in  most  cases,  as  the 
patient  succumbs  to  the  toxemia,  that  is,  during  the  second  week,  the 
headache,  restlessness,  and  insomnia  are  replaced  by  mental  dulness, 
hebetude,  and  delirium,  which  vary  considerably  in  different  cases,  and 
in  the  beginning  at  least  are  usually  most  marked  at  night.  The  patient 
becomes  listless  and  a])athetic,  and  is  more  or  less  unconscious  of  his 
surroundings,  althougli  he  may  lie  for  hours  at  a  time  with  his  eyes  wide 
open  (coma  vigil);  he  frecpiently  mutters  constantly,  picks  at  the  bed- 
clothing   or   at   imaginary   objects  (carphologia),  and  exhibits  general 


46  BACTERIAL  INFECTIONS 

muscular  twitchings,  especially  of  the  tongue,  lips,  hands,  and  fingers 
(subsultus  tendinum).  Often  the  undue  muscular  irritability  is  quite 
manifest  by  the  ready  production  of  myoidema.  In  this,  the  typhoid 
state,  the  urine  and  feces  may  be  voided  involuntarily,  and  the  patient 
knows  not  even  his  wants.  Not  infrequently  he  shows  a  disposition  to 
get  out  of  bed — whence  he  should  not  be  left  alone  for  even  an  instant, 
as  not  a  few  patients  have  thrown  themselves  from  a  window  during  the 
temporary,  though  only  momentary,  absence  of  the  nurse.  Occasion- 
ally, instead  of  a  quiet,  muttering  delirium,  the  patient  may  exhibit  a 
noisy,  hysterical  (emotional),  or  maniacal  delirium  (especially  alcoholic 
subjects,  in  whom  the  condition  quite  resembles  delirium  tremens). 

Occasionally  typhoid  fever  is  ushered  in  with  unusual  nervous  symp- 
toms. The  headache  and  backache  may  be  intense,  and  there  may  be 
also  photophobia,  pain,  tenderness,  and  rigidity  of  the  muscles  of  the 
neck,  sometimes  even  retraction  of  the  head,  and  rarely  convulsions 
(more  common  in  children  than  in  adults).  In  other  cases,  later  in  the 
course  of  the  disease,  similar  symptoms  arise.  These  cases  suggest  and 
are  only  with  difficulty  distinguished  from  meningitis;  three  types  may 
be  distinguished:  (1)  Cases  suggesting  meningitis,  but  in  which  no 
anatomical  lesions  can  be  demonstrated — the  so-called  meningism  of 
the  French,  probably  due  solely  to  toxemia;  (2)  cases  exhibiting  the 
lesions  of  serous  meningitis  and  perhaps  revealing  the  typhoid  bacillus  in 
the  cerebrospinal  fluid ;  and  (3)  cases  of  purulent  meningitis  from  which 
the  typhoid  bacillus,  either  alone  or  in  association  with  other  bacteria, 
may  be  isolated.  Circumscribed  encephalitis,  and  hemorrhage,  embolism, 
and  thrombosis  of  the  brain  (hemiplegia  with  or  without  aphasia)  have 
been  observed.  Myelitis  or  poliomyelitis  (spastic  or  flaccid  paralysis)  is 
still  more  uncommon.  Peripheral  neuritis  is  quite  frequently  observed, 
of  which  a  well-known  manifestation  is  the  rather  common  tender 
toes  and  tender  feet — believed  to  be  more  common  since  the  use  of  the 
cold-bath  treatment.  The  very  common  painful  calves  (observed  fre- 
quently during  convalescence),  as  well  as  the  much  less  common  painful 
muscles  in  other  parts  of  the  body,  are  not  infrequently  due  to  neuritis ;  but 
they  are  sometimes  due  to  myositis  or  to  thrombosis  of  a  vein.  Post- 
typhoidal  insanity  (confusional  insanity,  melancholia,  or  mere  mental 
dulness)  is  not  uncommon.  It  is  usually  attributed  to  toxemia  and 
impaired  nutrition,  and  in  the  majority  of  cases  soon  subsides.  Oculo- 
motor paralysis,  paralysis  of  accommodation,  iritis,  keratitis,  conjuncti- 
vitis, and  divers  other  ocular  complications  have  been  reported. 

Genito-urinary  System. — ^The  urine,  as  a  rule,  presents  the  features 
of  so-called  febrile  urine  (diminished  in  amount,  high  colored,  of  high 
specific  gravity,  abundance  of  urates,  etc.).  The  diazo  reaction  is  usually 
present.  At  least  three-fourths  of  the  patients  exhibit  slight  albumin- 
uria— attributable  to  toxic  degeneration  of  the  renal  epithelium.  Occa- 
sionally a  true  nephritis  (hemorrhagic  or  non-hemorrhagic)  occurs 
at  the  height  of  the  disease.  I  have  observed  acute  interstitial  non- 
suppurative nephritis  (the  so-called  lymphomatous  nephritis  of  Wagner). 


TYPHOID  FEVER  47 

Nephritis  during  convalescence  or  as  a  sequel  is  quite  rare,  the  lesions 
developing  during  the  course  of  the  disease  usually  subsiding  in  the 
non-fatal  cases.  Retention  of  urine  is  quite  common  and  often  occasions 
rather  severe  abdominal  pain.  Typhoid  bacilluria  is  present  in  at  least 
one-third  of  the  cases,  and  sometimes  lasts  for  months  after  apparent 
recovery  from  the  disease;  because  the  urine  is  often  not  disinfected  this 
bacilluria  is  answerable  for  some  epidemics.  The  bacilluria  may  be 
due  to  pyelitis,  cystitis,  spermatocystitis,  prostatitis,  or  orchitis,  or  it 
may  occur  without  noteworthy  lesions.  Diabetes  (or  glycosuria),  hema- 
turia, and  hemoglobinuria  are  rarely  observed.  Menstruation  is  not  infre- 
quent at  the  beginning  of  the  disease,  and  pregnant  women  usually  abort. 

Other  unusual  complications  comprise  osteomyelitis,  periostitis,  peri- 
chondritis, synovitis,  and  arthritis  (from  which  the  typhoid  bacillus  may 
be  cultivated  months  and  even  years  after  the  primary  infection).  Occa- 
sionally during  or  after  convalescence  the  patient  complains  of  pain, 
tenderness,  and  rigidity  in  the  lumbar  and  sacral  regions,  and  of  certain 
nervous  (sometimes  hysterical)  phenomena.  This  condition  (so-called 
typhoid  spine)  is  in  some  cases  a  pure  neurosis,  but  it  not  infrequently 
has  an  organic  basis — spondylitis  or  perispondylitis.  Perinephritic 
abscess  may  simulate  the  condition.  Fever  may  be  an  important  sign 
in  the  differential  diagnosis. 

Typhoid  fever  is  not  uncommonly  associated  with  other  diseases, 
especially  tuberculosis,  malaria,  measles,  diphtheria,  noma,  erysipelas, 
furunculosis,  etc.  Most  of  the  cases  of  so-called  typho-malarial  fever 
are  true  typhoid  fever;  others  are  remittent  malarial  fever;  in  a  few 
cases  only  do  two  diseases  co-exist. 

Varieties  of  Typhoid  Fever. — Many  different  varieties  of  typhoid  fever 
have  been  described;  but  the  infection  is  always  with  the  same  typhoid 
bacillus  (which,  however,  often  exhibits  variations  in  certain  of  its  biologi- 
cal characteristics) ;  the  clinical  differences  are  dependent,  therefore,  upon 
differences  in  the  virulence  of  the  infecting  agent,  upon  unusual  localiza- 
tions of  the  infection,  and  upon  variations  in  the  resistance  of  the  indi- 
vidual. Thus,  mild  (typhus  Ifevis  sive  Isevissimus,  Griesinger)  and  severe 
forms  are  readily  distinguished.  In  the  mild  forms,  which  are  frequently 
overlooked  and  especially  common  in  children,  the  clinical  and  anatomical 
manifestations  of  the  disease  are  ill  developed,  and  although  fever, 
an  enlarged  spleen,  rose-spots,  the  Gruber-Widal  reaction,  etc.,  often 
occur,  convalescence  is  not  infrequently  established  at  or  before  the  end 
of  the  second  week;  but  the  disease  may  run  the  more  usual  course  of 
three  to  four  weeks.  In  children  the  abdominal  symptoms  are  often 
slight  or  absent,  whereas  the  nervous,  cerebral  symptoms  are  likely  to  be 
marked. 

Unusually  acute  and  rapid  cases  are  sometimes  observed.  Doubtless 
an  abortive  form  occurs,  but  it  is  very  uncommon — more  especially 
since  the  general  use  of  the  (irul)er-Wi(lal  reaction.  As  described,  the 
onset  presents  nothing  unusual,  except  in  some  cases  rather  sudden  and 
marked  initial  fever;  but  at  the  end  of  the  first  week  the  fever  falls,  and 


48  BACTERIAL  INFECTIONS 

convalescence  goes  on  as  in  the  ordinary  cases,  though  relapses  may 
occur.  Latent  or  ambulatory  typhoid  fever  is  a  form  of  infection  in 
which  the  symptoms,  at  the  beginning  at  least,  are  so  mild  that  the  patient 
does  not  feel  the  necessity  of  going  to  bed,  and  therefore  continues  about 
until  some  unusual  phenomenon,  such  as  marked  diarrhoea,  delirium, 
intestinal  perforation,  or  hemorrhage,  etc.,  brings  him  under  the  atten- 
tion of  the  physician.  The  subsequent  course  of  the  disease  is  often 
severe  and  not  infrequently  fatal.  The  initial  symptoms  of  typhoid 
fever  sometimes  suggest  an  ordinary  "cold,"  influenza,  tonsillitis,  or 
gastritis.  An  afebrile,  exceedingly  rare,  form  of  the  infection  has  been 
described  by  Liebermeister.  The  severe  cases  are  characterized,  as  a 
rule,  by  unusual  severity  of  the  fever  and  of  the  nervous  symptoms 
(delirium,  prostration,  vasomotor  paralysis,  etc.) — whence  these  are 
sometimes  spoken  of  as  the  cerebrospinal  form.  In  other  cases  there 
is  unusual  localization  of  the  lesions  in  different  organs — whence  the 
terms  pneumo-typhoid,  pleuro- typhoid,  nephro-typhoid,  tonsillo-typhoid, 
pharyngo-typhoid,  meningo-typhoid,  etc.  A  few  severe  cases  have 
been  characterized  by  petechial  spots  and  hemorrhages  from  the  mucous 
membranes — so-called  hemorrhagic  form.  The  disease  often  runs  a 
severe  course  in  elderly,  alcoholic,  and  obese  subjects. 

Relapses. — A  relapse,  a  repetition  of  the  anatomical  and  clinical 
features  of  the  diease  and  due  to  re-infection,  is  not  an  uncommon 
event,  occurring  in  different  epidemics  in  from  3  to  15  per  cent,  of 
the  cases.  It  should  be  distinguished  from  recrudescence  of  the  fever 
(spurious  relapse,  previously  alluded  to),  as  well  as  from  complications, 
such  as  cholecystitis,  pleuritis,  etc.,  for  which  it  is  frequently  mistaken. 
It  is  not  always  possible  to  discover  the  source  of  re-infection:  some- 
times it  may  be  from  without;  usually  it  is  from  within,  and  one 
should  always  bear  in  mind  the  possibility  of  infection  from  the  gall- 
bladder which  frequently  harbors  typhoid  bacilli  without  obvious  local 
disease;  the  urinary  tract  also  may  be  the  source  of  reinfection; 
but  the  real  cause  of  the  relapse  is  most  likely  to  be  found  amongst  the 
problems  of  immunity — perhaps  in  temporary  exhaustion  or  over- 
powering of  the  bacteriolytic  activities  of  the  blood.  As  a  rule,  the 
relapse  comes  on  within  seven  days  of  the  beginning  of  the  convalescence; 
sometimes  it  develops  earlier,  even  before  the  temperature  has  reached 
normal  (intercurrent  relapse),  in  which  event  it  is  often  severe  and 
protracted;  occasionally  it  may  not  come  on  until  the  temperature 
has  been  normal  for  three  weeks  or  more.  The  period  of  apyrexia  is 
usually  without  noteworthy  manifestations.  The  onset  of  the  relapse, 
as  a  rule,  is  sudden,  the  temperature  rising  abruptly,  sometimes  with 
a  chill  or  chilliness.  Then  follow  usually  the  characteristic  step-ladder 
rise  of  the  temperature  (for  two  or  three  days),  new  roseolous  spots  (on 
the  second  to  the  fourth  day),  and  enlargement  of  the  spleen — two  of 
which  signs,  at  least,  should  be  present  to  warrant  the  diagnosis  of  a  true 
relapse.  As  a  rule,  the  relapse  does  not  last  more  than  ten  or  fourteen 
days,  and  the  clinical  signs  are  less  severe  than  in  the  primary  attack; 


TYPHOID  FEVER  49 

hut  occasionally  all  the  phenomena  of  the  disease  are  much  aggravated 
during  the  relapse,  and  the  patient  may  die  of  the  toxemia  or  of  one  of 
the  common  accidents,  such  as  hemorrhage  or  perforation.  There  may 
be  a  second,  a  third,  a  fourth,  and  even  a  fifth  relapse.  A  recurrence,  as 
contrasted  with  a  relapse,  means  another  attack  of  the  disease  occurring 
after  complete  restoration  to  health.  Usually,  typhoid  fever  confers 
lasting  immunity,  but  second  and  apparently  well-authenticated  third 
attacks  have  been  observed — a  period  of  years  intervening  between  the 
attacks. 

Diagnosis. — The  recognition  of  typhoid  fever  is,  in  the  one  case,  a 
matter  of  the  greatest  ease,  and  in  another,  of  the  greatest  uncertainty 
— for  a  time  at  least.  No  one  symptom  is  conclusive.  Of  special  value 
in  the  diagnosis  are  prodromal  symptoms  lasting  for  a  week  or  more,  the 
gradual  onset  of  fever  (of  characteristic  rise,  if  it  has  been  observed), 
persistent  headache,  nose-bleed,  roseolous  spots,  enlarged  spleen,  early 
dicrotism  of  the  pulse,  leukopenia,  and  the  diazo  reaction;  the  diagnosis 
is  made  conclusive  by  the  Gruber-Widal  reaction  (in  dilutions  of  1  to 
50  or  more),  and  the  cultivation  of  typhoid  bacilli  from  the  blood,  the 
rose-spots,  the  stools,  the  urine,  or  the  cerebrospinal  fluid.  In  some 
regions  continued  fever  for  seven  days  without  evidence  of  local  disease 
is  quite  suggestive.  Paratyphoid  fever,  as  a  rule,  is  first  suggested  by  the 
absence  of  the  Gruber-Widal  reaction  with  the  typhoid  bacilli.  It  may 
be  difficult  or  impossible  for  some  days  to  exclude  cerebrospinal  menin- 
gitis, since  typhoid  fever  sometimes  begins  with  severe  nervous  mani- 
festations, but  the  characteristic  course  of  the  fever,  the  erythematous 
rose  rash  (as  contrasted  with  a  petechial  eruption),  the  presence  of  ab- 
dominal symptoms,  the  absence  of  herpes  facialis,  the  presence  of  the 
Gruber-Widal  reaction,  and  the  negative  results  of  lumbar  puncture, 
serve  ultimately  to  distinguish  typhoid  fever.  The  continued  types  of 
malarial  fever,  which  much  resemble  typhoid  fever,  may  be  distinguished 
by  the  absence  of  the  Gruber-Widal  reaction,  the  presence  of  the  malarial 
parasite  in  the  blood,  and  by  the  administration  of  quinine.  Acute 
miliary  tuberculosis  is  often  differentiated  with  difficulty,  but  it  is  sug- 
gested by  absence  of  the  characteristic  fever  curve,  of  abdominal  symp- 
toms, of  erythematous  rose-spots,  of  leukopenia,  and  of  the  Gruber-Widal 
reaction,  and  by  the  presence  of  increased  pulse-rate,  of  dyspnoea,  of 
cyanosis,  of  occasionally  bloody  expectoration,  of  choroidal  tubercles, 
and  of  tubercle  bacilli  in  the  cerebrospinal  fluid  and  rarely  in  the  blood. 
Certain  pyemic  processes,  of  which  ulcerative  endocarditis  is  an  example, 
are  usually  diagnosticated  typhoid  fever,  but  they  may  sometimes  be 
differentiated  by  detecting  a  source  of  infection,  and  by  the  presence  of 
undue  dyspnoea,  irregular  heart  action,  a  peculiar  rough  systolic,  but 
more  especially  a  diastolic  murmur,  irregular  and  repeated  chills  or 
chilly  sensations,  profuse  sweats,  the  early  occurrence  of  marked  prostra- 
tion, the  rapid  development  of  anemia,  leukocytosis,  embolic  phenomena 
(petechial  helnorrhages,  infarctions,  etc.),  and  pyococci  in  the  blood,  and 
by  the  absence  of  a  characteristic  fever  curve,  of  persistent  headache, 
4 


.50  BACTERIAL  IXFECTIOXS 

of  epistaxis,  of  abdominal  symptoms,  and  of  the  Griiber-Widal  reaction. 
Acute  leukemia  without  noteworthy  enlargement  of  the  lymph  nodes, 
which  usually  resembles  typhoid  fever,  may  be  distinguished  by  the 
absence  of  the  Gruber-Widal  reaction  and  the  presence  of  leukocytosis 
(lymphocytosis).  Pneumonia,  appendicitis,  and  tuberculous  peritonitis 
also  must  be  considered  in  the  differential  diagnosis  in  certain  instances. 

Prognosis. — The  prognosis  is  always  doubtful,  since  no  one  can  fore- 
tell whether  or  not  one  of  the  two  accidents  (hemorrhage  and  perforation), 
responsible  for  almost  two-thirds  of  the  deaths,  will  occur.  The  mortality 
varies  much  in  different  epidemics — from  5  to  12  per  cent,  in  private 
practice  to  from  7  to  20  per  cent,  in  hospital  practice,  where  the  worst 
cases  are  encountered.  During  recent  years,  in  consequence  of  the 
general  use  of  the  cold-bath  treatment,  the  mortality  has  certainly  been 
reduced — in  some  hospital  statistics  to  less  than  4  per  cent.  The  prog- 
nosis in  general  depends  upon  the  severity  of  the  infection,  the  resistance 
of  the  individual,  and  the  presence  or  absence  of  complications.  Aside 
from  repeated  hemorrhages  and  perforation  (with  consecutive  peritonitis) 
answerable  for  almost  two-thirds  of  the  deaths,  especially  unfavorable 
symptoms  are  persistent  high  fever,  persistently  rapid  pulse  (above  1 20), 
profound  toxemia  and  delirimn,  marked  t^Tnpanites,  and  complications, 
such  as  pneumonia,  meningism,  meningitis,  etc.  Sudden  death  may 
occur  during  the  fastigium,  as  well  as  during  defen^escence  or  con- 
valescence, from  cardiac  collapse,  vasomotor  paralysis,  pulmonary  or 
cerebral  embolism  or  thrombosis,  etc.  The  passage  of  eighty  to  one 
hundred  or  more  ounces  of  urine  daily  is  one  of  the  most  favorable 
prognostic  signs  The  prognosis  of  relapses  is  not  essentially  different 
from  that  of  the  primary  attack.  The  prognosis  in  children,  as  a  rule, 
is  good. 

Treatment. — In  t^'phoid  fever  probably  as  much  as,  if  not  more  than, 
in  any  other  disease,  our  duty  is  not  to  our  patient  alone,  but  in  a  special 
sense  to  the  community  at  large  Since  t}-phoid  fever  is  a  preventable 
disease,  it  should  be  prevented;  the  duty  of  preventing  it  falls  upon 
the  physician  no  less  than  upon  the  public  health  authorities.  The 
general  measures  of  prophylaxis  set  forth  on  page  29  should  be 
scrupulously  followed. 

AMiether  Wright's  preventive  inoculation  will  ultimately  commend 
itself  to  the  profession  is  at  least  doubtful.  According  to  British 
armv  surgeons,  typhoid  fever  is  more  than  two  and  a  half  times  as 
common,  and  one  and  a  half  time  as  fatal,  among  the  uninoculated 
as  compared  with  the  inoculated  troops.  Of  possible  value  during 
times  of  war,  inoculation  is  not  likely  soon  to  attain  much  vogue  in  civil 
practice;  it  may  prove  of  service  among  hospital  attendants.  The  serum 
treatment  of  the  disease,  for  which  Chantemesse  and  others  claim  good 
results,  has  not  commended  itself  to  the  profession  at  large.  A  satis- 
factory vaccine  (bacterin)  treatment  has  not  yet  been  devised. 

Since  t}-phoid  fever  is  a  self-limited  infection,  the  special  function  of 
the   physician  is  to   assist,  never   thwart,   the  well-directed  efforts  of 


TYPHOID  FEVER  51 

nature.  This  comprises  attention  to,  (1)  the  general  management  of 
the  patient,  (2)  the  diet,  (3)  hydrotherapy,  and  (4)  medicinal  and 
other  measures  indicated  symptomatically. 

General  Maxagemext. — ^Miether  the  patient  shall  be  treated  in 
his  home  or  in  a  hospital  is  a  matter  to  be  decided  in  each  individual 
case ;  in  general  the  hospital  patient  has  the  advantage,  since  the  nursing, 
as  a  rule,  is  better  and  the  necessary  manipulations  can  be  more  easily 
carried  out;  disinfection  is  more  thoroughly  practised;  complications 
are  likely  to  be  sooner  recognized  (since  a  physician  is  always  at  hand) ; 
and  in  the  event  of  surgical  intervention  being  necessary,  it  can  be 
undertaken  sooner  and  under  better  auspices  than  in  the  patient's  home. 
But  under  proper  supervision,  the  patient  may  be  very  well  treated  at 
his  home.  Under  all  circumstances,  he  should  be  isolated — in  the 
hospital,  in  a  ward  or  room  set  apart  for  this  purpose;  at  home,  in  a 
room  affording  abundance  of  sunlight  and  fresh  air.  He  should  be 
confined  absolutely  to  bed  until  he  is  well  along  in  convalescence,  and 
he  must  use  a  bed-pan  and  a  urinal.  Special  attention  should  be 
directed  to  avoiding  creases  in  the  bed-linen  so  as  to  promote  the  comfort 
of  the  patient  and  prevent,  as  far  as  possible,  the  development  of  bed 
sores.  The  patient  should  be  turned  on  his  side  from  time  to  time,  and 
his  skin,  especially  of  the  back,  should  be  frequently  sponged  with 
dilute  alcohol  (50  per  cent.)  or  with  equal  parts  of  alcohol  and  alum 
water;  following  this  a  drying  powder  may  be  applied,  such  as  zinc 
stearate,  or  equal  parts  of  powdered  zinc  oxide  and  boric  acid.  Should 
the  skin  become  irritated,  one  may  substitute  a  mixture  consisting  of 
boric  acid  10  grains  (0.65  gram),  zinc  oxide  1  to  2  drams  (4  to  8  grams), 
and  castor  oil  1  ounce  (30  grams) .  The  mouth  and  throat  should  be 
kept  clean  and  sweet  by  the  use  of  mild  antiseptic  solutions,  such  as 
boric  acid  (3  per  cent.) ;  or  boric  acid  (1  dram,  4  grams) ,  glycerin  (6  drams, 
25  grams) ,  and  rose  water  (6  ounces,  200  grams) ;  or  liquor  antisepticus 
(U.  S.  P.);  or  the  following: 

I^ — Carbolic  acid 6  minims  0  40 

Oil  of  eucalyptus 10  minims         0  60 

Sodium  borate 1  dram.  4  00 

Glycerin 3  drams  12|00 

Distilled  wat3r,  sufficient  to  make    .      .      .  3  ounces  100  00.— M. 

The  physician  should  always  write  his  orders  in  detail,  rather  than 
trust  to  the  memory  of  even  a  well-trained  nurse;  in  the  absence  of  a 
trained  nurse,  this  is  all  the  more  imperative. 

The  general  management  of  convalescence  often  demands  much 
tact  on  the  part  of  the  physician — to  withstand  the  importunities  of  the 
patient  and  the  usually  well-meant,  but  often  ill-advised,  endeavors  of 
his  solicitous  friends.  Could  solicitous  friends  be  banished  for  a  while, 
most  typhoid-fever  patients  would  fare  better;  at  all  events,  the  visits 
should  be  as  short  as  possible,  and  all  matters  that  may  excite  the  patient 


52  BACTERIAL  INFECTIONS 

or  disturb  his  emotions  should  be  scrupulously  avoided.  On  the  fifth  or 
the  sixth  day  of  normal  temperature,  in  the  ordinary  case,  the  patient 
may  be  propped  up  in  bed  for  a  while,  and  on  the  eighth  day  or  there- 
abouts he  may  sit  in  a  chair.  A  general  tonic  is  usually  advantageous, 
though  often  not  necessary;  anemia,  however,  calls  for  the  administra- 
tion of  iron.  Return  to  ordinary  avocations  should  be  postponed 
as  long  as  possible,  especially  after  severe  infections;  return  to  mental 
work  and  study,  in  particular,  should  be  delayed,  since  a  too  early 
return  not  infrequently  results  in  a  prolonged  spell  of  cerebral  asthenia. 
A  sea  voyage  subserves  a  most  useful  purpose  following  convalescence. 

Diet. — ^The  diet  should  be  suited  to  the  individual  patient,  rather 
than  to  the  disease.  The  physician  should  remember  that  during 
typhoid  fever  the  digestive  juices  are  lessened  or  perverted,  and  that 
some  at  least  of  the  toxemia  is  due  to  the  poisonous  effects  of  the  end- 
products  of  destructive  katabolism  of  the  body  protein;  and  while  he 
should  endeavor  as  far  as  possible  to  supply  a  sufficiency  of  calories  in 
foodstuffs  to  satisfy  dynamic  needs  and  to  minimize  loss  of  weight,  he 
must  be  careful  to  avoid  improper  food  and  that  excess  of  food  which  is 
certainly  productive  of  digestive  disorders.  If  in  the  past  we  have 
been  perhaps  too  much  committed  to  a  diet  insufficient  in  calories  and 
relatively  too  rich  in  protein,  a  diet  of  too  high  caloric  value  may  be 
productive  of  much  harm;  certain  carbohydrates,  under  circumstances, 
may  be  of  value;  fats,  at  least  in  excess,  are  not  well  borne.  In  many 
respects  the  appetite  is  a  good  index  of  the  amount,  although  not  of  the 
character  of  the  food  that  may  be  permitted. 

There  can  be  no  doubt  that  at  present,  as  in  the  past,  the  majority  of 
patients  do  best  on  a  diet  consisting  largely,  if  not  wholly,  of  milk.  To 
an  adult  one  may  give  four,  six,  or  eight  ounces  of  milk  every  two  hours 
during  the  day,  and  every  four  hours  at  night — nine  or  ten  feedings  in 
the  twenty-four  hours.  This  furnishes  from  780  to  1750  calories 
(650  to  700  calories  to  a  quart  or  liter).  The  milk  may  be  given  hot 
or  cold;  it  may  be  diluted  with  lime  water  or  some  carbonated  water, 
such  as  Vichy;  it  may  be  flavored  with  salt,  vanilla,  coffee,  tea,  cocoa, 
or  port  or  sherry  wine;  or  it  may  be  given  as  buttermilk,  koumiss, 
matzoon,  junket,  or  in  part  as  ice  cream.  Twice  a  day,  the  white  of  an 
egg  (20  calories)  or  the  whole  egg  (80  calories) ,  if  w^ell  borne,  may  be 
added  to  the  milk.  In  case  of  objection  on  the  part  of  the  patient, 
albumen  water  (the  whites  of  two  eggs  added  to  four  to  six  ounces  of 
water,  and  flavored  with  lemon,  lime,  or  orange  juice)  may  be  substituted 
for  the  milk  at  every  other  feeding.  In  ordinary  cases,  throughout  the 
febrile  period,  I  commonly  adhere  to  this  diet  of  milk  and  egg-albumen 
— the  advantage  of  which  is  seen  in  the  freedom  from  intestinal  dis- 
orders, the  good  general  condition  of  the  patient,  and  the  usually  prompt 
convalescence  without  noteworthy  untoward  symptoms.  However,  in 
the  event  of  very  serious  objection  to  milk  on  the  part  of  the  patient,  or  an 
obvious  poor  general  condition,  I  have  no  hesitation  in  substituting  the 
milk  in  whole  or  in  part,  or  adding  to  it,  cream,  milk  sugar,  eggs,  meat  and 


TYPHOID  FEVER  53 

veo-etable  soups^  strained  and  thickened  with  flour,  powdered  rice  or 
barley,  cream,  egg,  etc.,  or  strained  oatmeal  gruel,  cornstarch,  arrow-root, 
potato  puree,  gelatine  flavored  with  wine,  etc. 

In  the  event  of  tympanites  or  diarrhcea,  the  milk  should  be  reduced  in 
amount;  usually,  under  these  circumstances,  too  much  rather  than  too 
little  is  being  given,  and  curds  frequently  appear  in  the  stools.  Whey, 
l)oiled  milk,  peptonized  or  pancreatized  milk,  or  koumiss  may  be  substi- 
tuted; but  if  the  unfavorable  symptoms  do  not  subside  promptly  the 
milk  should  be  entirely  withheld  for  twenty-four  to  thirty-six  hours, 
and  albumen  water  given  instead.  Thereafter  one  may  cautiously 
recommence  with  peptonized  milk  in  small  amounts,  or  resort  to  some 
of  the  other  mentioned  foodstufi^s.  If  the  patient  has  done  well  on  the 
milk  and  egg-albumen  dietary,  toward  the  end  of  the  third  week,  in  the 
absence  of  definite  indications  to  the  contrary,  two  raw  eggs  daily  should 
be  added  to  the  diet;  and  during  the  following  week,  the  aforementioned- 
gruels,  broths,  soups,  cornstarch,  etc.,  as  well  as  very  soft-boiled  eggs. 
At  the  end  of  four  to  seven  days  of  normal  temperature,  soft  puddings, 
milk  toast,  scraped  beef,  mashed  potato,  apple  sauce,  etc.,  may  be 
allowed;  and  a  day  or  two  later,  sweetbreads,  the  white  meat  of  chicken, 
stewed  fruit,  etc.  The  return  to  the  ordinary  diet  should  be  gradual. 
Thus,  while  I  incline  to  liberality  in  the  matter  of  diet,  especially  toward 
the  end  of  the  disease,  I  have  yet  to  see  any  general  good  come  from  the 
unusually  generous  dietary,  even  solid  food,  sometimes  advocated,  and 
I  have  seen  it  do  positive  harm. 

Of  quite  as  much  importance  as  food  is  water.  A  minimum  of 
three  or  four  liters,  in  stated  amounts  between  the  feedings,  should  be 
given  in  the  twenty-four  hours;  often  much  more  can  be  taken  with 
great  advantage  to  the  patient.  The  daily  amount  of  urine  is  the  best 
indication  of  the  amount  of  water  that  should  be  given,  and  we  may 
be  sure  that  that  patient  who  passes  eighty,  one  hundred,  or  more 
ounces  of  urine  daily  will  recover  unless  he  suffers  a  severe  hemor- 
rhage or  a  perforation. 

Hydrotherapy. — Hydrotherapy  constitutes  an  essential  part  of  the 
treatment  of  every  typhoid-fever  patient.  Advocated  originally  by 
Currie,  of  England,  hydrotherapy  was  systematized  in  1861,  and  sub- 
secjuently,  by  Brand,  and  is  commonly  known  as  the  Brand  treatment. 
Its  advantages  are  many,  the  most  important  of  which  is  not  the 
reduction  in  temperature  which  it  effects.  Its  greatest  claim  to  our 
attention  is  that  it  unquestionably  reduces  the  mortality — large  statistics 
showing  undoul)tedly  that   from   five   to  seven  of  every  one   hundred 

'  Houghton  giv'es  the  following  formula  for  the  preparation  of  a  vegetable  soup:  00  grams 
(2  ounces)  each  of  green  or  canned  French  peas,  white  dry  beans,  potato,  rice,  and  noodles,  antl 
15  grams  (J^  ounce)  of  carrot,  should  be  boiled  in  water  for  at  least  four  hours.  Thereupon 
sufficient  water  should  be  added  to  make  one  liter  (1  quart),  which  is  sufficient  for  four  feedings. 
This  yields  760  calories,  of  which  6.3  per  cent,  is  protein,  4.3.9  per  cent,  carbohydrate,  and  les.s 
than  0.2  per  cent.  fat.  When  ready  to  use,  the  sediment  should  be  stirred  up,  and  the  patient 
allowed  to  eat  everytlung  except  the  pea-  and  bean-skins.  Oiuon  may  be  added  for  flavoring, 
if  <lesired. 


54  BACTERIAL  INFECTIONS 

typhoid-fever  patients  are  saved  by  its  use.  The  patients  saved  are  not 
the  unfortunate  subjects  of  compHcations  such  as  hemorrhage  and 
perforation,  but  patients  who  otherwise  would  die  of  toxemia.  Hydro- 
therapy, therefore,  does  good  by  reducing  toxemia,  and  largely  through 
an  influence  on  the  nervous  system. 

Although,  for  obvious  reasons,  the  degree  of  temperature  is  taken  as 
the  indication  for  repeating  the  hydrotherapeutic  measures,  the  influence 
of  the  bath  on  the  fever,  especially  during  the  fastigium,  is  often  com- 
paratively slight,  though  the  toxemia  may  be  notably  influenced.  Com- 
monly, however,  more  or  less  bodily  heat  is  abstracted;  reduction  of  the 
temperature  of  from  2°  to  4°  after  the  baths  is  frequent,  especially  after 
the  treatment  has  been  in  use  for  several  days ;  and  the  ill  effects  of  long- 
continued  fever  are  obviated.  The  notable  influence,  however,  is  on 
the  toxemia :  the  nervous  manifestations  of  the  toxemia,  mental  dulness, 
stupor,  delirium,  muscular  twitchings,  etc.,  are  much  improved,  the 
"typhoid  state"  of  our  forefathers  is  rarely  seen  in  patients  subjected 
to  the  bath  treatment  from  the  beginning,  and  insomnia  and  coma  vigil 
when  present  often  after  a  bath  give  way  to  several  hours  of  refreshing- 
sleep  ;  the  toxic  weakness  of  the  heart  and  circulation  (low  blood  pressure) 
is  replaced  by  fuller,  slower,  and  stronger  heart  beats,  the  blood  pressure 
is  increased,  and  peripheral  cyanosis,  hypostatic  congestion  of  the  lungs, 
venous  thromboses,  and  other  ill  consequences  of  low  blood  pressure 
are  warded  off;  shallow  breathing  gives  way  to  full  and  deep  inspirations, 
the  cyanosis  of  ill-ventilation  is  lessened,  the  good  results  of  improved 
oxygenation  are  obtained,  and  the  bronchitis  is  improved,  whence  the 
likelihood  of  bronchopneumonia  is  lessened;  the  kidneys  are  stimulated 
to  increased  functional  activity,  and  typhotoxins  are  excreted  in  in- 
creased amount;  and  the  invigorating  action  of  the  baths  and  friction  on 
the  skin  and  the  cutaneous  capillaries  improves  the  general  tone  of  the 
system  and  diminishes  the  likelihood  of  bed  sores. 

Objections  to  the  cold-bath  treatment  are:  that  it  is  troublesome 
— which  is  true,  especially  in  private  homes ;  that  it  is  attended  by  no 
better  results  than  other  forms  of  treatment — which  is  not  true;  that  it 
increases  the  likelihood  of  hemorrhage  and  perforation — which  is  not  true, 
although  certain  series  of  cases  may  show  somewhat  higher  percentage 
incidence  of  these  complications:  they  show  also  a  higher  percentage 
of  recoveries;  that  it  is  cruel,  inhuman,  and  barbarous — which  contains 
an  apparent  modicum  of  truth,  but  in  reality  the  treatment  does  not  add 
notably  to,  in  many  respects  it  reduces,  the  discomfort  of  the  attack  of 
typhoid  fever,  and  assuredly  it  is  better  to  suffer  the  ills  of  two  or  three 
weeks  of  cold-bath  treatment  than  fly  to  those  we  know  not  of;  and  that 
it  is  not  necessary  in  all  cases — but  the  good  results  of  the  treatment  are 
seen  to  best  advantage  only  when  it  is  instituted  early  and  continued 
systematically  throughout  the  attack,  and  not  when  postponed  until 
the  patient  is  "sick  enough,"  a  practice  that  unfortunately  still  obtains 
among  some  practitioners.  No  one  can  foretell  at  the  beginning  of  an 
attack  how  severe  it  is  likely  to  become. 


TYPHOID  FEVER  55 

The  hydrotherapeutic  measures  to  be  commended  in  typhoid  fever 
are  the  cold  bath  and  sponging;  the  cold  pack,  sprinkling,  and  fanning 
are  more  or  less  unsatisfactory  substitutes — available,  however,  in  some 
cases. 

The  cold  bath  is  the  most  preferable  and  is  in  general  use  in  most 
modern  hospitals,  and  as  far  as  circumstances  will  permit  is  largely  used 
by  many  physicians  in  their  private  practice.  The  common  practice  is 
to  give  the  patient  a  bath  at  70°  F.,  for  fifteen  or  twenty  minutes,  every 
three  hours,  if  his  temperature  reaches  or  is  above  102.5°  F.  While  in 
the  water,  the  patient's  body  should  be  submerged,  a  cold  cloth  or  an 
ice-bag  should  be  applied  to  his  head,  the  exposed  neck,  shoulders,  and 
chest  should  be  douched  repeatedly  with  cold  water,  and  his  extremities, 
back,  and  chest  should  be  rubbed  vigorously  and  continuously — an 
essential  of  the  treatment.  At  the  termination  of  the  bath  the 
patient  should  be  wrapped  in  a  dry,  preferably  warmed,  sheet  (pre- 
viously, with  a  blanket,  spread  upon  the  bed);  the  sheet  should  be  care- 
fully tucked  about  the  patient's  extremities  and  trunk,  and  gentle  friction 
made  to  remove  the  excess  of  water;  hot-water  bottles  may  be  applied 
to  his  feet  and  legs,  and  then  he  should  be  covered  with  the  blanket. 
After  the  patient  is  dry,  the  sheet  may  be  removed  and  the  patient 
allowed  to  rest  in  the  blanket  for  twenty  to  thirty  minutes,  whereupon 
a  dry  nightdress  should  be  provided.  The  rectal  temperature  should 
be  taken  at  the  termination  of  the  bath,  and  again  at  the  end  of  a 
half-hour.  Usually  a  fall  of  temperature  of  from  1°  to  2°  will  have 
been  attained;  this  is  sufficient,  marked  falls  (4°  and  thereabouts)  being 
undesirable. 

Certain  deviations  from  this  strict  regimen  are  not  only  permissible, 
but  often  desirable — due  attention  being  paid  to  the  patient  rather  than 
to  the  disease.  Thus,  it  is  by  no  means  necessary  that  the  water  should 
be  always  at  70°  F. ;  it  may  vary  from  70°  to  85°  F.,  and  it  is  often  desir- 
able to  begin  with  a  temperature  of  85°  F.  in  adults,  and  sometimes  to  con- 
tinue with  this  temperature  throughout  the  attack  in  children.  Beginning 
with  85°  in  apprehensive  adults,  the  temperature  may  be  reduced  5° 
while  the  patient  is  in  the  bath,  by  the  addition  of  ice  or  cold  water — the 
cold  water  being  preferable,  since  it  is  less  likely  to  add  to  the  appre- 
hensiveness  of  the  patient.  Each  succeeding  or  every  second  bath  may 
begin  at  a  temperature  of  5°  less,  until  the  desired  and  the  best  tempera- 
ture for  the  particular  patient  is  obtained.  Some  patients,  however, 
never  do  well  with  a  temperature  as  low  as  70°  F.  It  is  usually  desirable 
to  have  the  first  })ath  last  not  more  than  five  or  ten  minutes  and  gradually 
to  lengthen  the  time  of  succeeding  baths  until  the  desired  fifteen  or  twenty 
minutes  is  attained. 

While  in  the  bath  some  patients  complain  much  of  the  low  temperature; 
others  shiver  much,  their  teeth  chatter,  and  they  become  more  or  less 
cyanosed;  while  others  do  not  complain  at  all.  Much  dejjends  upon  the 
skill  and  tact  with  which  the  bath  is  given.  Brand  originally  recom- 
mended that  a  glass  of  red  wine  be  given  the  patient  before  and  after 


56  BACTERIAL  INFECTIONS 

the  bath;  whiskey  has  been  largely  substituted  in  this  country,  but  it 
is  not  necessary  as  a  routine  measure.  In  the  event  of  unusual  shivering 
or  of  cyanosis,  especially  of  the  face  (rather  than  of  the  extremities, 
which  occurs  in  practically  all  patients),  a  half-ounce  (15  c.c.)  of  whiskey 
may  be  given;  but  equally  good  results  attend  the  use  of  hot  coffee, 
hot  broth  or  milk,  aromatic  spirit  of  ammonia,  Hoffmann's  anodyne, 
etc.  The  patient  should  be  removed  immediately  from  the  bath  upon 
the  occurrence  of  marked  cyanosis  (especially  of  the  face),  cardiac  col- 
lapse, acute  abdominal  pain,  vomiting,  or  intestinal  hemorrhage.  The 
baths  are  contraindicated  in  the  event  of  severe  abdominal  pain, 
hemorrhage,  perforation  (peritonitis),  cholecystitis,  thrombophlebitis, 
unusual  prostration,  and  cardiac  weakness. 

More  than  six  tub  baths  are  rarely  required  in  the  twenty-four  hours. 
The  patient  should  be  allowed,  if  he  will,  to  sleep  at  night;  should 
the  temperature  be  unusually  high,  cold  sponging  may  be  substituted 
for  the  bath  at  night.  Following  the  suggestion  of  Dr.  John  H.  Musser, 
I  have  been  in  the  habit,  for  a  number  of  years,  of  giving  a  tub  bath  for 
fifteen  minutes  when  the  temperature  is  above  103°  F.,  and  a  sponge 
bath  when  the  temperature  is  above  102°  F.;  thus  while  the  treatments 
are  increased  in  number,  the  number  of  tub  baths,  especially  troublesome 
in  private  practice,  are  reduced.  Various  portable  bath-tubs  have  been 
devised  for  use  in  private  practice. 

Cold  sponging  is  an  alternative  hydrotherapeutic  measure  often 
necessary  in  private  practice,  and  sometimes  advisable  in  children  and 
elderly  persons.  The  water  may  be  at  70°  F.,  or  less,  even  ice  water, 
depending  upon  the  indications  in  the  case  and  the  reaction  of  the 
patient.  The  general  indications,  and  the  frequency  and  duration  of  the 
spongings,  are  similar  to  those  of  the  tub  baths.  While  it  is  best  to 
expose  only  that  of  the  body  being  sponged,  the  patient  should  not  be 
dried  until  the  process  is  completed,  since  to  insure  reduction  of  the 
temperature  a  layer  of  water  must  be  provided  for  evaporation. 

The  cold  pack  is  sometimes  serviceable  in  children.  The  patient  should 
be  wrapped  in  a  sheet  (previously  doubled  and  wrung  out  of  water  at 
60°  to  70°  F.),  and  then  covered  with  a  blanket — where  he  may  remain 
for  from  thirty  minutes  to  an  hour.  The  patient  sometimes  sweats 
considerably,  and  the  temperature  may  be  reduced  a  degree  or  two; 
but  the  reaction  and  the  influence  on  the  toxic  and  nervous  symptoms 
are,  as  a  rule,  not  so  marked  as  after  the  cold  tub  bath.  Sprinkling  the 
patient  with  cold  water  from  a  watering-pot,  or  by  means  of  a  spray- 
nozzle  attached  to  an  irrigating  reservoir,  is  also  efficacious  in  some  cases. 
Evaporation  may  be  facilitated  by  fanning  the  patient  after  the  applica- 
tion of  a  wet  sheet,  which  may  be  sprinkled  from  time  to  time.  The 
application  of  continuous  cold  to  the  abdomen  by  means  of  an  ice-bag 
or  a  Leiter's  coil  is  favored  by  some  practitioners,  who  believe  that  it 
reduces  the  temperature  and  lessens  the  likelihood  of  intestinal  hemor- 
rhage and  tympanites.  If  none  of  the  foregoing  measures  is  resorted 
to  systematically,  the  patient  should  he  bathed  at  least  once,  prefer- 


TYPHOID  FEVER  57 

ably  twice,  daily,  merely  as  a  matter  of  cleanliness,  to  prevent  bed  sores, 
and  to  equalize  the  circulation. 

Medicine. — Medicines  should  be  given  only  when  clearly  indicated. 
I  believe  it  good  practice,  though  often  not  necessary,  following  ancient 
custom,  if  the  patient  comes  under  observation  before  the  tenth  day, 
and  especially  in  the  event  of  constipation,  to  give  an  aperient  dose  of 
blue  mass  (5  grains,  0.3  gram)  or  of  calomel  (5  to  10  grains  at  one  dose, 
or  \  grain,  0.008  gram,  every  fifteen  miniltes  for  eight  doses),  followed  by 
an  enema  or  a  saline  cathartic.  In  view  of  the  common  deficiency  of 
gastric  juice,  and  the  occurrence  of  a  dry,  brown,  coated  tongue,  it  is 
advisable,  especially  in  private  practice,  to  give  10  to  15  minims  (0.6 
to  1  c.c.)  of  dilute  hydrochloric  acid,  three  times  daily.  Aside  from 
this,  many  patients  may  require  no  medicine  throughout  the  entire 
course  of  the  disease. 

The  so-called  intestinal  antiseptics  are  of  little  use,  since  they  do  not 
achieve  the  object  for  which  they  are  intended  (the  harmful  bacteria 
are  not  those  in  the  lumen  of  the  intestine,  but  those  in  the  lymphatic 
and  the  blood  streams);  they  sometimes  do  some  good,  however,  in 
preventing  or  limiting  tympanites.  The  best  is  probably  salol,  which  I 
believe  I  have  seen  do  good.  I  have  rarely  seen  any  indication  for  ad- 
ministering carbolic  acid,  the  mercurials,  iodine,  /?-naphthol,  menthol, 
thymol,  guaiacol,  chlorine,  acetozone,  etc.  Those  who  desire  only  to 
reduce  the  temperature  may  use  guaiacol,  30  minims  (2  c.c),  painted 
on  the  skin  of  the  abdomen  and  flank.  Since  I  have  never  used  any 
of  the  coal-tar  antipyretics,  except  in  an  occasional  dose,  in  the  early 
stages  of  the  disease,  to  relieve  headache  or  severe  neuromuscular 
pains,  I  am  happy  in  the  conviction  that  I  have  avoided  doing  my 
patients  considerable,  sometimes  even  fatal,  harm — of  which  these 
drugs  are  unquestionably  capable. 

Alcohol  should  not  be  used  as  a  routine  measure,  but  should  be  with- 
held until  it  is  clearly  indicated,  when  without  doubt  it  does  considerable 
good.  When  the  pulse  becomes  weak  and  dicrotic,  the  first  sound  of  the 
heart  weak  and  valvular;  when  insomnia  is  persistent  and  the  fever  high; 
and  when  the  typhoid  state  develops,  alcohol  renders  excellent  service. 
It  should  be  given  carefully  and  not  in  too  large  amounts — beginning 
with  a  half  ounce  three  or  four  times  daily.  In  some  cases  the  poor 
condition  of  the  patient  is  due  largely  to  the  amount  of  alcohol  given, 
and  improvement  immediately  follows  its  discontinuance.  Headache, 
in  the  early  stages,  is  usually  relieved  by  an  ice-bag,  sodium  bromide,  or 
a  small  dose  of  codeine  or  morphine;  rarely  one  of  the  coal-tar  deriva- 
tives, such  as  acetphenetidin  or  acetanilide,  may  be  given  in  small  doses, 
but  a  few  doses  only.  Insomnia  is  best  relieved  by  hydrotherapeutic 
measures,  the  patient  not  iiifre((uently  enjoying  a  refreshing  sleep  after 
the  badis.  (jeneral  restlessness,  particularly  at  night,  is  best  controlled 
by  a  Dover's  powder  or  a  small  dose  of  morphine  hyjxxlernu'cly.  The 
bromides,  codeine,  chlorahunide,  trional,  sulfonal,  and  similar  remedies 
are  sometimes  useful. 


58-  BACTERIAL  INFECTIONS 

Delirium  and  other  manifestations  of  severe  intoxication  are  best  con- 
trolled by  hydrotherapeutic  measures.  An  ice-bag  should  be  kept  to 
the  head  continuously.  Alcohol  is  useful,  and  is  often  required  in  rela- 
tively large  amounts,  but  the  caution  already  mentioned  should  be 
heeded.  With  the  development  of  the  typhoid  state,  stimulation  must 
be  more  active,  and  special  efforts  must  be  made  to  rid  the  patient  of 
toxins.  Water  should  be  given  in  very  large  amounts,  and  hot  enteroc- 
lysis  and  hypodermoclysis  (0.9  per  cent,  saline  solution)  are  extremely 
serviceable.  Cocaine,  camphor,  and  codeine  hypodermicly  often  con- 
trol markedly  the  mental  wandering,  the  carphologia,  and  the  subsultus 
tendinum.  Strychnine  (^^-^  to  ^V  grain;  0.0015  to  0.003  gram)  is  often 
of  value,  but  it  should  not  be  given  continuously,  since  it  often  tends  to 
aggravate  the  condition.  In  cases  of  marked  cardiac  asthenia  with  low 
blood  pressure,  the  addition  to  the  saline  solution  by  hypodermoclysis 
of  2  to  4  c.c.  of  adrenalin  chloride  is  often  followed  by  good  results. 
Digitalin  germanicum  (Merck),  ^^  to  |^  grain  (0.005  to  0.01  gram) 
hypodermicly,  also  often  seems  to  do  good,  although  it  is  said  to  lose 
much  of  its  efficiency  during  states  of  fever.  The  meningism  that 
much  simulates  meningitis  is  often  markedly  relieved  by  lumbar 
puncture. 

Constipation  rarely  requires  much  treatment,  and  constipation  as 
such  is  much  to  be  preferred  to  diarrhoea.  A  simple  soap-suds  enema 
or  an  oil  enema  should  be  given  every  other  day  if  the  bowels  do  not 
move  spontaneously.  During  the  height  of  the  disease  no  purgatives 
whatever  should  be  given  by  the  mouth.  During  convalescence  special 
attention  should  be  paid  to  the  bowels,  since,  despite  a  daily  evacuation, 
even  of  liquid  feces,  the  patient  may  be  constipated;  that  is,  his  rectum 
and  colon  may  be  more  or  less  filled  with  hardened  feces.  The  rectum, 
the  urinary  bladder,  and  the  gall-bladder  should  be  the  special  objects 
of  concern  in  delayed  convalescence.  Well  on  in  convalescence  castor 
oil  often  subserves  a  useful  purpose. 

Diarrhoea  should  not  be  checked  unceremoniously,  not  unless  there 
are  more  than  four  movements  in  the  twenty-four  hours,  and  they  are 
distressing  and  weakening  to  the  patient.  Since  ill-digested  food  is 
usually  the  cause,  the  milk  should  be  stopped,  temporarily  at  least,  and 
albumen  water  substituted.  Bismuth,  salol,  and  chalk  mixture,  or  a  lead 
and  opium  pill,  or  aromatic  sulphuric  acid  and  other  astringents,  may  be 
administered  for  a  few  days,  but  care  should  be  exercised  that  scybalous 
masses  do  not  form.  Tympanites,  often  associated  with  diarrhoea,  is  by 
no  means  so  common  as  in  the  days  prior  to  the  cold-bath  treatment. 
When  developed  it  may  usually  be  controlled  by  withholding  the  milk, 
temporarily  at  least,  and  administering  turpentine  externally  (hot  stupes), 
by  the  mouth,  and  by  the  rectum,  if  necessary.  Charcoal,  resorcin, 
/?-naphthol,  zinc  sulphocarbolate,  etc.,  by  the  mouth,  and  milk  of 
asafoetida,  by  the  rectum,  are  also  sometimes  of  service.  A  rectal  tube 
may  be  inserted  high  up  in  the  sigmoid.  A  hypodermic  injection  of 
eserine  (y^^  ^^to  gi'ain,  0.0006  to  0.C013  gram)  is  sometimes  efficacious 


TYPHOID  FEVER  59 

in  causing  the  expulsion  of  considerable  gas.  Vomiting  is  rarely  severe, 
and  when  present  is  usually  controlled  by  withholding  food  for  a  time, 
and  giving  lime  water  with  creosote  or  carbolic  acid  (in  \  grain,  0.008 
gram,  doses),  bismuth,  cerium  oxalate,  sips  of  hot  water,  brandy,  or  dry 
champagne.     Hot  applications  to  the  abdomen  are  also  of  service. 

Hemorrhage  is  best  treated  by  securing  absolute  rest  to  the  patient 
and  his  intestines — by  disturbing  the  patient  as  little  as  possible,  even 
for  evacuating  his  bowels,  withholding  all  food  for  at  least  ten  or  twelve 
hours,  and  giving  morphine  hypodermicly.  An  ice-bag  may  be  applied 
to  the  abdomen,  except  in  the  event  of  marked  collapse  and  lowered 
temperature;  custom  sanctions  the  use  of  ice  internally.  How  long 
the  morphine  should  be  continued  must  be  determined  in  individual 
cases — remembering  that,  though  it  inhibits  peristalsis,  it  favors  intestinal 
distention,  and  in  the  event  of  perforation  (associated  in  from  15  to  20 
per  cent,  of  the  cases  of  hemorrhage)  it  masks  the  symptoms  and  may 
prevent  their  recognition.  Turpentine  is  recommended  to  control  re- 
peated oozings.  I  have  never  seen  undoubted  good  follow  the  use  of 
any  of  the  styptics,  but  lead  (in  the  well-known  lead  and  opium  pill), 
Monsel's  solution  of  iron  sulphate,  tannic  acid,  etc.,  may  be  used  by 
those  committed  to  the  practice.  Calcium  chloride  seems  indicated 
theoretically  to  promote  the  coagulation  of  the  blood,  but  its  effects 
are  lost  after  several  days'  use.  Gelatine  has  largely  gone  out  of 
use  hypodermicly,  but  it  may  be  given  by  the  mouth,  especially  when 
food  is  recommenced,  in  the  hope  that  it  will  favor  the  coagulation  of 
the  blood;  but  its  action  is  at  least  doubtful.  In  the  event  of  collapse, 
the  foot  of  the  bed  should  be  elevated,  hot-water  bags  should  be  applied 
about  the  patient,  and  hypodermoclysis  and  diffusible  stimulants,  such 
as  ether  and  camphor,  should  be  administered.  Recently  operation 
has  been  advised  to  control  severe  bleeding. 

Perforation  and  peritonitis  (which  may  be  due  to  causes  other  than 
perforation)  calls  for  immediate  operation — now-a-days  done  largely 
under  local  anesthesia.  The  mortality  without  operation  is  at  least 
95  to  98  per  cent.,  an  occasional  patient  seeming  to  recover  without 
operation,  but  in  such  cases  the  diagnosis  must  always  remain  more 
or  less  in  doubt.  With  improved  technique  and  early  operation  the 
mortality  is  becoming  less  and  less,  and  is  now  probably  not  more  than 
60  to  65  per  cent. ;  that  is  from  30  to  35  per  cent,  of  patients  are  saved 
who  otherwise  would  inevitably  perish.  Without  operation,  the  treat- 
ment consists  of  supportive  measures:  opium  to  relieve  pain,  and  hot 
water  botdes,  hypodermoclysis,  and  stimulants  to  combat  shock  and 
peritoneal  sepsis. 

Cholecystitis  usually  subsides  without  untoward  symptoms,  though  it 
is  usually  the  first  of  a  train  of  serious  symptoms  (gallstones,  etc.)  that 
may  develop  in  later  life.  If  the  symptoms  are  acute,  however,  if 
they  increase  rather  than  subside,  and  especially  if  there  is  reason  to 
suspect  suppuration  or  perforation,  operation  should  be  undertaken. 
In  all  cases  the  patient  must  be  under  continuous  competent  observa- 


60  BACTERIAL  INFECTIONS 

tion,  so  that  should  operation  be  called  for  it  may  be  undertaken  without 
delay.  There  is  much  to  commend  operation  following  recovery  with 
a  view  to  prevent  the  later  development  of  gallstones. 

Bed  sores  are  better  prevented  than  cured.  Perfect  cleanliness  is 
imperative;  the  bed-linen  should  be  well  cared  for  and  creases  pre- 
vented; the  patient  should  be  turned  frequently  from  side  to  side,  and 
he  should  be  bathed  frequently  with  alcohol,  alum  water,  etc.;  and 
should  any  redness  develop  he  should  be  placed  upon  an  air  cushion, 
and  the  reddened  area  painted  with  a  5  per  cent,  silver  nitrate  solution. 
If  a  bed  sore  develops,  all  pressure  must  be  removed,  by  the  use  of 
the  air-cushion,  pads,  or  a  water-bed  or  an  air-bed;  the  ulcer  should 
be  treated  antiseptically  and  with  a  drying  dusting  powder  consisting  of 
boric  acid,  zinc  steorate,  and  bismuth  subnitrate;  all  dead  tissue 
should  be  removed,  and  if  the  granulations  are  sluggish,  stimulating 
applications  of  silver  nitrate  should  be  made. 

Thrombosis  of  the  femoral  or  other  veins  should  be  treated  by  rest  of 
the  limb  in  an  elevated  position,  and  the  application  of  cotton  wool, 
an  ichthyol  ointment  (33  per  cent.),  a  lead  and  opium  lotion,  or  a 
saturated  solution  of  magnesium  sulphate.  In  the  early  days  an  ice-bag 
over  the  thrombosis  will  relieve  the  pain.  Later,  mercury,  belladonna, 
and  iodine  ointment  (equal  parts)  is  useful,  but  rough  handling  must 
be  avoided  on  account  of  the  possibility  of  embolism.  Tender  toes 
(peripheral  neuritis)  may  be  relieved  by  alcohol  rubbings,  massage, 
counterirritation  (iodine,  etc.),  ichthyol  ointment,  and  aconitine  oint- 
ment (2  per  cent.).  Bacilluria,  a  frequent  and  unsuspected  source  of 
infection,  is  usually  controlled  by  hexamethylenamine,  10  to  15  grains 
(0.6  to  1  gram)  three  times  daily.  It  is  advisable  to  give  this  as  a 
routine  measure  for  four  or  five  days  in  the  early  days  of  convalescence. 
Should  cystitis  develop,  we  may  use,  in  addition  to  the  hexamethylena- 
mine, irrigations  of  the  bladder  with  mercuric  bichloride,  1  to  50,000. 
As  previously  stated,  the  urine  of  every  typhoid-fever  patient  should 
be  disinfected. 

PARATYPHOID  FEVER. 

Paratyphoid  fever  is  an  acute  infectious  disease  caused  by  Bacillus 
paratyphosus  (Archard  and  Bensaude);  clinically  it  is  characterized 
by  symptoms  that  do  not  distinguish  it  from  typhoid  fever. 

Etiology. — ^The  term  Bacillus  paratyphosus  is  used  as  a  convenient 
designation  for  a  group  of  bacilli  intermediate  in  biological  type  between 
the  typhoid  and  the  colon  groups.  Of  the  many  subdivisions  of  these 
organisms,  one  much  resembles  Bacillus  typhosus,  another  Bacillus  coli, 
while  others  exhibit  biological  characteristics  pertaining  to  Bacillus 
enteritidis,  Gartner  (the  meat  poisoning  bacillus).  Bacillus  suipestifer 
(hog  cholera),  and  Bacillus  psittacosis.  Following  Schottmiiller  and 
I3uxton  the  paratyphoid  bacilli  are  commonly  divided  into:  (1)  The 
paracolon   bacilli,  a  group  of    organisms   differing    somewhat  among 


PYOGENIC  INFECTIONS  61 

themselves  but  culturally  very  much  alike,  and,  as  a  rule,  not  causing 
typhoid-fever  symptoms  in  man;  and  (2)  the  paratyphoid  bacilli,  a 
group  of  organisms  that  do  cause  typhoid  fever  in  man  and  are  sub- 
divided into  Bacillus  paratyphosus  a,  distinctly  unlike  the  paracolon 
bacilli,  and  Bacillus  paratyphosus  [^,  resembling  the  paracolons,  but  a 
distinct  species.  Bacillus  coli  and  Bacillus  fsecalis  alcaligenes  also  seem 
to  be  capable  of  causing  a  typhoid-like  infection,  so  that  the  term 
typhoidal  disorders  is  sometimes  used  to  include  this  whole  group  of 
diseases.  Aside  from  the  specific  cause,  the  etiological  factors  of  para- 
typhoid fever  are  similar  to  those  of  typhoid  fever. 

Pathology. — The  disease  is  a  general  bacteremia,  and  local  lesions 
may  be  inconspicuous  or  entirely  absent.  The  common  noteworthy 
lesion  is  enlargement  of  the  spleen.  Otherwise  the  disorder  resembles 
most  of  the  bacteremias.  The  characteristic  lesions  of  typhoid  fever 
are  usually  absent;  Beyer's  patches  and  the  solitary  glands  are  slightly 
if  at  all  altered;  intestinal  ulceration,  in  the  few  cases  observed,  has 
resembled  dysenteric  rather  than  typhoid  ulceration;  proliferative  changes 
in  the  endothelium  and  endothelial  phagocytosis,  so  characteristic  of 
typhoid  fever,  have  not  been  observed.  Doubtless,  many  of  the  cases 
of  so-called  typhoid  fever  without  intestinal  lesions  have  been  examples 
of  paratyphoid  infection. 

Symptoms. — In  general  the  symptoms  are  those  of  typhoid  fever,  but 
as  a  rule,  paratyphoid  fever  has  a  shorter  period  of  invasion,  and  the 
fever  is  less  high,  exhibits  more  marked  diurnal  variations,  has  a  shorter 
course  (twelve  to  twenty  days),  and  ends  rather  rapidly  (crisis  or  rapid 
lysis).  Prolonged  (eighty-four  day),  severe,  and  even  fatal  cases, 
however,  have  been  observed.  Diarrhoea  appears  to  be  somewhat 
more  common  than  in  typhoid  fever.  Intestinal  hemorrhage  occurs  in 
from  5  to  10  per  cent,  of  the  cases.  Pratt  has  emphasized  the  frequency 
of  complications — which  are  often  purulent  in  character.  Relapses  are 
about  as  frequent  as  in  typhoid  fever. 

Diagnosis. — The  disease  is  usually  suspected  to  be  typhoid  fever 
luitil  the  Gruber-Widal  reaction  with  the  typhoid  bacillus  is  found  to  be 
absent.  The  diagnosis  depends  then  upon  the  recovery  of  the  infecting 
microorganism — from  the  blood,  the  spleen,  the  urine,  the  feces,  the 
sputum,  the  rose-spots,  or  the  complicating  lesions;  or  the  diagnosis 
may  be  made  by  the  agglutination  reaction  with  known  strands  of 
paratyphoid  bacilli. 

Prognosis. — The  mortality  is  low — not  more  than  3  per  cent. 

Treatment. — The  treatment  is  similar  to  that  of  typhoid  fever. 

PYOGENIC  INFECTIONS. 

(Pyococcic  Infeclionsi;  Septic  Infections;  Snpremin;  Septicemia;  Pj/emia; 
Septicopyemia;  Toxemia;  Bacteremia.) 

The  pyogenic  infections  comprise  a  group  of  non-specific  infectious 
diseases,  some  local  and  some  general,  caused  by  the  dift'erent  pyogenic 


62  BACTERIAL  INFECTIONS 

microorganisms,  and  characterized  by  fever,  leukocytosis,  a  variable 
degree  of  systemic  intoxication,  sometimes  by  bacteremia,  chills,  and 
sweats,  and  often  by  at  least  a  local  focus  of  inflammation  or  suppuration. 

Etiology. — The  pyogenic  infections  occur  in  all  parts  of  the  world 
and  at  all  seasons;  they  are  common  at  all  ages,  and  under  like  conditions 
they  affect  the  sexes  equally — but  for  very  obvious  reasons  women  alone 
suffer  from  that  form  known  as  puerperal  infection.  While  the  robust 
are  by  means  immune,  these  infection?  are  especially  common  in  persons 
debilitated  from  any  cause,  and  they  are  often  the  terminal  event  in  the 
course  of  many  other  diseases  (terminal  infections). 

The  exciting  causes  of  these  infections  are  especially  the  pyogenic 
cocci — Staphylococcus  pyogenes  aureus  (citreus  et  albus),  Streptococcus 
pyogenes,  Diplococcus  pneumonife.  Micrococcus  gonorrhoese,  Micro- 
coccus intracellularis  meningitidis,  and  Micrococcus  tetragenus.  Many 
bacilli  and  certain  streptothrix  also  give  rise  to  pyogenic  infections, 
of  which  the  more  important  are  Bacillus  coli  communis,  Bacillus 
typhosus,  Bacillus  pyocyaneus.  Bacillus  aerogenes  capsulatus.  Bacillus 
tuberculosis.  Bacillus  anthracis.  Bacillus  mallei,  Bacillus  pestis,  and 
Friedlander's  pneumobacillus.  Although  these  bacilli  unquestionably 
may  produce  suppuration,  the  pyococci  are  not  infrequently  associ- 
ated with  them,  as  well  as  with  other  bacilli  (the  diphtheria  bacillus,  for 
instance);  that  is,  mixed  infections  are  quite  common.  Infection  may 
be  transmitted  by  direct  inoculation  (such  as  infected  sutures  at  opera- 
tion), contact  (such  as  necropsy  and  dissection  wounds),  or  proximity 
(infected  wounds  and  gangrene  in  hospitals  and  other  infected  localities), 
by  a  third  person,  and  by  fomites  of  all  kinds.  Susceptibility  to  the  in- 
fection is  much  enhanced  by  a  wound,  abrasion,  or  traumatism  of  the 
skin  or  mucous  membrane ;  in  fact,  were  it  not  for  the  protection  afforded 
by  the  skin  and  the  mucous  membranes  these  infections  would  be  much 
more  common  than  they  are,  since  pathogenic  staphylococci  and  often 
streptococci  may  readily  be  cultivated  from  the  skin  and  certain  mucous 
surfaces  of  the  most  human  beings  and  lower  animals,  and  they  abound 
in  the  air,  dust,  and  soil  about  us.  Infection  may  be  acquired  by  inhala- 
tion or  ingestion,  but  it  is  much  more  commonly  acquired  by  direct  inocu- 
lation into  the  blood  stream  or  the  lymph  stream  (through  a  wound  or 
abraded  surface). 

Pathology. — These  pyogenic  infections  still  labor  under  the  embar- 
rassment of  descriptive  terms  born  of  ignorance  and  perpetuated  in  this 
day  of  comparative  enlightenment — such  as  sapremia,  septicemia,  and 
pyemia.  Sapremia  was  understood  to  be  a  condition  due  to  poisoning 
by  the  chemical  products  of  bacteria,  but  unattended  by  the  entrance  of 
the  bacteria  themselves  into  the  blood;  septicemia  (septic  infection, 
putrid  material  in  the  blood)  was  a  condition  due  to  the  growth  and 
development  of  microorganisms  in  the  circulating  blood,  as  well  as  to 
poisoning  by  their  chemical  products;  and  pyemia  (pus  in  the  blood), 
also  called  septicopyemia,  comprised  in  addition  to  the  foregoing  the 
development  of  multiple  abscesses  in  different  parts  of  the  body.     And 


PYOGENIC  INFECTIONS  63 

when  the  source  of  the  infection  was  not  discoverable  the  condition  was 
spoken  of  as  cryptogenetic.  These  distinctions,  however,  are  strained 
and  artificial:  except  when  introduced  intentionally  or  taken  in  certain 
forms  of  food  poisoning,  poisoning  of  the  body  by  the  products  of  bacteria 
cannot  occur  independently  of  the  presence  of  bacteria  in  the  body,  and 
contrary  to  former  opinions,  we  now  know  that  bacteria  enter  and  circulate 
in  the  blood  stream  much  more  frequently  than  was  formerly  supposed, 
and  that  abrasions  and  other  small  and  inconspicuous  wounds  of  the 
skin  and  mucous  membranes  are  frequently  the  infectious  atria  of  what 
formerly  would  have  been  regarded  as  cryptogenetic  sepsis  or  infection. 
Since,  therefore,  it  is  impossible,  clinically  as  well  as  anatomically,  to 
separate  the  one  of  these  conditions  from  the  others,  since  in  reality  they 
are  but  stages  of  the  one  process,  it  is  much  preferable  to  speak  of  them 
as  pyococcic  (or  other)  infections;  when  possible  to  qualify  these  by 
adjectives  such  as  staphylococcic,  streptococcic,  pneumococcic,  gono- 
coccic,  etc.;  and  to  use  the  terms  toxemia  and  bacteremia  in  their  very 
obvious  meanings.  It  is  desirable  to  bear  in  mind  also  that  it  is  usually 
impossible  to  distinguish  between  bacterial  intoxication  and  bacteremia. 

The  pyogenic  infections  may  be  classified  as  follows :  (1)  Local  infec- 
tions; (2)  general  infections  (a)  with  and  (b)  without  obvious  infectious 
atria;  and  (3)  terminal  or  secondary  infections. 

Local  Infections. — The  local  infections  provoked  by  pyogenic 
microorganisms,  especially  staphylococci  and  streptococci,  are  legion, 
and  comprise  the  inflammatory  processes  which  arise  in  all  parts  of  the 
body  and  which  may  or  may  not  progress  to  suppuration,  such  as  fur- 
uncle, carbuncle,  abscess,  phlegmon,  cellulitis,  erysipelas,  lymphangitis, 
phlebitis,  bronchitis,  pleuritis,  pericarditis,  endocarditis,  peritonitis, 
appendicitis,  cholangitis,  salpingitis,  osteomyelitis,  arthritis,  puerperal 
infection,  etc.  As  long  as  these  (and  other)  infections  remain  local,  the 
systemic  intoxication  is  due  solely  to  the  soluble  toxins  produced  by 
the  bacteria  and  absorbed  into  the  lymphatic  and  blood  streams;  in 
this  respect  these  infections  resemble  certain  specific  infections, 
such  as  diphtheria  and  tetanus,  in  which  the  systemic  symptoms  are 
toxic  solely.  The  severity  of  the  symptoms,  the  toxemia,  is  proportionate 
to  the  amount  and  virulence  of  toxins  absorbed,  and  since  the  toxin 
is  being  constantly  excreted,  especially  by  the  kidneys,  removal  of  the 
toxin-producing  focus,  such  as  a  putrescent  placenta,  a  pelvic  abscess, 
an  empyema,  etc.,  results  in  almost  immediate  lessening  of  the  toxic 
manifestations,  and  unless  irreparable  damage  has  already  been  done, 
recovery  usually  ensues.  Contrary  to  former  opinions,  we  now  know 
that  in  many  of  these  local  infections  there  is  a  disposition  to  an  early 
invasion  of  the  lymphatic  and  blood  streams,  whence  to  the  toxemia 
bacteremia  is  added.  The  bactericidal  properties  of  the  blood  serum, 
however,  are  considerable,  and  though  invasion  of  the  blood  may  occur, 
general  infection  is  often  prevented. 

General  Infections. — Frequently  on  account  of  the  virulence  of  the 
invading  microorganisms  the  bactericidal  properties  of  the  blood  are 


64  BACTERIAL  INFECTIONS 

overcome  and  general  infection  (bacteremia)  occurs.  This  may  or 
may  not  be  associated  with  multiple  abscess  formation,  whence  it  is 
spoken  of  as  septicemia  or  pyemia,  respectively.  The  term  septicemia 
is  also  employed  to  designate  the  bacteremia  that  sometimes  occurs  in 
other  infections,  such  as  typhoid  fever  (typhoid  septicemia),  gonococcic 
infection,  anthrax,  .etc. 

These  general  infections  may  occur  with  or  without  an  obvious  local 
lesion.  Much  interest  attaches  to  those  cases,  by  no  means  rare,  in 
which  no  local  infection  can  be  found  during  life  or  after  death — 
so-called  cryptogenetic  infection  or  septicemia.  Diligent  search  often 
results  in  the  discovery  of  a  small  local  lesion  that  otherwise  would 
have  gone  undetected,  but  in  some  cases  the  most  rigorous  investigation 
fails  to  reveal  any  local  source  of  infection.  In  the  majority  of  cases, 
however,  general  infection  is  preceded  by  some  local  lesion,  inconspicu- 
ous or  apparently  insignificant  though  it  may  apparently  be,  such  as  an 
acne  pustule,  a  furuncle,  a  stitch  abscess,  a  small  abrasion;  a  latent  or 
masked  osteomyelitis,  otitis  media,  adenitis,  empyema,  cholecystitis,  or 
appendicitis;  an  unsuspected  abortion,  retained  placenta,  etc.  Infection 
may  be  transmitted:  (1)  Along  the  lymphatics  (which  may  or  may  not 
become  actively  inflamed) ;  (2)  by  way  of  the  venous  circulation,  in 
which  event  the  venules  frequently,  and  the  larger  veins  sometimes, 
become  thrombosed ;  and  (3)  sometimes  by  way  of  the  arterial  stream, 
especially  in  pulmonary  or  endocarditic  lesions,  or,  as  rarely  happens, 
when  a  local  focus  of  suppuration  ruptures  directly  into  an  artery. 
Should  the  venous  thrombi  soften  (a  rather  common  event),  the  emboli 
carried  to  different  parts  of  the  body  act  either  mechanically,  producing 
infarction,  or,  if  they  contain  virulent  bacteria,  setting  up  disseminated 
foci  of  suppuration:  metastatic  or  embolic  abscesses  (so-called  pyemia, 
or  septicopyemia).  Similar  results  ensue  if  the  infectious  matter  is 
transported  by  the  arterial  stream.  These  metastatic  phenomena  occur 
especially:  (1)  In  the  lungs,  particularly  when  the  emboli  have  been 
transported  by  way  of  the  systemic  venous  circulation;  (2)  in  other 
parts  of  the  body,  when  the  arterial  stream  has  become  infected,  either 
from  rupture  of  a  purulent  focus  into  it,  or  from  endocarditic  thrombi, 
or  from  metastatic  foci  in  the  lungs,  or  by  the  passage  of  small  emboli 
through  the  pulmonary  capillaries ;  and  (3)  in  the  liver  (suppurative 
pylephlebitis),  when  the  primary  focus  is  in  the  area  of  collection  of  the 
portal  vein. 

Terminal  or  Secondary  Infections. — Terminal  or  secondary 
infections  deserve  special  mention.  In  the  majority  of  debilitating  and 
wasting  diseases,  such  as  arteriosclerosis,  chronic  nephritis,  cirrhosis  of 
the  liver,  myocarditis,  etc.,  the  final  event  is  determined  not  by  the  primary 
disease,  but  by  some  secondary  or  so-called  terminal  infection.  This  is 
usually  caused  by  streptococci,  staphylococci,  or  pneumococci,  and  less 
commonly  by  Bacillus  coli,  Bacillus  tuberculosis,  Bacillus  pyocyaneus. 
Bacillus  proteus,  etc. ;  and  the  infection  may  be  local  or  general.  The 
local  infections  are  the  more  common,  especially  pyococcic  or  tuber- 


PYOGENIC  INFECTIONS  65 

culous  infection  of   the  serous   membranes — pleura,   peritoneum,   and 
pericardium. 

In  the  milder  pyogenic  infections  (pyococcic  toxemia,  sapremia)  the 
lesions  consist  of — usually  a  local  focus  of  suppuration,  cloudy  swelling 
of  the  organs,  especially  the  liver,  kidneys,  and  heart,  enlargement  and 
softening  of  the  spleen,  lessened  coagulability  of  the  blood,  and  often 
small  hemorrhages  in  the  serous  membranes  (pleura,  peritoneum,  and 
pericardium).  In  more  severe  cases,  associated  with  bacteremia  (septi- 
cemia), the  foregoing  lesions  are  aggravated:  to  the  cloudy  swelling  of 
the  organs  foci  of  necrosis  are  added,  the  general  lymphatics  are  enlarged 
and  softened,  and  small  hemorrhages  appear  not  only  in  the  serous 
membranes  (including  the  pia-arachnoid),  but  also  in  the  mucous  mem- 
branes and  the  skin.  In  the  cases  usually  described  as  pyemia,  in  addi- 
tion to  the  foregoing,  thromboses,  especially  in  the  region  of  the  primary 
focus,  and  embolism  with  infarction  and  metastatic  abscesses  in  different 
parts  of  the  body,  are  found.  Lesions  of  the  endocardium  (acute  benign 
and  malignant  endocarditis)  are  common  in  all  forms  of  pyogenic  infec- 
tions, and  although  they  often  materially  modify  the  course  and  the  symp- 
tomatology of  the  disease,  they  scarcely  merit  separate  classification;  in 
fact,  the  nature  of  the  disease  is  better  understood  by  bearing  in  mind 
that  the  involvement  of  the  endocardium  is  a  more  or  less  accidental 
factor  in  the  pyogenic  infection,  and  that  although  the  lesion  may  be 
serious  the  essential  factor  is  the  general  pyogenic  infection,  of  which 
the  endocardial  lesion  may  be  the  least  important.  The  infective  bacteria 
may  be  recovered  (in  pure  or  mixed  culture)  from  the  local  lesions  and 
the  blood. 

Symptoms. — The  symptoms  vary  with  the  severity  of  the  infection. 
Frequently  the  onset  of  the  symptoms  is  insidious,  and  in  case  a  primary 
local  focus  (furuncle,  wound,  puerperium,  etc.)  is  present,  a  period  of 
incubation,  varying  from  one  to  three  or  four  days,  may  be  quite  obvious. 
Occasionally  the  onset  is  sudden,  with  chill  or  chilliness,  fever,  malaise, 
headache,  general  neuromuscular  pains  and  aching,  and  sometimes 
vomiting  and  diarrhoea.  Especially  characteristic  is  intermittent  fever, 
with  notable  diurnal  fluctuations  (4°  to  6°  F.),  accompanied  by  irregularly 
occurring  chills  and  sweats  (often  the  chief  complaint).  Sometimes  the 
fever  occurs  in  paroxysms  of  hyperpyrexia,  between  which  the  tempera- 
ture may  be  of  the  continuous-fever  type,  or  almost  if  not  quite  normal 
(apyrexia).  In  addition,  the  pulse  is  rapid  and  weak,  the  spleen  is 
enlarged,  diarrhoea  may  continue,  and  the  headache  gives  way  to  restless- 
ness, hebetude,  stupor,  and  delirium;  the  patient  becomes  markedly 
prostrated,  polynuclear  leukocytosis  is  present,  and  a  high-grade  anemia 
develops  rapidly.  A  subicteric  hue  or  even  jaundice  is  not  uncom- 
mon, and  certain  cutaneous  phenomena,  such  as  roseola,  erythema, 
urticaria,  etc.,  doubtless  toxic  in  nature,  may  be  observed. 

In  the  so-called  pyemic  cases,  embolic  phenomena  (mechanical  and 
septic  infarctions)  may  occur  in  all  parts  of  the  body,  especially:     In 
the  skin — petechial  hemorrhages  and  furuncles;  in  the  heart — ulcerative 
5 


66  BACTERIAL  INFECTIONS 

endocarditis,  septic  myocarditis,  and  fibrinopurulent  pericarditis;  in 
the  lungs — hemorrhagic  infarcts  (pain,  dyspnoea,  cyanosis,  hemoptysis, 
localized  dulness,  bronchial  breathing,  and  fine  rales),  abscesses,  or 
fibrinopurulent  pleuritis ;  in  the  kidneys — renal  pain,  albumin,  blood,  and 
tube  casts  in  the  urine ;  in  the  spleen — splenic  pain,  audible  and  palpable 
frictions;  in  the  eye — retinal  hemorrhages,  choroiditis,  optic  neuritis, 
panophthalmitis;  in  the  brain — -hemorrhage  (hemiplegia,  monoplegia, 
aphasia,  blindness,  convulsions)  or  abscess;  in  the  long  bones — 
periostitis  and  osteomyelitis  (local  pain  and  tenderness);  in  the  joints 
— arthritis  (local  pain,  swelling,  and  tenderness). 

The  course  of  these  infections  is  sometimes  extremely  rapid,  especially 
when  a  large  amount  of  toxin  is  suddenly  thrown  into  the  circulation; 
death  may  result  within  twenty-four  or  forty-eight  hours.  Com- 
monly the  symptoms  last  for  from  one  to  three  weeks;  occasionally 
several  months. 

Diagnosis. — A  primary  focus  of  infection,  irregularly  occurring  fever, 
chills,  and  sweats,  prostration,  leukocytosis,  anemia,  cutaneous  hemor- 
rhages and  other  embolic  phenomena,  render  the  diagnosis  easy  in  the 
majority  of  cases.  Confirmation  may  be  obtained  by  cultivating  the 
infective  microorganisms  from  the  blood.  Involvement  of  the  endo- 
cardium (malignant  endocarditis)  is  suggested  by  embolic  phenomena 
and  instability  of  the  cardiac  activity  (rapid  changes  in  frequency  of 
beat).  Malaria  may  be  excluded  by  the  presence  of  leukocytosis,  the 
irregularity  of  the  rigors  and  sweats,  absence  of  the  plasmodium,  and  the 
non-response  to  quinine.  In  acute  tuberculosis,  as  contrasted  with 
pyogenic  infection,  variations  in  the  temperature  and  pulse-rate  and 
excessive  perspirations  occur  with  more  regularity,  wasting  is  more  rapid, 
a  local  focus  of  tuberculous  disease  may  be  detected  in  some  part  of  the 
body — in  the  lungs  (tubercle  bacilli  in  the  sputum),  in  the  pleura,  in  the 
abdomen,  in  the  brain  (tubercle  bacilli  in  the  cerebrospinal  fluid  obtained 
by  lumbar  puncture) — and  embolism  does  not  occur.  The  detecting  of 
chloroidal  tubercles  in  the  one  case,  and  of  retinal  hemorrhages  in  the 
other,  is  of  the  greatest  diagnostic  value.  In  case  of  doubt  as  regards 
typhoid  fever,  persistent  headache,  persistent  but  not  intermittent  fever, 
comparative  infrequency  of  the  pulse,  roseola,  tympanites,  the  Gruber- 
Widal  reaction,  the  recovery  of  typhoid  bacilli  from  the  urine,  feces, 
roseola,  blood,  etc.,  and  the  absence  of  petechise  and  of  embolism, 
suggest  typhoid  fever,  whereas  pyogenic  infection  is  suggested  by  a  local 
source  of  infection,  undue  dyspnoea,  irregular  and  repeated  rigors,  pro- 
fuse sweats,  early  marked  prostration,  the  rapid  development  of  anemia, 
leukocytosis,  embolism,  and  the  recovery  from  the  blood  of  pyogenic 
microorganisms.  In  obscure  cases  of  evident  intoxication,  hidden  or 
latent  foci  of  infection,  such  as  gonorrhoea,  prostatic  abscess,  pyelitis, 
osteomyelitis,  cholecystitis,  etc.,  should  be  diligently  searched  for.  We 
are  not  yet  able  to  distinguish  clinically  between  the  different  pyogenic 
infections,  but  in  general  the  streptococcic  infections  are  the  more  serious, 


ERYSIPELAS  67 

give  rise  to  a  more  rapid  and  progressive  anemia,  greater  prostration, 
and  often  an  unusual  mental  alertness. 

Prognosis. — The  outlook  depends  upon  the  severity  of  the  infection, 
the  resistance  of  the  patient,  and  the  possibility  of  removing  the  infectious 
foci.  Remarkable  improvement  often  ensues  immediately  after  the  local 
foci  are  removed;  if,  however,  the  patient's  tissues  are  already  seriously 
damaged,  this  may  avail  little,  if  anything. 

Treatment. — ^The  prime  indication  is  to  remove  the  infectious  foci — 
whence  the  treatment  is  largely  surgical.  Little  can  be  expected  of 
medicinal  measures  if  the  remnants  of  a  putrid  placenta  are  allowed  to 
remain  in  the  uterus,  or  if  a  liver  abscess,  brain  abscess,  or  an  empyema 
is  permitted  to  go  undrained.  In  addition  to  surgical  measures,  the 
patient's  strength  must  be  conserved,  by  fresh  air,  sunshine,  and  good 
nutritious  food.  Wliiskey,  quinine,  iron  (tincture  of  the  chloride),  and 
strychnine  are  useful  adjuvants — supportive  and  restorative,  and  hot 
saline  solutions  (hypodermoclysis  and  enteroclysis)  assist  in  eliminating 
the  toxins.  The  coal-tar  antipyretics  should  never  be  employed.  The 
sweats  may  be  controlled  by  alcohol  baths,  atropine,  and  aromatic  sul- 
phuric acid.  Crede's  colloid  silver  (1  per  cent,  solution,  hypodermically 
and  intravenously)  has  been  suggested,  but  the  results  have  not  been 
very  encouraging.  Antistreptococcic  serum  has  not  proved  of  great 
service.  The  best  results  recently  have  followed  the  use  of  autogenous 
vaccines  (bacterins) ;  that  is,  isolating  from  a  local  lesion  or  the  patient's 
blood  the  infecting  microorganism  and  from  this  preparing  a  vaccine. 


ERYSIPELAS. 

(St.  Anthony's  Fire.) 

Erysipelas  is  an  acute,  perhaps  specific,  infectious,  and  moderately 
contagious  disease  caused  by  Streptococcus  erysipelatus  (Fehleisen), 
and  characterized  by  high  fever,  marked  toxemia,  and  inflammation 
of  the  skin  and  subcutaneous  and  the  mucous  and  submucous  tissues. 
The  disease  in  reality  is  merely  one  manifestation  of  pyococcic  infection. 

Etiology. — Erysipelas  occurs  at  all  ages,  being  common  in  early  life, 
in  adolescence,  and  in  adult  life;  but  it  is  rather  uncommon  in  old  age. 
It  affects  males  more  frequently  than  females.  It  is  endemic  in  most 
large  cities,  and  frequently  prevails  epidemically,  especially  during  the 
late  winter  and  spring;  but  sporadic  cases  are  common.  Recurrences 
are  rather  frequent;  indeed,  in  some  persons  one  attack  seems  to 
predispose  to  subsequent  attacks. 

The  exciting  cause  of  the  disease  is  Streptococcus  erysipelatus,  which, 
however,  is  now  believed  to  be  identical  with  Streptococcus  pyogenes. 
Infection  may  be  transmitted  by  direct  inoculation,  contact,  or  proximity 
(possibly  transmitted  })y  the  air),  by  a  third  person,  and  by  fomites — 
whence  the  frequent  occurrence  of  epidemics  (less  common  recently 
than  in  former  years)  in  insanitary  hospitals,  institutions,  barracks,  etc. 


68  BACTERIAL  IXFECTIOXS 

Susceptibility  to  the  disease  is  much  enhanced  by  a  wound  of  the  skin  or 
of  a  mucous  membrane — whence  the  frequent  occurrence  of  the  disease 
(traumatic  erysipelas)  after  parturition,  operations,  traumatic  wounds, 
etc.  In  many  of  the  so-called  idiopathic  cases  a  history  of  previous 
nasal  catarrh  may  be  elicited,  and  in  many  others  there  are  doubtless 
unsuspected  wounds  or  abrasions  of  the  nasal  or  oral  mucous  mem- 
brane— whence  the  frequent  occurrence  of  facial  erysipelas.  Debili- 
tating influences,  such  as  those  connected  with  chronic  alcoholism, 
chronic  nephritis,  cirrhosis  of  the  liver,  etc.,  also  favor  the  development 
of  the  disease.  Infection  apparently  is  usually  acquired  directly  into  the 
blood  or  the  lymph  channels. 

Pathology. — The  lesions  consist  of  the  ordinary  changes  of  inflamma- 
tion with  marked  oedema  and  cellular  infiltration.  The  streptococci  are 
found  especially  in  the  lymphatic  channels  (lymphangitis),  and  in  large 
numbers  in  the  zone  of  spreading  inflammation  and  beyond  (where  active 
phagocytosis  may  be  observed).  The  visceral  lesions  are  those  common 
to  severe  pyococcic  infections.  Suppuration  of  the  seroiLS  membranes  is 
rather  common — pleuritis,  pericarditis,  endocarditis,  meningitis,  arthritis, 
etc. 

Symptoms. — In  so-called  idiopathic  (non-surgical)  erysipelas,  the 
period  of  incubation  varies  from  three  to  seven  or  ten  days.  Often 
prodromal  symptoms  are  absent,  but  usually  there  is  headache,  malaise, 
restlessness,  general  aching,  and  loss  of  appetite ;  possibly  also  slight  eleva- 
tion of  the  temperature.  The  onset  is  usually  abrupt  with  a  chill  or  chilli- 
ness (which  may  be  repeated),  high  fever  (104°  to  105°  F.),  sometimes 
nausea  and  vomiting,  followed  soon  by  the  specific  cutaneous  manifesta- 
tions. These  develop  first  on  the  bridge  of  the  nose  or  on  one  cheek 
near  the  nose,  or  at  a  mucocutaneous  junction  (in  the  event  of  a  wound, 
however,  immediately  about  the  wound).  They  consist  at  first  of  slight 
redness ;  at  the  end  of  twenty-four  hours,  however,  the  skin  has  become 
red  and  hot,  smooth  and  glistening,  swollen  and  quite  tense  (inflammatory 
oedema).  The  lesions  spread  by  peripheral  extension,  and  are  usually 
sharply  demarcated  from  the  adjacent  unaffected  skin  by  a  well-defined, 
elevated,  rather  pale,  and  indurated  ridge.  Often  the  cheeks,  the  eyelids, 
the  forehead,  the  ears,  sometimes  the  entire  scalp  and  even  the  neck 
become  involved,  and  give  rise  to  extreme  disfiguration.  As  the  disease 
spreads,  the  swelling  and  redness  of  the  parts  first  affected  gradually 
subside.  Blebs  not  infrequently  form,  especially  on  the  eyelids,  fore- 
head, and  ears.    The  cer^-ical  lymph  nodes  are  generally  much  enlarged. 

The  systemic  disturbance  varies  much  in  different  cases;  it  is  often 
remarkably  slight,  as  contrasted  with  the  rather  severe  cutaneous  mani- 
festations, but  it  may  be  extreme.  Usually  the  fever  remains  high,  with 
slight  remissions,  for  four  or  five  days,  and  then  falls  by  a  rather  rapid 
lysis  (sometimes  even  a  crisis).  The  pulse  is  rapid ;  albumin  is  frequently 
present  in  the  urine;  and  there  is  often  stupor  and  a  moderate  amount  of 
delirium.  Leukocytosis  is  present.  In  favorable  cases  the  subsidence 
of  the  cutaneous  lesions  is  followed  by  desquamation  (the  scales  being 


ERYSIPELAS  69 

infectious),  and  the  patient  enters  upon  convalescence.  In  unfavorable 
cases,  the  fever  remains  high,  the  typhoid  state  develops,  the  delirium 
becomes  more  marked,  the  urine  lessened  in  amount,  the  albuminuria 
more  marked,  and  in  convulsions  or  coma  the  patient  may  die.  In  severe 
cases  that  do  not  go  on  immediately  to  death,  more  or  less  extensive 
suppurative  (phlegmonous)  inflammation,  and  in  some  cases,  even  gan- 
grene, supervenes.  Small  abscesses  are  cpiite  common  in  many  other\\'ise 
mild  cases. 

An  unusual  form  of  erysipelas  has  been  described — in  which  the 
cutaneous  lesions  spread  from  the  face  to  the  neck,  to  the  chest,  and 
may  even  gradually  involve  the  entire  body — erysipelas  migrans. 
Occasionally  the  lesions  involve  the  mucous  membrane  of  the  nose  and 
mouth  (usually  secondarily,  but  sometimes  primarily),  and  occasion  an 
erysipelatous  faucitis  which  may  go  on  to  the  most  extensive  phlegmon- 
ous inflammation  and  lead  to  oedema  of  the  glottis,  otitis  media,  inflam- 
mation of  the  eye  and  the  other  orbital  tissues,  etc.  More  or  less  swelling 
and  redness  of  the  fauces,  however,  is  not  uncommon  in  cases  of  ordinary 
erysipelas,  and  oedema  of  the  glottis  may  result  from  extension  of  inflam- 
mation from  without  (from  the  neck). 

Complications. — Pneumonia,  pleuritis,  pericarditis,  malignant  endo- 
carditis, meningitis  (rarely,  however,  from  extension  through  the  skull, 
as  erroneously  believed),  arthritis,  nephritis,  and  metastatic  abscesses 
are  the  more  common  complications. 

Diagnosis. — As  a  rule,  the  disease  is  readily  recognized.  Erythema, 
urticaria,  and  acute  eczema  should  be  distinguished.  Erysipeloid  of 
Rosenbach  (erythema  migrans)  occurs  especially  in  those  who  handle 
meat,  crabs,  and  other  shellfish,  and  occasionally  in  laboratory  workers; 
it  is  characterized  by  an  area  of  inflammation,  usually  on  the  hands, 
sharply  outlined,  dark,  reddish  purple  in  color;  and  it  usually  subsides 
within  ten  days  or  two  weeks. 

Prognosis. — The  disease  lasts  usually  ten  to  fourteen  days.  The  mor- 
tality varies  from  4  to  7  per  cent.  The  prognosis  is  bad  in  newborn 
infants,  in  whom  the  region  about  the  umbilicus  is  often  involved,  in 
unusually  severe  infections,  and  in  aged,  debilitated,  and  alcoholic 
subjects.  Recurrences  which  are  not  uncommon  are  frequently  due  to 
unsuspected  erosions  of  the  nasal  mucous  membrane. 

Treatment. — The  regulations  enforced  in  infectious  diseases  (page  29) 
should  )je  carried  out.  The  patient  should  be  confined  to  bed,  and  given 
a  light,  nutritious  diet.  Since  the  disease  usuafly  pursues  a  self-limited 
course,  it  is  doubtful  if  medicines  exert  any  specific  influence;  but  I  am 
in  the  habit  of  giving  quinine  and  iron,  which  are  sanctioned  by  age 
and  long  experience,  and  seem  to  do  good : 

I^ — Quinine  sulphate 48  grains  3  0 

Tincture  of  iron  chloride G  drams  22  5 

Glycerin 4  drams  15  0 

Distilled  water,  sufficient  to  make       ....         6  ounces  200  0 — M. 

S.— Two  teaspoonfuls  (10  c.c),  in  water,  four  times  a  day. 


70  BACTERIAL  INFECTIONS 

In  mild  cases  stimulants  are  not  required,  but  alcohol  and  strychnine 
should  always  be  given  in  severe  infections,  in  the  aged,  and  in  the 
debilitated.  Da  Costa  obtained  good  results  with  pilocarpine  subcu- 
taneously,  ^  grain  (0.01  gram)  every  two  or  three  hours  for  three  or  four 
doses,  in  the  early  stages;  but  assuredly  it  should  be  given  only  to 
sthenic  subjects,  and  never  when  the  disease  is  advanced.  The  coal-tar 
products  are  absolutely  contra-indicated.  Antistreptococcic  serum  has 
not  yet  sustained  the  claims  originally  made  for  it.  Better  results  are 
to  be  expected  from  the  use  of  autogenous  vaccines  (bacterins). 

Locally  a  saturated  aqueous  solution  of  magnesium  sulphate,  applied 
on  a  gauze  mask,  and  renewed  twice  in  the  twenty-four  hours,  is  the 
best  form  of  treatment;  but  one  may  use  also  applications  of  cold  water, 
lead  water  and  laudanum,  mercuric  bichloride  (1  to  4000),  carbolized 
vaseline,  or  ichthyol  ointment  (33  per  cent.).  The  injection  of  carbolic 
acid  (2  per  cent.),  mercuric  bichloride,  or  mercuric  biniodide  into  the 
area  of  advancing  oedema  has  been  practised  with  some  good  results 
and  many  failures;  this  is  also  true  of  painting  the  area  with  silver 
nitrate.  Judd  extols  the  value  of  painting  the  inflamed  area  and  one- 
half  inch  of  the  surrounding  apparently  healthy  skin  with  95  per  cent, 
carbolic  acid,  and  after  the  painted  region  has  become  white  applying 
pure  alcohol  until  it  becomes  pink.  Should  suppuration  ensue,  the  pus 
should  be  evacuated  surgically. 

For  the  nervousness,  headache,  and  insomnia,  one  may  use  the 
bromides,  chloral,  opium,  and  hyoscine.  Large  amounts  of  water 
should  always  be  given  (as  in  every  toxic  process)  to  facilitate  elimina- 
tion of  the  toxins.  The  fever,  if  high,  calls  for  hydropathic  measures 
— upon  general  principles. 


PNEUMOCOCCIC  INFECTIONS. 

By  pneumococcic  infection  is  understood  an  infection  of  the  body  by 
the  pneumococcus,  a  microorganism  first  discovered  by  Sternberg,  in 
1880,  later  studied  by  Fraenkel  and  Weichselbaum,  and  sometimes  de- 
scribed as  Diplococcus  pneumoniae,  or  Micrococcus  lanceolatus.  The 
most  common  manifestation  of  such  infection  is  the  ordinary  croupous 
or  lobar  pneumonia,  of  genuine  cases  of  which  the  pneumococcus 
is  probably  the  sole  etiological  factor.  The  pneumococcus,  however, 
is  causative  of  many  other  diseases,  such  as  bronchopneumonia,  pleuritis, 
pericarditis,  endocarditis,  peritonitis,  meningitis,  arthritis,  otitis,  etc. 
Although  these  are  sometimes  primary,  they  are  commonly  secondary 
infections,  and  they  may  be  the  result  of  mixed  infections.  A  number 
of  terminal  infections  in  other  diseases  also  are  due  to  the  pneumococcus. 
Furthermore,  a  distinct  pneumococcic  infection  without  local  lesions, 
a  pneumococcic  septicemia  (bacteremia),  may  occur.  This,  which  is 
somewhat  comparable  to  typhoid  septicemia,  typhoid  fever  without 
intestinal  lesions,  is  usually  sudden  in  onset  with  cliill  and  fever,  but 


PNEUMOCOCCIC  INFECTION  OF  THE  LUNG;  PNEUMONIA      71 

with  few  if  any  local  symptoms,  and  it  progresses  rapidly  to  a  fatal 
termination  under  manifestations  of  profound  intoxication — coma  and 
collapse  of  the  circulation.  The  pneumococcus  may  be  cultivated  from 
the  blood  and  other  tissues  of  the  body. 


PNEUMOCOCCIC  INFECTION  OF  THE  LUNG;  PNEUMONIA. 

(Pneumonitis;   Crouporis,  Fibrinous,  or  Lobar  Pneumonia;  Lung  Fever.) 

Pneumonia  is  an  acute,  specific,  infectious,  and  mildly  contagious  dis- 
ease caused  by  Diplococcus  pneumoniae  (Sternberg,  Fraenkel-Weichsel- 
baum);  it  is  characterized  anatomically  by  bacteremia  and  a  local 
inflammation  in  the  lung  proceeding  to  solidification,  and  clinically  by 
initial  chill,  rusty  expectoration,  and  high  fever  that  usually  ends  by 
crisis. 

Etiology. — Pneumonia  occurs  at  all  ages,  being  common  prior  to  the 
sixth  year  and  in  adult  life  and  old  age.  It  is  less  frequent  during  ado- 
lescence than  at  any  other  period  of  life.  It  affects  males  more  than 
females,  and  the  urban  more  than  the  rural  population;  and,  while  it 
frequently  attacks  those  apparently  in  robust  health,  it  is  especially 
prone  to  attack  those  debilitated  by  fatigue,  starvation,  unhygienic 
surroundings,  exposure  to  the  inclemencies  of  the  weather,  and  over- 
indulgence in  alcohol,  and  those  subject  to  or  convalescent  from  certain 
diseases,  such  as,  influenza,  typhoid  fever,  Bright's  disease,  diabetes, 
etc.  It  sometimes  follows  traumatism  to  the  chest  (traumatic  pneu- 
monia), and  it  frequently  follows  "catching  cold" — although  this  is 
now  thought  to  act  merely  by  reducing  the  resistance  of  the  individual. 
Recurrences  are  common,  one  attack  seemingly  predisposing  to  others. 
It  is  especially  fatal  in  the  negro. 

Pneumonia  prevails  in  all  parts  of  the  world,  and  may  be  said  to  be 
endemic  in  most  large  cities.  It  is  especially  prevalent  during  the 
winter  and  spring,  more  particularly  in  February  and  March,  when 
marked  and  sudden  variations  in  temperature  and  humidity  are  common. 
Small  epidemics,  especially  house  (jail,  barrack,  ship,  etc.)  epidemics 
are  not  infrequent. 

The  exciting  cause  of  the  disease  is  the  pneumococcus,  which  may  be 
found  in  the  lesions  in  the  lung,  in  the  secretions  of  the  entire  respiratory 
tract  (sputum),  in  the  blood,  and  sometimes  in  the  complicating  lesions. 
It  has  been  found  also  in  the  mouths  of  healthy  persons,  as  well  as  in 
the  dust  and  hangings  of  rooms.  Pneumonia  is  slightly  contagious — 
some  outbreaks  more  so  than  others.  Infection  is  usually  transmitted 
directly,  by  a  third  person,  or  by  the  air,  although  it  may  be  transmitted 
by  fomites;  it  is  usually  acquired  by  inhalation,  the  lung  being  first 
affected.  There  is  some  evidence,  however,  that  the  blood  may  be 
primarily  infected,  through  a  wound  or  the  tonsil,  for  instance,  and 
the  lung,  or  other  organ,  secondarily.  Secondary  infections  witli  the 
ordinary  pyogenic  microorganism  are  not  uncommon. 


72  BACTERIAL  INFECTIONS 

The  pneiimococcic  process  may  also  be  set  up  by  other  microorganisms, 
such  as  Friedlander's  pneumobaciUus,  the  influenza  baciUus,  the  t}^hoid 
baciUus,  the  plague  bacillus,  streptococci,  staphylococci,  etc.,  but  the 
processes  induced  by  these  microorganisms  difl^er  somewhat  anatomically, 
as  well  as  clinically,  from  true  pneumococcic  infection  of  the  lung. 

Pathology. — ^The  pneumonic  process  involves  the  right  lung  more 
frequently  than  the  left,  because  the  right  bronchus  is  larger  and  more 
in  a  straight  line  with  the  trachea  than  the  left,  and  the  lower  lobe  more 
frequently  than  the  upper.  Involvement  of  the  upper  lobe  in  adults 
is  often  more  serious  and  more  likely  to  terminate  fatally  than  involve- 
ment of  the  lower  lobe;  but  the  upper  lobe  is  often  involved  in  children 
and  usually  ends  favorably.  In  some  cases  both  lungs  are  involved, 
whereas  in  other  cases  first  one  portion  and  then  another  portion  of  the 
lung  becomes  involved. 

Four  stages  of  the  process  may  be  described:  (1)  Congestion;  (2) 
red  hepatization;  (3)  gray  hepatization;  and  (4)  resolution.  Fre- 
quently, however,  the  lung  reveals  several  stages  side  by  side.  In 
the  first  stage,  or  stage  of  congestion,  the  lung  is  markedly  congested, 
dark  red  in  color,  and  of  increased  consistence,  although  it  still  crepi- 
tates and  floats  on  water.  The  capillary  bloodvessels  are  much  con- 
gested and  dilated — protruding  into  the  alveolar  air  spaces,  which 
are  much  encroached  upon,  and  which,  together  with  the  infundibula 
and  the  commencements  of  the  bronchi,  are  more  or  less  filled  with  a 
tenacious  exudate  containing  erythrocytes,  a  few  leukocytes,  and  desqua- 
mated alveolar  epithelium.  As  the  disease  progresses,  the  exudation  in- 
creases until  it  entirely  displaces  the  air  in  the  alveoli — the  second  stage 
or  stage  of  red  hepatization.  Not  only  the  fluid,  but  also  the  cellular 
exudate,  consisting  of  erythrocytes,  mononuclear  and  polynuclear  leuko- 
cytes, desquamated  epithelium,  and  pneumococci,  is  increased  in  amount, 
and  the  entire  exudate  becomes  coagulated  to  form  a  fibrinous  mass — 
whence  the  term  fibrinous  or  croupous  pneumonia.  The  interstitial 
tissues  of  the  lung  also  show  inflammatory  phenomena.  In  this  stage 
the  affected  portion  of  the  lung  is  increased  in  consistency,  weight,  and 
volume  (often  revealing  indentations  from  the  ribs);  it  is  dark,  reddish 
brown  in  color  (although  less  congested  than  in  the  first  stage);  it  no 
longer  crepitates,  and  it  sinks  in  water — in  a  word,  it  much  resembles 
liver  tissue,  whence  the  term  hepatization.  The  section  surface  is  con- 
gested (motded),  dry,  dull,  granular  (due  to  the  fibrinous  plugs  in  the 
alveoli),  and  the  organ  is  quite  friable.  Red  hepatization  gradually 
merges  into  gray  hepatization — evidence  of  increased  leukocytic  infil- 
tration, lessening  of  the  congestion  from  pressure  upon  the  bloodvessels 
by  the  exudation,  and  beginning  autolysis  of  the  exudate.  The  lung 
becomes  motded,  grayish  red  in  color,  its  surface  less  granular  and 
more  moist  than  previously — the  result  of  degeneration  and  necrosis  of 
the  exudate  and  of  the  transudation  of  serum  from  the  bloodvessels. 
Tlie  exudate  consists  in  large  part  of  polynuclear  leukocytes  (phago- 
cytes), although  degenerated  erythrocytes  and  desquamated  epithelium 


PNEUMOCOCCIC  INFECTION  OF  THE  LUNG:  PNEUMONIA     73 

may  be  distinguishable.  As  the  exudate  becomes  softened,  in  conse- 
(juence  of  autolytic  processes,  it  is  removed,  in  large  part  by  absorption, 
in  small  part  by  expectoration;  resolution  occiu's,  and  gradually  the 
lung:  returns  to  its  normal  condition.  In  less  favorable  cases  the  lung 
may  become  the  seat  of  purulent  infiltration — diffusely  infiltrated  with 
polynuclear  leukocytes  and  appearing  yellowish,  soft,  and  puriform 
to  the  naked  eye.  In  other  cases  the  lung  process  goes  on  to  abscess 
formation  (one  large  abscess  or  several  small  abscesses  that  usually 
fuse  to  form  a  large  one) — due  often  to  secondary  infection  with 
streptococci  and  other  pyogenic  microorganisms;  or  a  portion,  or  an 
entire  lobe,  becomesg  angrenous — due  to  defective  blood  supply  and  to 
secondary  infection  with  putrefactive  bacteria.  In  other  cases  resolution 
is  delayed  and  may  be  followed  by  induration  of  the  lung  or  tuberculosis. 

The  non-solidified  portion  of  the  lung  may  be  normal,  but  it  usually 
shows  more  or  less  congestion  and  oedema.  Sometimes  there  is  an 
associated  bronchitis,  and  the  fibrinous  plugs  may  extend  far  into  the 
bronchi,  forming  veritable  casts.  The  pleura  investing  the  affected 
portion  of  the  lung  is  almost  always  more  or  less  inflamed,  revealing 
usually  a  fibrinous  exudate,  although  the  lesions  may  progress  to  serous- 
fibrinous  exudation  (pleuropneumonia;  metapneumonic  pleuritis),  or  to 
suppuration  (metapneumonic  empyema).  The  organs  in  general  show 
the  results  of  toxemia  and  infection.  Thus,  the  bronchial  lymph  nodes 
are  swollen  and  soft,  the  myocardium,  kidneys,  and  liver  the  seat  of 
parenchymatous  and  sometimes  fatty  degeneration,  and  the  spleen  is 
swollen.  The  heart  is  frequently  markedly  dilated  (especially  the  right 
side),  and  it  may  contain  firm  coagula  (attributable  to  increased  fibrin 
in  the  blood),  which  may  lead  to  sudden  death.  Complications  such 
as  pericarditis,  endocarditis,  meningitis,  enteritis,  and  other  evidences 
of  infection  are  not  infrequent. 

Symptoms. — The  period  of  incubation  is  not  definitely  known,  although 
it  probably  varies  from  a  few  hours  to  several  days.  Usually  there  are 
no  prodromal  symptoms,  but  in  some  cases  the  patient  may  complain 
for  a  day  or  two  of  slight  catarrh  of  the  upper  respiratory  tract,  malaise, 
loss  of  appetite,  headache,  and  dull  pains  in  the  limbs.  In  the  majority 
of  the  cases,  however,  the  onset  of  the  disease  is  sudden — usually  with 
a  severe  chill,  but  sometimes  in  children,  with  a  convulsion  or  vomiting. 
Concurrent  with  the  chill  the  temperature  rises  rapidly  and  attains  its 
maximum,  104°  F.  or  more,  within  a  few  hours.  At  the  same  time  the 
patient  complains  of  headache  and  general  muscular  or  neuromuscular 
pains,  severe  stabbing  pain  in  the  side,  cough,  rusty  expectoration, 
dyspnoea,  and  the  usual  concomitants  of  fever,  such  as  rapid  pulse, 
dry  skin,  a  flushed  face,  loss  of  appetite,  concentration  of  tlie  urine,  etc. 
Soon  the  physical  signs  of  solidification  of  the  limg  and  the  general 
evidences  of  toxemia  with  delirium  become  apparent.  The  clinical  mani- 
festations continue  usually  unabated  for  from  five  to  nine  days,  in  the 
majority  of  cases,  when  the  crisis  occurs,  and  the  patient  enters  upon 
what  is  usually  a  rapid  convalescence. 


74 


BACTERIAL  INFECTIONS 


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PNEUMOCOCCIC  INFECTION  OF  THE  LUNG;  PNEUMONIA     75 

The  Fever. — The  fever  of  pneumococcic  infection  of  the  lung  is 
quite  characteristic  (Fig.  2).  As  already  stated,  it  rises  rapidly  and 
may  reach  104°  F.  or  more,  within  a  few  hours.  In  most,  especially 
asthenic,  cases  the  temperature  is  usually  stable,  that  is,  for  several  days 
the  diurnal  variations  may  be  not  more  than  a  degree.  By  the  third  day, 
however,  there  may  be  a  slight  remission  and  the  subsequent  diurnal 
variations  may  amount  to  1.5°  F.,  but  the  temperature  remains  high  until 
some  time  between  the  fifth  and  ninth  days  (usually  the  fifth,  seventh, 
or  ninth,  rarely  the  third,  day)  when  the  characteristic  crisis  occurs — a 
sudden  fall  of  the  temperature,  within  two  to  ten  hours,  to  normal  or  less, 
accompanied  by  profuse  sweating,  lessening  of  the  dyspnoea  and  the 
general  toxic  manifestations,  increase  in  the  strength  of  the  pulse  and 
the  amount  of  urine,  and  marked  improvement  in  the  general  condition 
of  the  patient,  without  however,  in  many  cases,  any  noteworthy  changes 
in  the  physical  condition  of  the  lung.  Frequently  the  crisis  is  followed 
by  a  prolonged  and  refreshing  sleep.  Occasionally  the  crisis  is  unduly 
protracted — beyond  twenty-four  hours.  Not  infrequently  on  the  day  or 
the  second  day  preceding  the  crisis  the  temperature  falls  to  between  99° 
and  101.5°  F.  and  rises  again — a  pseudocrisis.  On  the  other  hand,  in 
cases  with  prodromal  symptoms  and  sometimes  in  children  the  onset 
may  be  gradual,  and  in  debilitated  and  alcoholic  subjects  the  temperature 
range  is  likely  to  be  relatively  low — 102°  to  102.5°  F.  In  cases  protracted 
beyond  the  tenth  day  the  fall  of  temperature  is  frequently  by  lysis.  In 
some  cases  the  temperature  rises  before  the  crisis — a  so-called  precritical 
rise.  Such  rise,  however,  may  be  merely  a  forerunner  of  death,  but  in 
most  cases  the  temperature  falls  just  before  death.  Aside  from  the  pre- 
critical hyperpyrexia,  the  temperature  may  be  unusually  high  throughout 
the  course  of  the  disease — 106°  to  107°  F.  (usually  fatal  cases);  in  other 
cases  there  is  no  elevation  of  the  temperature  whatever — afebrile  pneu- 
monia. 

Respiratory  Symptoms. — Dyspnoea  is  a  constant  and  characteristic 
symptom,  the  respirations  varying  from  30  or  more  per  minute  on  the 
first  day,  to  50  or  60  per  minute  on  the  third  or  fourth  day;  sometimes 
however,  reaching  80  to  100  per  minute  in  children.  The  breathing 
is  superficial,  repressed,  and  evidently  painful;  and  the  expiration  is 
usually  accompanied  by  an  almost  pathognomonic  grunt.  The  dyspnoea 
is  not  entirely  dependent  upon  the  solidification  of  the  lung,  being  due  also 
to  pain,  fever,  toxemia,  and  loss  of  functionating  lung  surface;  it  is 
frequently  out  of  proportion  to  the  extent  of  the  lung  involvement  and 
it  disappears  with  the  occurrence  of  the  crisis,  although  the  physical 
condition  of  the  lung  may  persist  unchanged  for  several  days.  The  pulse- 
respiration  ratio  may  become  2  to  1,  even  1.5  to  1,  instead  of  the  normal 
4  to  1.  Pain  is  an  early  and  distressing  sign,  and  is  usually  attributable 
to  associated  involvement  of  the  pleura.  It  is  severe,  stabbing  in 
character,  and  much  increased  by  deep  inspiration  and  by  coughing. 
It  is  generally  referred  to  the  region  of  the  nipple  or  the  lower  ribs  on  the 
affected  side,  rarely  to  the  opposite  side,  or  to  the  abdomen,  back,  or 


76  BACTERIAL  INFECTIONS 

shoulder.  It  gradually  disappears  after  the  third  or  fourth  day.  It  may 
be  slight  or  absent  in  central  and  in  apical  pneumonias.  Cough  and  ex- 
pectoration are  initial  symptoms.  In  the  early  stages  the  cough  is  short, 
harsh,  and  restrained  on  account  of  the  pain  that  it  provokes.  The 
expectoration,  which  may  be  mucous  in  character  for  a  few  hours,  speedily 
takes  on  almost  pathognomonic  characteristics,  becoming  rusty,  viscid, 
and  tenacious.  Rarely  there  is  a  distinct  hemoptysis.  In  certain  asthenic 
cases,  the  sputum  may  be  thin,  less  viscid,  and  darker  (more  hemorrhagic) 
in  color  (prune-juice  sputum).  After  the  crisis  the  cough  usually  becomes 
less  harsh  and  the  sputum  less  viscid  and  more  mucopurulent  in  char- 
acter. Cough  and  expectoration  may  be  almost,  if  not  entirely,  absent 
in  certain  asthenic  cases,  in  much  debilitated  and  alcoholic  subjects, 
and  in  the  very  young  and  the  very  aged.  Microscopic  examination  of 
the  sputum  reveals  Diplococcus  pneumoniae  (often  in  pure  culture,  though 
frequently  associated  with  other  microorganisms),  erythrocytes,  leuko- 
cytes, mucus,  alveolar  epithelium,  and  sometimes  fibrinous  plugs  from 
the  alveoli  and  casts  of  the  finer  bronchioles. 

Circulatory  Symptoms. — In  ordinary  cases  the  pulse  is  usually  100 
to  110  or  120,  in  children  140  to  160,  per  minute,  and  full  and  bounding 
in  the  height  of  the  disease.  Late  in  the  disease,  especially  if  the  attack 
be  severe,  the  pulse  loses  its  strength  and  becomes  more  rapid  (160  or 
more  per  minute).  A  pulse  of  more  than  120  per  minute,  as  well  as 
a  small,  weak,  and  irregular  pulse,  always  occasions  concern.  In  ordinary 
cases  the  heart  sounds  are  clear  and  the  pulmonary  second  sound  accen- 
tuated. In  the  height  of  the  disease  functional  murmurs  are  common; 
with  dilatation  of  the  heart  due  to  weakness  of  the  myocardium,  the 
result  of  toxic  degeneration  and  excessive  pressure  in  the  pulmonary 
circulation,  relative  insufficiency  of  the  mitral  and  tricuspid  valves  may 
develop.  Early  evidence  of  cardiac  embarrassment  is  furnished  by  lack 
of  muscular  tone  of  the  first  sound  of  the  heart  and  weakening  of  the 
previously  accentuated  pulmonary  second  sound ;  later,  there  may  be  an 
extension  of  the  cardiac  dulness  to  the  right,  epigastric  pulsation,  and 
embryocardia.  Sudden  collapse  of  the  circulation — weakness  and  irregu- 
larity of  the  heart  and  the  pulse,  low  blood  pressure,  subnormal  tempera- 
ture, cyanosis,  and  sweating,  are  by  no  means  unknown,  and  are  the 
result  of  toxic  paralysis  of  the  vasomotor  centres,  toxic  degeneration  of 
the  myocardium,  and  excessive  pressure  in  the  pulmonary  circulation. 
Though  it  may  prove  fatal,  it  may  be  recovered  from. 

Blood. — Polynuclear  leukocytosis  is  a  diagnostic  feature  of  most  cases. 
The  leukocytes  usually  number  from  18,000  to  45,000  per  c.mm.; 
they  may  be  more  numerous  (rare),  and  in  extremely  asthenic  and 
toxic  cases  there  may  be  little  or  no  leukocytosis  (a  bad  prognostic 
sign).  Leukocytosis  begins  with  the  onset  of  the  disease,  persists  through- 
out its  course,  and  falls  with  and  after  the  true  crisis.  During  the 
height  of  the  disease  the  eosinophiles  are  much  reduced  or  absent; 
they  reappear  with  or  just  prior  to  the  crisis.  The  other  blood  changes 
consist  of  a  secondary  oligocythemia  and  oligochromemia,  rapid  clotting 


PXEUMOCOCCIC  INFECTION   OF   THE   LUNG;  PNEUMONIA      77 

of  the  blood,  due  to  increase  of  the  fibrin  elements,  and  the  presence  of 
the  diplococcus  in  some  cases. 

Nervous  Symptoms. — Nervous  symptoms  are  a  characteristic  of 
all  cases.  Headache,  mental  dulness,  and  at  least  slight  mental  wander- 
ing, are  rarely  missed.  In  well-developed  cases,  delirium  is  constant, 
although  it  varies  in  character.  It  may  be  maniacal,  but  it  is  usually 
of  a  low  adynamic  muttering  character  (profound  toxemia),  or  it  may 
resemble  delirium  tremens  (true  delirium  tremens  is  the  rule  in  alcoholic 
subjects).  Convulsions  are  common  at  the  onset  in  children,  and  some 
cases  of  pneumonia  in  children  run  their  course  altogether  under  the 
guise  of  meningitis  (so-called  cerebral  pneumonia).  Cerebral  symptoms 
sometimes  develop  about  the  time  of,  or  persist  after,  the  crisis,  and,  con- 
sisting of  mental  hebetude,  delirium,  rarely  of  insanity,  they  may  continue 
for  several  days. 

Digestive  Symptoms.— Initial  vomiting  is  common,  especially  in 
children.  The  tongue  is  coated  with  a  white  or  yellowish  white  fur  and 
later  sordes  not  infrequently  collect  upon  the  teeth  and  gums,  and  the 
tongue  may  become  fissured.  Thirst  is  marked,  the  appetite  is  lost, 
and  the  patient  is  usually  constipated,  unless  enteritis  or  colitis  develops. 
INIeteorism,  sometimes  of  dangerous  grade,  since  it  embarrasses  the 
already  embarrassed  heart  and  lungs,  may  accompany  the  pneumococcic 
enteritis  or  colitis,  or  it  may  be  due  to  toxic  paresis  of  the  intestine. 
The  spleen  is  usually  enlarged  and  palpable,  and  the  liver  can  often 
be  felt,  especially  in  right-sided  pneumonias,  in  which  an  apparent 
enlargement  may  be  due  only  to  displacement  of  the  liver  downward. 

Cutaneous  Symptoms. — Herpes  occurs  in  about  one-third  of  the  cases 
on  the  lips  and  about  the  alee  of  the  nose,  but  occasionally  also  on  the 
cheek,  ear,  arms,  genitals,  etc.  It  develops  usually  on  the  second, 
third,  or  fourth  day  of  the  disease,  and  sometimes  comes  out  in  successive 
crops.  Moderate  sweating  is  common  throughout  the  latter  half  of  the 
disease,  and  profuse  sweating  occurs  with  the  crisis.  A  dusky  flush 
on  the  cheek,  said  to  be  homolateral  with  that  of  the  lung  aft'ected,  is 
(|uite  common;  sometimes  the  flush  occurs  on  both  cheeks,  being  more 
marked  on  that  of  the  side  affected  with  pneumonia. 

Urinary  Symptoms. — The  urine  presents  the  characteristics  of  feljrile 
urine — concentrated,  lessened  in  amount,  high  colored,  increased  in 
specific  gravity,  and  depositing  a  copious  sediment  of  urates  and  uric 
acid.  Albumin,  referable  to  toxic  changes  in  the  renal  epithelium,  is 
common;  sometimes  a  true  nephritis  (much  albumin,  blood,  and  tube 
casts)  develops.  The  chlorides  are  usually  much  diminished,  or  al)sent 
throughout  the  height  of  the  disease.  The  diazo  reaction  is  sometimes 
present. 

Physical  Signs. — In  the  first  stage,  or  stage  of  congestion  (usually 
of  not  more  than  twenty-four  hours'  duration),  the  respiratory  move- 
ments over  the  aft'ected  portion  of  the  lung  are  restricted;  there  is  slight 
increase  of  tactile  fremitus  and  of  vocal  resonance;  the  percussion  note 
may  be  normal,  but  is  usually  higher  pitched  and  somewhat  tympanitic 


78  BACTERIAL  INFECTIONS 

(Skodaic  resonance) ;  and  the  breath  sounds  are  weak  or  bronchovesicular 
in  character.  The  crepitant  rale  of  Laennec  may  be  heard.  This  is 
usually  said  to  be  due  to  forcible  separation  of  the  alveolar  walls  and 
infundibula  rendered  adherent  by  the  viscid  exudation;  in  some  cases, 
however,  a  sound  indistinguishable  therefrom  is  more  likely  a  pleural 
friction,  since  it  is  not  heard  in  all  cases,  and  not  until  the  end  of  the 
first  stage,  when  the  pleura  may  be  covered  with  a  layer  of  fibrin. 

In  the  second  stage,  or  stage  of  solidification,  the  respiratory  move- 
ments over  the  affected  portion  of  the  lung  are  much  restricted,  while 
those  over  the  other  lung  are  exaggerated;  the  affected  side  may  be 
somewhat  enlarged  (1  to  1.5  cm.),  but  the  intercostal  depressions  are  not 
obliterated.  Tactile  fremitus  and  vocal  resonance  are  much  increased, 
except  in  the  exceptional  cases  in  which  the  bronchi  are  plugged  by 
mucus  or  fibrinous  exudate,  or  when  there  is  an  associated  pleuritis.  The 
percussion  note  is  dull — there  being  varying  grades  of  dulness  from  the 
slight  dulness  of  the  first  stage  to  marked  dulness  or  flatness,  present 
especially  posteriorly,  in  the  fully  developed  disease.  With  the  dulness 
there  is  increased  resistance  to  the  percussing  finger,  but  neither  the 
dulness  nor  the  resistance  are  as  marked  as  in  pleuritis  with  effusion. 
Dulness  is  less  marked  in  incomplete  solidification,  especially  in  pneu- 
monias that  do  not  fully  reach  to  the  surface  (central  pneumonias), 
in  the  very  young,  and  in  the  aged  (on  account  of  senile  changes  in  the 
ribs  and  cartilages).  Skodaic  resonance  may  be  elicited  above  the 
solidified  area.  The  breath  sounds  are  bronchial  or  tubular  in  character, 
though  rarely  they  may  be  absent  in  case  the  bronchi  are  plugged  with 
exudate;  a  voluntary  cough,  however,  will  usually  dislodge  such  plug, 
which,  being  followed  immediately  by  bronchial  breathing,  is  conclusive 
evidence  of  solidification.  Bronchophony,  sometimes  egophony,  may 
be  elicited  (unless  the  bronchi  be  plugged).  I  have  known  Wintrich's 
change  of  note  and  amphoric  breathing  to  lead  to  confusion  with  a 
cavity.  In  associated  bronchitis,  fine,  crackling  rales  may  be  heard, 
and  usually  with  undue  distinctness  on  account  of  the  solidification. 
The  uninvolved  lung  reveals  exaggerated  vesicular  breathing,  and  occa- 
sionally, especially  in  children  and  young  subjects,  bronchial  breathing 
due  to  conduction  from  the  diseased  lung. 

With  the  onset  of  resolution  there  is  a  gradual  return  to  the  normal 
conditions.  Movement  returns  to  the  previously  immobile  chest,  tactile 
fremitus  and  vocal  resonance  lessen,  and  the  percussion  note  becomes 
less  dull,  more  tympanitic,  and  finally  resonant  (although  more  or  less 
impairment  of  the  note  may  persist  for  a  long  time).  The  breath  sounds 
become  less  bronchial,  bronchovesicular,  and  finally  (but  often  not  for 
a  long  time)  purely  vesicular,  and  coarse  and  fine  bubbling  rales,  together 
with  in  some  cases  the  recurrence  of  the  crepitant  rale  (so-called  redux 
crepitus),  make  their  appearance.  In  some  cases  the  physical  signs  are 
much  delayed,  although  the  diagnosis  is  quite  evident  from  the  symp- 
toms— chill,  fever,  pain,  cough,  rusty  expectoration,  and  dyspnoea.     In 


PNEUMOCOCCIC  INFECTION  OF  THE  LUNG;  PNEUMONIA     79 

some  cases  physical  signs  are  never  found.  I  have  known  them  to  be 
delayed  until  nearly  or  about  the  time  of  the  occurrence  of  the  crisis. 

Clinical  Varieties. — A  number  of  terms  have  been  employed  to  designate 
different  varieties  of  pneumonia.  Thus  basal  pneumonia  is  sufficiently 
explanatory  of  the  majority  of  cases.  Apical  pneumonia  is  common  in 
children,  more  likely  to  be  attended  by  cerebral  symptoms  and  profound 
intoxication,  and  often  escapes  detection  because  of  the  frequent  slight 
cough  and  expectoration,  and  because  the  apices  posteriorly  are  not  care- 
fully examined.  In  adults  it  is  said  to  be  more  fatal  than  the  basal  form. 
Double  pneumonia  is  that  form  in  which  both  lungs,  or  portions  of  both 
lungs,  are  involved.  Migratory,  or  creeping  pneumonia,  is  that  in  which 
different  portions  of  one  or  both  lungs  are  successively  involved.  In  this 
the  onset  may  be  gradual,  the  course  is  prolonged,  exacerbations  are 
common,  and  the  disease  usually  ends  by  lysis.  Massive  pneumonia 
is  a  form  in  which  an  entire  lung,  or  at  least  a  large  portion  of  a 
lung,  is  involved  and  the  fibrinous  exudate  extends  from  the  alveoli  to 
the  bronchi.  Casts  of  the  bronchi  revealing  dichotomous  divisions  mav 
appear  in  the  sputum.  The  physical  signs  much  simulate  those  of 
pleurisy — there  being  flatness,  absence  of  breath  sounds,  and  of  tactile 
fremitus  and  vocal  resonance.  The  diagnosis  is  sometimes  suddenly 
cleared  up  by  the  expectoration  (by  voluntary  or  involuntary  coughing) 
of  obstructing  plugs  of  exudate,  and  the  immediate  development  of 
characteristic  physical  signs.  Central  pneumonia  is  that  in  which  the 
process  commences  in  the  centre  of  a  lobe,  and,  spreading  gradually 
to  the  surface,  does  not  immediately  occasion  demonstrable  physical 
signs,  and  in  which  the  diagnosis,  for  a  time  at  least,  rests  upon  the  symp- 
toms. Latent  pneumonia  is  that  which  pursues  its  course  unsuspected 
for  some  time,  or  altogether.  Many  cases  of  central  pneumonia  are  of 
this  nature,  as  is  also  pneumonia  in  the  aged,  and  many  cases  develop- 
ing in  the  course  of  Bright's  disease,  insanity,  and  alcoholism.  In 
alcoholics,  especially,  pneumonia  is  frequently  entirely  unsuspected, 
the  symptoms  being  attributed  to  meningitis,  delirium  tremens,  or 
uremia. 

Epidemic  pneumonia,  as  the  term  implies,  is  an  epidemic  form  of 
the  disease.  It  maybe  widespread  or  local.  Thus,  family,  house,  jail, 
ship,  etc.,  epidemics  are  well  recognized.  These  often  have  a  high  mor- 
tality rate,  and  may  be  associated  with  influenza.  Larval,  or  abortive, 
pneumonia  is  a  form  of  short  duration  and  usually  mild  symptoms,  com- 
mon especially  during  epidemics.  The  initial  chill,  fever,  cough,  rusty 
expectoration,  and  ill-defined  or  negative  physical  signs  may  be  followed 
by  complete  recovery  in  a  few  days.  x\lcoholic  pneumonia,  pneu- 
monia in  alcoholics,  is  usually  attended  by  marked  nervous  symptoms 
and  delirium,  and  is  often  devoid  of  suggestive  local  manifestations.  It 
is  insidious  in  onset,  has  a  relatively  low  fever  range  (101°  to  102°  F.), 
and  a  very  high  death  rate.  Typhoid  pneumonia  is  a  pneumonia  charac- 
terized by  marked  asthenia  or  adynamia  (asthenic  or  adynamic  pneu- 
monia) or  the  t}'phoid  state  (and  has  nothing  whatever  to  do  with  typhoid 


80  BACTERIAL  INFECTIONS 

infection  or  typhoid  fever).  The  characteristic  of  the  disease  is  extreme 
toxemia  (toxic  pneumonia) — whence  it  indicates  severity  of  infection 
and  sometimes  double  infection  (pneumococcic  and  streptococcic  or 
staphylococcic,  bacteremia  being  common).  It  must  be  distinguished 
from  pneumotyphoid — typhoid  infection  of  the  lung  occurring  in  the 
course  of  typhoid  fever.  It  is  also  true  that  pneumococcic  infection 
of  the  lung  may  occur  in  typhoid  fever.  Bilious  or  malarial  pneumonia 
is  a  term  used  by  some  writers  to  designate  pneumonia  occurring  espe- 
cially in  malarious  regions,  and  attended  by  jaundice,  vomiting,  and 
severe  nervous  symptoms.  The  complicating  symptoms  are  usually 
due  to  an  associated  duodenal  catarrh,  and  bear  no  relation  to  the 
malarial  parasite,  although  infection  with  the  pneumococcus  and  the 
malarial  parasite  (as  well  as  with  other  microorganisms)  may  be  con- 
current. 

Secondary  pneumonia  is  common  in  many  of  the  acute  infective 
diseases.  It  may  be  due  to  the  pneumococcus  or  to  the  microorgan- 
isms provocative  of  the  primary  disorder  (typhoid  fever,  diphtheria, 
etc.),  or  to  mixed  infection  with  streptococci,  staphylococci,  and  colon 
bacilli,  etc.  It  is  generally  bronchopneumonic  in  type,  and  devoid  of 
most  of  the  characteristic  clinical  and  anatomical  features  of  true  lobar 
pneumonia.  Terminal  pneumonia  (usually  bronchopneumonia)  is  a 
common  event  in  the  final  stage  of  many  cases  of  Bright's  disease, 
diabetes,  carcinoma,  heart  disease,  and  the  adynamia  of  senility.  The 
onset  is  gradual  and  the  symptoms  slight  and  not  suggestive;  there 
may  be,  indeed,  few  clinical  manifestations  aside  from  dyspnoea  and 
slight  fever. 

Pneumonia  in  the  aged  is  often  latent,  and  may  be  terminal.  The 
onset  may  be  sudden,  but  it  is  usually  insidious,  and  the  local  symptoms 
and  physical  signs  are  slight,  although  the  patient  is  manifestly  seriously 
ill  and  usually  soon  dies  from  cardiac  debility.  This  is  a  hypostatic  or 
bronchopneumonia,  and  is  especially  common  in  the  aged  who  are  con- 
fined to  bed — as  with  a  fractured  femur,  for  instance.  Pneumonia  in 
children  and  infants  often  begins  with  a  convulsion  or  vomiting,  the 
apex  is  often  involved,  cerebral  symptoms  are  marked  (the  disorder 
much  simulating  meningitis),  expectoration  is  absent,  and  the  disease 
usually  ends  in  recovery. 

Postoperative  and  ether  pneumonia  occurs  sometimes  after  operation 
and  anesthetization,  especially  after  abdominal  operations  (probably 
because  the  bronchial  secretions  are  allowed  to  accumulate  on  account 
of  the  pain  provoked  by  coughing).  The  development  of  the  disease 
is  much  favored  by  winter  season,  by  prolonged  anesthetization,  general 
debility  of  the  patient,  disease  of  the  respiratory  tract,  such  as  bronchitis 
or  chronic  congestion  from  heart  disease,  and  by  the  aspiration  of  irrita- 
ting particles  (aspiration  or  inhalation  pneumonia).  It  is  often  lobular 
(that  is,  bronchopneumonia)  rather  than  lobar,  insidious  in  onset,  latent 
in  course,  and  frequently  due  to  microorganisms  other  than  the  pneu- 
mococcus. 


PNEUMOCOCCIC  INFECTION  OF  THE  LUNG;  PNEUMONIA     SI 

Complications  and  Sequels. — Inflammations  of  the  serous  membrane, 
pleuritis,  pericarditis,  endocarditis,  and  meningitis,  are  common  com- 
plications— pleuritis  the  most  common,  and  meningitis  the  most  serious. 
In  most  of  these  comphcating  exudates,  the  pneumococcus  may  be 
detected,  sometimes  alone,  sometimes  in  association  with  the  strepto- 
coccus, staphylococcus,  etc.  Pleuritis  is  a  part  of  the  pneumonic  process 
rather  than  a  complication,  since  it  occurs  in  all  cases  in  which  the  inflam- 
mation reaches  the  surface  of  the  lung.  In  most  cases  the  exudate  is 
slight  in  amount  and  fibrinous  in  character;  in  other  cases  it  is  serofibrin- 
ous, and  more  or  less  abundant  (pleuropneumonia,  metapneumonic 
pleuritis).  In  still  fewer  cases,  however,  but  rather  commonly  in  children 
and  youths,  the  exudate  is  purulent  (metapneumonic  empyema):  most 
cases  of  supposed,  unresolved  pneumonia.  Unusual  prolongation  of 
the  disease,  chills,  fever,  sweats,  leukocytosis,  flatness  on  percussion, 
markedly  increased  resistance,  absence  of  breath  sounds  and  of  rales, 
suggest  the  presence  of  the  pleural  lesions;  but  an  absolute  diagnosis 
may  require  the  use  of  the  exploring  needle.  Pericarditis  is  a  rather 
unusual  complication,  more  common  in  left-sided  than  in  right-sided 
pneumonias.  It  is  usually  fibrinous,  but  may  be  serofibrinous  or  puru- 
lent. Its  presence 'may  be  inferred  from  the  development  of  undue  dys- 
pnoea and  pericardial  distress,  but  its  diagnosis  depends  upon  the  detection 
of  the  physical  signs.  Acute  endocarditis,  both  simple  and  malignant,  is 
more  common;  it  affects  the  left  side  of  the  heart  rather  than  the  right, 
especially  if  there  be  an  old  valvular  lesion.  The  diagnosis  rests  upon 
detecting  the  ordinary  manifestations  of  acute  endocarditis — sepsis 
and  embolic  phenomena.  Acute  meningitis,  usually  fibropurulent,  is 
a  rather  uncommon,  and  usually  fatal,  complication.  Frequently  it 
cannot  be  distinguished  from  the  meningism  of  many  cases  of  pneumonia 
without  resort  to  lumbar  puncture,  which  may  reveal  pneumococci  in 
the  meningeal  exudate.  That  the  pneumococcic  process  is  a  more  or 
less  widespread  infection  in  many  cases  is  evident  from  the  occurrence 
together  of  inflammation  in  divers  organs,  such  as  the  lung,  pleura, 
endocardium,  meninges,  etc.  Rarer  complications  are  bronchitis, 
pneumococcic  synovitis  and  arthritis,  toxic  degeneration  of  the  myo- 
cardium, gastritis,  duodenitis  (causing  jaundice),  enteritis,  colitis, 
nephritis,  peritonitis,  neuritis,  phlebitis,  heart  clots,  etc. 

Sequels  are  rare,  inasmuch  as  most  cases  result  in  recovery.  In  some 
cases,  however,  relapse  occurs;  that  is,  a  few  days  after  the  crisis  the 
fever  returns  and  persists  for  several  (two  to  seven  or  eight)  days. 
Recurrences  are  common — one  attack  seemingly  predisposing  to  others, 
and  eighth,  ninth,  and  tenth  attacks  being  by  no  means  unknown.  In 
some  cases  resolution  is  much  delayed,  and  although  it  may  ultimately 
occur  after  many  days  or  several  weeks,  the  lung  being  restored  to 
the  normal,  fibroid  induration  (chronic  interstitial  pneumonia)  is  a 
very  likely  event.  In  other  cases  purulent  infiltration  or  abscess  (single 
or  multiple),  gangrene,  or  tuberculosis  results. 
6 


82  BACTERIAL  INFECTIONS 

Diagnosis. — In  the  majority  of  cases,  especially  in  sthenic  subjects, 
the  disease  is  rarely  overlooked — the  abrupt  onset,  initial  chill,  pain  in 
the  side,  dyspnoea,  cough,  rusty  expectoration,  herpes,  leukocytosis, 
physical  signs  of  solidification  of  the  lung,  and  the  course  of  the  fever, 
being  unequivocal.  In  debilitated  subjects,  in  those  the  subject  of 
chronic  disease,  and  in  the  aged,  the  disease  setting  in  insidiously  may 
escape  recognition.  Undue  dyspnoea  and  fever  should  suggest  a  physical 
exploration  of  the  lungs.  The  association  of  fever  and  delirium  tremens 
should  lead  to  the  suspicion  of  pneumonia  in  an  alcoholic  subject. 

The  diseases  with  which  pneumonia  is  most  likely  to  be  confounded 
are  typhoid  fever,  pleuritis  with  effusion,  meningitis,  bronchopneumonia, 
and  acute  pneumonic  tuberculosis.  Cases  of  acute  pneumonic  tuber- 
culosis, often  said  to  be  the  consequence  of  the  engrafting  of  tuberculosis 
upon  a  primary  pneumococcic  infection,  are  almost  always  tuberculous 
from  the  onset.  In  the  majority  of  cases  the  tuberculous  nature  of  the 
infection  is  not  recognized  until  the  expected  crisis  does  not  occur  or 
tubercle  bacilli  and  elastic  fibers  are  detected  in  the  sputum.  The  tuber- 
culous nature  of  the  disorder,  however,  may  be  suggested  by  previous 
ill  health  of  the  patient,  tuberculosis  in  the  antecedents,  a  gradual 
onset,  an  intermittent  and  later  remittent  fever,  hemorrhagic-purulent 
and  non-viscid  sputum,  profuse  sweats,  rapid  emaciation,  and  the  physical 
signs  of  cavity  formation.  In  other  cases,  a  later  involvement  of  one 
apex  suggests  that  the  primary  lesions  (which  are  more  frequent  in  the 
upper  than  in  the  lower  lobe)  were  tuberculous. 

Prognosis. — Pneumonia  is  a  very  fatal  disease — the  mortality  rate  being 
from  15  to  40  per  cent.  The  prognosis  is  influenced  by:  (1)  The  age 
of  the  patient.  Children  usually  recover;  the  aged  usually  die.  The 
mortality  rate  increases  with  each  decade  beyond  the  second.  (2)  Race. 
The  disease  is  more  fatal  in  the  negro  than  in  the  white  race.  (3)  The 
previous  health  of  the  patient.  The  death  rate  is  high  in  those  debili- 
tated from  any  cause.  It  is  almost  always  fatal  in  alcoholic  subjects. 
(4)  The  severity  of  the  infection.  The  prognosis  is  bad  in  patients  with 
marked  toxemia,  persistently  high  temperature  (105°  F.  and  more), 
cardiac  weakness,  and  absence  of  leukocytosis.  The  extent  of  the  lung 
involvement,  unless  it  be  extreme  and  bilateral,  has  very  little  influence 
on  the  severity  of  the  symptoms  (the  degree  of  toxemia).  (5)  The  pres- 
ence of  complications  renders  the  prognosis  much  more  anxious,  as  almost 
all  deaths  in  previously  healthy  subjects  occur  in  complicated  cases. 
Death  in  uncomplicated  cases  is  due  to  the  general  eft'ects  of  the  toxemia, 
or  to  the  special  effects  of  the  toxemia  on  the  heart  associated  with  the  em- 
barrassing results  of  increased  intrapulmonary  pressure,  or  to  heart  clot. 

Treatment. — Although  the  patient  is  not  notably  infectious  to  those 
about  him,  it  is  well  that  he  be  isolated;  the  sputum  undoubtedly  should 
be  destroyed,  since  it  unquestionably  is  the  chief  source  of  infection; 
and  it  is  wise  also,  especially  if  several  cases  of  pneumonia  have  occurred 
in  the  same  room  or  the  same  bed  to  disinfect  the  bed  and  the  room 
(see  page  29). 


PNEUMOCOCCIC  INFECTION  OF  THE  LUNG;  PNEUMONIA     S3 

Our  general  management  of  the  patient  should  always  be  guided  by  a 
knowledge  of  the  fact  that  pneumococcic  infection  of  the  lung  is  self- 
limited,  and  that  we  are  apparently  unable  to  shorten  it  or  to  influence  the 
crisis.  Still  we  can  unquestionably  do  a  great  deal  for  our  patients.  I 
have  not  been  able  to  assure  myself  that  the  disease  can  be  aborted,  even 
in  its  very  earliest  stages;  from  time  to  time  I  have  used  the  different 
measures  recommended  for  this  purpose,  such  as  venesection,  aconite, 
veratrum  viride  (to  bleed  the  patient  within  his  own  vessels),  large 
doses  of  digitalis  (with  a  view  forcibly  to  stimulate  the  heart  and  re- 
establish the  cardiopulmonary  circulation);  but,  although  the  patients 
recovered  without  untoward  symptoms,  the  disease  was  not  aborted. 
After  the  disease  has  become  established,  that  is,  after  the  first  twenty- 
four  hours,  these  methods  of  treatment,  except  bleeding  (to  be  referred  to 
presently),  are  as  harmful  as  they  are  irrational. 

The  patient  should  be  placed  in  a  large,  readily  ventilated  room,  and 
the  windows  should  be  kept  wide  open  all  the  time,  so  as  to  provide  an 
abundance  of  fresh  air.  When  available,  as  in  hospital  practice,  the 
best  results  are  achieved  by  placing  the  patient  out-of-doors,  as  on  a 
porch,  for  instance;  he  should,  of  course,  be  well  protected  by  a  suffi- 
ciency of  bed-clothes.  The  fresh  air  tends  to  promote  an  efficient  aera- 
tion of  the  blood,  it  lessens  the  cyanosis,  invigorates  the  cardiovascular 
system,  reduces  the  general  intoxication,  etc.  There  can  be  no  com- 
parison between  the  results  attained  by  affording  the  patient  from  the 
beginning  an  abundant  supply  of  fresh  air,  and  those  that  ensue  upon 
the  giving  of  canned  oxygen  when  cyanosis  has  become  extreme  and 
the  patient's  vitality  has  been  almost  if  not  quite  depleted  by  the 
intoxication. 

In  the  early  stages  of  the  disease,  at  least,  the  diet  should  be  largely 
fluid,  that  is,  largely  milk;  but  the  milk  may  be  flavored,  as  recom- 
mended for  the  typhoid-fever  subject,  or  it  may  be  given  as  junket,  etc.; 
and  there  can  be  no  serious  objection  to  egg-white  or  the  whole  egg  (if 
well  borne),  or  to  meat  and  vegetable  soups  thickened  with  a  little 
flour,  powdered  rice,  or  barley,  or  strained  oatmeal  gruel,  cornstarch, 
arrow-root,  blanc-mange,  gelatine  flavored  with  wine,  calf's-foot  jelly, 
etc.  Care  must  be  taken  not  to  overfeed  the  patient.  After  the  crisis, 
milk  toast,  scraped  meat,  soft-boiled  eggs,  potato  puree,  stewed  fruits, 
etc.,  may  be  added,  and  in  a  day  or  two  sweetbreads,  chicken,  etc. 

The  special  indications  for  treatment  are  to  combat  the  toxemia,  to 
support  the  overtaxed  heart,  to  relieve  certain  symptoms,  and  to  treat 
the  complications  as  they  arise.  As  yet  we  have  no  specific.  Anti- 
pneumococcic  serum  has  not  realized  the  claims  originally  made  for  it; 
nor  is  this  to  be  expected  a  priori,  since  the  pneumococ-cic*  toxin  is  an 
intracellular  rather  than  an  extracellular  toxin — whence  the  difficulty  of 
producing  an  efficient  antitoxin.  I  have  used  the  serum  in  a  few  cases, 
apparently  with  some  influence  on  the  temperature,  and  a  slight,  though 
doubtful,  influence  on  the  toxemia.  Encouraging  results  have  recently 
followed  the  use  of  bacterial  vaccines  and  of  extracts  of  washed  leuko- 


84  BACTERIAL  INFECTIONS 

cytes;  but  sufficient  use  has  not  yet  been  made  of  these  forms  of  treat- 
ment to  determine  finally  their  value. 

The  pain  of  the  early  stages  is  best  relieved  by  twenty  to  forty  dry  cups 
placed  on  one  or  both  sides;  these  not  only  relieve  the  pain,  but  also 
lessen  the  dyspnoea.  The  cupping  may  be  repeated  twice  or  thrice 
within  the  first  twenty-four  hours,  and  again  during  the  second  twenty- 
four  hours,  if  required.  Should  this  be  ineffectual,  morphine  should 
be  given  hypodermicly,  since  pain  itself  is  depressing  to  the  patient  and 
must  be  relieved.  Dover's  powder,  deodorized  tincture  of  opium,  an 
ice-bag,  a  Leiter's  coil,  a  light  application  of  the  Paquelin  cautery,  or 
strapping  the  side,  also  may  be  used;  or  one  may  give  every  three  or  four 
hours  a  pill  containing  quinine  sulphate,  2  grains  (0.13  gram),  and 
powdered  opium,  ^  grain  (0.03  gram).  This  not  only  reheves  the  pain 
and  promotes  a  feeling  of  general  well-being,  but  is  believed  to  exert 
also  some  antiphlogistic  action.  I  have  long  since  given  up  the  use  of 
poultices,  the  newer  clay  poultices  as  well  as  the  better,  though  more  old- 
fashioned,  flaxseed  poultices — with  considerable  increase  in  the  general 
comfort  of  my  patients.  A  cotton  jacket  may  be  applied  to  a  child — 
and  will  do  the  mother  considerable  good.  During  this  stage  the  blood 
pressure,  if  high,  may  be  reduced — by  bleeding,  free  catharsis,  and 
diaphoresis.  The  abstraction  of  twenty  ounces  of  blood  in  sthenic 
subjects  is  often  followed  by  relief  of  pain,  dyspnoea,  and  cerebral 
(toxic)  symptoms;  but  it  should  not  be  practised  indiscriminately,  and 
not  in  debilitated  subjects.  An  initial  dose  of  10  grains  (0.6  gram)  of 
calomel,  followed  by  a  saline  cathartic,  subserves  a  very  useful  purpose, 
promoting  free  evacuation  of  the  bowels  and  reducing  the  blood  pressure. 
If  given  dry  on  the  tongue  and  allowed  to  mix  with  the  secretions  of  the 
mouth  and  throat  it  exerts  also  a  local  antiseptic  action.  Potassium 
citrate,  solution  of  ammonium  acetate,  spirit  of  nitrous  ether,  etc.,  also 
promote  the  comfort  of  the  patient  by  inducing  sweating,  reducing  the 
blood  pressure,  and  promoting  diuresis  and  elimination  of  toxins. 

The  use  of  hydrotherapy,  of  water  internally  and  externally,  is  the 
best  means  at  our  command  to  combat  the  effects  of  the  toxemia:  given 
internally,  being  our  best  diuretic,  it  promotes  the  free  discharge  of  toxin 
with  the  urine ;  applied  externally,  by  its  stimulating  effects,  it  counteracts 
the  depressing  effects  of  the  toxins.  An  excellent  procedure  is  to  envelop 
the  chest  with  cloths  wrung  out  of  water  at  a  temperature  of  from 
50°  to  32°  F.,  to  cover  these  with  several  thicknesses  of  dry  flannel,  and 
to  leave  them  on  for  from  fifteen  to  thirty  minutes,  depending  upon  the 
reaction.  Often  the  dyspnoea  and  the  cyanosis  are  relieved,  the  pulse 
becomes  stronger,  fuller,  and  less  rapid,  the  manifestations  of  cerebral 
intoxication  lessen,  and  the  temperature  falls  to  100°  F.  or  less.  The  pro- 
cedure may  be  repeated  every  two  to  four  hours,  should  the  temperature 
again  become  high  and  other,  especially  nervous,  evidences  of  toxemia 
ao-ain  become  marked.  In  other  cases  excellent  results  follow  the  appli- 
cation of  cloths  wrung  out  of  ice  water  and  changed  every  fifteen  minutes 
for  two  hours ;  the  treatment  may  be  repeated  after  an  interval  of  two 


PNEUMOCOCCIC  INFECTION  OF  THE  LUNG;  PNEUMONIA     85 

hours  during  the  day  and  of  four  to  six  hours  at  night.  The  indication 
for  repeating  the  hydrotherapeutic  measures  is  found  in  the  reaction  of 
the  patient.  Cool  spongings  also  are  sometimes  of  service.  Full  tub 
baths  have  been  recommended,  but  I  have  not  been  convinced  of 
their  utility.  Warm,  full  baths,  however,  are  often  useful  in  children. 
Although  the  degree  of  the  temperature  is  utilized  as  one  of  the  indica- 
tions for  the  use  of  hydrotherapy,  the  fever,  as  such,  unless  very  high, 
really  does  very  little  harm,  and  it  is  not  necessary  to  reduce  it  at  all 
hazards;  when  very  high  it  may  be  reduced  by  hydrotherapeutic 
measures.  Under  no  circumstances  whatever  should  any  of  the  anti- 
pyretic drugs  be  used;  they  are  a  distinct  menace  to  the  pneumonic 
patient,  reducing  his  vitality,  weakening  the  heart,  lowering  the  tone 
of  the  cardiovascular  or  vasomotor  system,  and  reducing  the  oxygen- 
ation of  his  tissues  (increasing  cyanosis) — only  assisting,  therefore,  the 
pneumococcic  toxin  to  kill  the  patient.  That  they  are  sometimes  given 
to  patients  who  recover  is  but  one  of  the  many  indications  of  the  wonder- 
ful resisting  powers  of  the  human  system. 

WTiether  or  not  the  temperature  is  high,  the  patient  should  be  sponged 
two  or  three  times  in  the  twenty-four  hours  with  cool  or  tepid  water — to 
promote  cleanliness  and  a  general  feeling  of  well-being,  to  allay  nervous 
irritability  and  induce  sleep;  if  the  temperature  is  also  somewhat  reduced 
this  is  an  additional  advantage. 

Water  internally  is  of  even  greater  service,  since  it  promotes  the  free 
elimination  of  the  toxins.  At  least  three  liters  should  be  given  to  an 
adult  within  the  twenty-four  hours.  One  of  the  mild  alkaline  diuretics, 
such  as  potassium  bicarbonate,  acetate,  or  citrate,  or  lemon  juice,  lime 
juice,  or  other  fruit  juice  may  be  added  to  it.  In  the  event  of  renal 
elimination  being  inadequate  and  toxemia  increasing,  hot  enteroclysis 
and  hypodermoclysis  (sometimes  even  intravenous  injection)  of  normal 
saline  solution  should  be  used  systematically  and  repeatedly. 

Delirium  and  other  nervous  manifestations  of  toxemia  call  for  stimu- 
lants, of  which  strychnine  and  alcohol  are  the  best.  Strychnine  may  be 
given  routinely  to  all  patients  when  toxemia  is  marked,  the  heart  weak, 
and  renal  elimination  low;  it  is  wise  to  begin  it  early  in  the  hope  of  averting 
some  of  the  dangers  that  threaten.  Alcohol  had  best  be  withheld  imtil 
it  is  required — when  it  will  often  tide  the  patient  over  the  critical  period 
of  his  disease.  From  four  to  eight  ounces  of  whiskey  or  brandy  daily 
usually  suffices.  Champagne  is  excellent  for  a  short  time.  The  more 
diffusible  stimulants,  such  as  cocaine,  the  aromatic  spirit,  the  carbonate, 
and  other  preparations  of  ammonium,  compound  spirit  of  ether,  camphor, 
etc.,  are  useful  adjuvants  when  the  heart  is  failing.  Late  in  the  course 
of  the  disease,  when  the  heart  is  dilating  from  increased  intrapulmonary 
pressure,  I  have  seen  excellent  results  from  the  use  of  tincture  of  digitalis, 
8  to  10  minims  (0.5  to  0.6  c.c),  combined  with  5  to  8  minims  (0.3  to 
0.5  c.c.)  of  tincture  of  belladonna  (to  increase  the  vascular  tone),  every 
three  or  four  huurs.  Digitalin,  y^  grain  (0.005  gram)  hypodermicly, 
may  be  substituted  for   the  tincture  of  digitalis.     Caffeine   also   is  of 


86  BACTERIAL  INFECTIONS 

much  value.  Atropine  hypodermicly  is  of  good  service  when  there  is 
oedema  of  the  lungs  and  the  vascular  tone  is  low ;  but  when  vasomotor 
paralysis  supervenes  the  best  results  follow  the  use  of  hypodermoclysis 
or  intravenous  transfusion  of  physiological  saline  solution  with  adrenalin 
chloride.  Finally,  when  the  cyanosis  becomes  marked,  the  heart's  action 
feeble  and  irregular,  the  muscular  element  of  the  first  sound  of  the  heart 
indistinct,  and  the  previously  accentuated  pulmonary  second  sound  weak, 
when,  in  other  words,  dilatation  is  marked,  good  results  attend  vene- 
section, which  may  be  followed  by  hypodermoclysis  or  intravenous  in- 
jection of  normal  saline  solution  with  adrenalin  chloride.  Nitroglycerin 
is  said  to  be  of  value  when  the  blood  pressure  is  high,  but  this  is  seldom 
the  case.  I  have  never  seen  much  good  from  its  use :  indeed,  it  is  usually 
directly  contra-indicated.  ^Vhen  the  toxemia  increases  to  such  an  extent 
as  to  simulate  meningitis  (the  meningisin  of  the  French)  lumbar  puncture 
may  be  practised  with  hope  of  good  results. 

A  sufficiency  of  sleep  should  be  assured  the  patient — by  the  mentioned 
hydrotherapeutic  measures,  a  Dover's  powder  at  night,  hot  whiskey,  a 
small  dose  of  morphine,  or  one  of  the  hypnotics.  Cough,  as  such, 
rarely  requires  treatment,  but  in  case  it  is  painful  and  distresses  the 
patient  it  may  be  controlled  by  an  occasional  Dover's  powder,  codeine, 
or  heroin.  Expectorants,  as  a  rule,  are  not  indicated,  usually  not  until 
the  stage  of  resolution,  when,  if  the  sputum  is  viscid  and  tenacious, 
ammonium  chloride,  iodide,  or  carbonate,  terpene  hydrate,  terbene, 
and  similar  drugs  may  be  used.  Should  tympany  develop  it  must  be 
relieved  immediately — since  it  adds  to  the  already  existing  embar- 
rassment of  the  heart  and  lungs;  the  diet  must  be  regulated,  milk 
stopped,  the  bowels  opened  freely,  eserine,  y^  to  -^j-  grain  (0.00065 
to  0.0013  gram)  given  hypodermicly,  and  efforts  made  to  increase  the 
usually  low  blood  pressure. 

The  complications  and  sequels  are  to  be  treated  on  general  principles. 
General  tonics,-  iron,  quinine,  strychnine,  cod-liver  oil,  phosphorus, 
etc.,  are  valuable  during  convalescence.  In  delayed  resolution,  recourse 
may  be  had  to  these  general  measures,  and  to  counterirritation  (iodine, 
blisters,  the  Paquelin  cautery),  the  iodides  internally,  and  perhaps  the 
cautious  use  of  the  a;-rays,  which  although  not  free  from  danger,  are 
said  to  foster  resolution.  Pilocarpine  has  been  recommended,  but  it  is 
doubtful  if  it  does  any  good. 


MENINGOCOCCIC  INFECTION;  CEREBROSPINAL  FEVER. 

{Epidemic  Cerebrofspinal  Meningitis^;  Spotted  Fever.) 

Cerebrospinal  fever  is  an  acute,  specific,  infectious,  and  slightly  con- 
tagious disease  caused  by  Diplococcus  intracellularis  meningitidis  (Weich- 
selbaum) ;  it  is  characterized  anatomically  by  fibrinopurulent  inflamma- 
tion of  the  pia-arachnoid,  and  clinically  by  irregular  course,  fever,  and 
divers  nervous  symptoms. 


MENINGOCOCCIC  INFECTION;  CEREBROSPINAL  FEVER      87 

Etiology. — Cerebrospinal  fever,  though  it  occurs  at  all  ages  and  in 
both  sexes,  is  more  common  in  children  and  young  adults,  and  in  the  male 
sex.  It  occurs  both  epidemically  and  sporadically,  especially  in  the 
winter  and  spring;  epidemics  are  usually  circumscribed,  rarely  wide- 
spread, are  often  more  common  in  country  villages  and  towns  than  in 
larger  cities,  and  are  much  favored  by  overcrowding  and  general  insani- 
tary conditions  (institutions,  barracks,  jails,  etc.). 

The  exciting  cause  of  the  disease  is  Diplococcus  intracellularis  menin- 
gitidis (or  meningococcus),  which  is  found  in  the  cerebrospinal  exudate, 
and  sometimes  in  the  nasal  secretions  and  the  blood.  The  disease  does 
not  appear  to  be  especially  contagious.  How  the  contagium  is  spread 
is  not  definitely  known,  but  acute  and  chronic  meningococcic  "carriers" 
seem  sometimes  to  be  the  active  factor.  Fomites  are  not  unduly  active. 
Infection  is  believed  to  be  acquired  through  the  nose  (infecting  the  men- 
inges through  the  cribriform  plate  of  the  ethmoid  bone  or  through  the 
sphenoidal  cells);  doubtless  the  ear  is  sometimes  the  portal  of  entry, 
and  possibly  the  blood  is  sometimes  primarily  involved  (by  way  of  the 
tonsils,  etc.).  Recurrences  are  not  uncommon;  one  attack  does  not 
confer  immunity. 

An  infection  almost  if  not  quite  identical,  anatomically  and  clinically, 
with  cerebrospinal  fever  may  be  caused  by  the  pneumococcus,  strepto- 
coccus, staphylococcus,  influenza  bacillus,  etc.,  but  these  are  usually 
secondary  infections. 

Pathology. — In  the  early  stages  there  is  intense  hyperemia  of  the  pia- 
arachnoid;  in  fulminant  cases  these  maybe  the  only  lesions  observed. 
In  the  ordinary  acute  cases,  there  is  sero-fibrino-purulent  inflammation 
of  the  pia-arachnoid,  especially  marked  at  the  posterior  basic  region  of  the 
brain,  and  the  dorsal  surface  of  the  thoracic  and  lumbar  cord ;  but  the  exu- 
date may  extend  to  the  convexity  of  the  brain,  and  indeed  involve  the  entire 
pia-arachnoid.  The  cranial  nerves  (especially  the  second,  third,  fourth, 
fifth,  sixth,  seventh,  and  eighth)  are  often  embedded  in  a  thick,  fibrino- 
purulent  exudate,  whereby  irreparable  damage  results.  In  more  chronic 
cases  the  pia-arachnoid  is  irregularly  thickened,  the  ventricles  are  dis- 
tended with  turbid  fluid,  and  irregular  foci  of  hemorrhage,  softening, 
and  encephalitis  are  encountered.  Microscopically  the  exudate  consists 
largely  of  polynuclear  leukocytes,  which  contain  the  meningococcus  and 
certain  unusually  large  endothelial  cells;  there  is  also  leukocytic  infiltra- 
tion of  the  brain  and  cord,  foci  of  hemorrhage  and  suppuration,  and 
swelling  of  the  ganglion  and  neuroglia  cells.  The  lesions  common  to 
most  toxemias  are  found  in  the  other  organs. 

Symptoms. — ^The  period  of  incubation  is  probably  short— one  to  four 
days.  Usually  prodromes  are  slight— malaise,  headache,  pains  in  the 
back,  etc. ;  but  they  may  be  entirely  absent.  The  onset  of  the  disease 
is  commonly  abrupt,  with  severe  chill  (sometimes  chilliness),  fever 
(102°  to  103°  F.),  severe  headache,  vomiting,  soon  followed  by  pain  and 
stiffness  in  the  muscles  of  the  neck.  Evidences  of  general  involvement 
of  the  nervoas  system  are  soon  manifest  in  increasing  headache,  vertigo, 


88  BACTERIAL  INFECTIONS 

vomiting  (sometimes  intractable),  delirium,  which  in  the  early  stages 
may  be  wild  and  maniacal,  but  with  increasing  exudation  gives  way  to 
stupor  and  finally  coma.  Involvement  of  the  special  senses  is  seen  in 
early  photophobia  and  intolerance  of  noises,  followed  by  paretic  phenom- 
ena— dimness  of  vision  and  deafness.  Evidences  of  motor  irritability 
are  always  seen,  and  consist  especially  of  spasm  of  the  muscles  of  the 
neck  (painful  retraction  of  the  head)  and  of  the  spine  (opisthotonos), 
increased  reflexes,  tremors  and  clonic  and  tonic  spasms  of  other  muscles, 
of  which  Kernig's  sign  is  an  important  evidence — inability  to  extend  the 
leg  when  the  thigh  has  been  flexed  upon  the  abdomen;  this,  which  may 
be  readily  accomplished  in  health,  is  rendered  impossible  in  most  cases 
of  meningitis  by  the  tonic  spasm  of  the  flexors  of  the  leg  (the  ham-string 
tendons).  The  ocular  and  the  facial  muscles  also  may  be  implicated 
in  the  spasms.  Later,  evidences  of  paresis  or  paralysis  become  manifest; 
these,  while  they  may  be  present  in  the  extremities  (monoplegia,  para- 
plegia, etc.),  are  commonly  most  marked  about  the  eye  (ptosis,  unequal 
pupils,  strabismus,  etc.)  and  the  face.  Evidences  of  sensory  irritability 
are  found  in  the  general  cutaneous  hyperesthesia,  tenderness  of  the 
skull  and  along  the  spine,  and  sometimes  of  the  peripheral  nerves. 
Anesthesia  sometimes  replaces  the  hyperesthesia. 

The  fever  is  irregular — remittent  and  intermittent,  sometimes  sub- 
normal, sometimes  very  high  (105°,  106°,  even  108°  F.  or  more  just  before 
death).  The  pulse  is  variable;  it  is  often  accelerated  at  first,  especially 
in  children,  but  in  many  cases,  especially  in  adults,  it  soon  becomes 
very  slow — 60,  40 — and  irregular,  and  it  varies  much  from  time  to  time. 
The  respirations  are  often  increased  at  first;  soon  they  become  normal 
(except  in  the  event  of  pneumonia  or  bronchitis) ;  later  they  may  take  on 
the  Cheyne-Stokes  type.  Herpes  facialis  occurs  in  about  60  per  cent, 
of  the  cases.  Petechiae  (whence  the  name  spotted  fever)  occur  in  some- 
what more  than  one-half  of  the  cases  in  most  epidemics;  in  sporadic 
cases  they  are  often  missed;  and  when  present  may  be  few  or  many 
(universal).  Trousseau's  tache  cerebrale  (persistence  of  a  red  line 
after  striking  the  skin)  can  usually  be  elicited.  Erythema,  urticaria, 
and  even  gangrene  have  been  observed.  The  abdomen  is  often  retracted. 
Leukocytosis  (25,000  to  40,000)  is  usually  present,  and  is  polynuclear 
in  type.  Slight  albuminuria,  rarely  glycosuria,  may  be  encountered. 
The  bowels  are  usually  constipated.  The  spleen  may  be  enlarged,  but 
often  is  not  demonstrably  so. 

Varieties. — The  following  t}^es  may  be  recognized:  Abortive  cases, 
in  which  there  are  severe  initial  symptoms,  which,  however,  soon  subside, 
and  the  patient  convalesces.  Slight  cases,  in  which  there  is  moderate 
fever  of  slight  duration,  ill-developed  cerebrospinal  symptoms  of  short 
duration,  and  a  rather  quick  and  satisfactory  convalescence.  Malignant 
or  fulminant  cases,  in  which  the  symptoms  are  of  great  severity,  and  the 
temperature  very  high  (108°  F.  or  more),  and  in  which  death  results  within 
thirty-six  or  forty-eight  hours.  Apoplectiform  cases,  in  which  the  patient 
suddenly   becomes    unconscious,    possibly   paralyzed,    and   soon   dies. 


MENINGOCOCCIC  INFECTION;  CEREBROSPINAL  FEVER      89 

Intermittent  cases,  in  which  the  fever  and  the  other  manifestations  vary 
much  from  time  to  time,  remit  and  intermit.  Chronic  cases,  in  which 
the  disease  lasts  for  months,  relapses  and  improvements  occurring  from 
time  to  time. 

Complications  and  Sequels. — Complications  and  sequels  are  many  and 
various.  Pneumonia,  pleuritis,  pericarditis,  arthritis,  nephritis,  and 
parotitis  are  not  infrequent  during  the  height  of  the  disease.  The  most 
common  sequels  are  optic  neuritis  and  atrophy,  parotitis,  iritis,  and 
panophthalmitis,  leading  to  blindness;  otitis  media  and  mastoiditis, 
leading  to  deafness,  and  when  occurring  in  young  subjects  to  deaf- 
mutism;  paralysis  of  the  different  cranial  nerves,  aphasia,  hydrocephalus, 
monoplegia,  hemiplegia,  etc. 

Diagnosis. — The  diagnosis  is  usually  evident  from  the  foregoing 
symptoms.  Variability  in  the  intensity  of  the  symptoms  from  time  to 
time  is  one  of  the  most  characteristic  phenomena  of  the  disease.  With 
a  view  to  confirm  the  diagnosis,  lumbar  puncture  should  be  resorted  to 
— a  three-inch  needle  with  a  good-sized  caliber  being  introduced  into 
the  fourth  intervertebral  space  (just  below  a  line  drawn  between  the 
crests  of  the  ilium).  Cytodiagnosis  may  be  resorted  to:  in  cerebro- 
spinal meningitis  the  polynuclear  cells  predominate  in  the  exudate, 
whereas  in  tuberculous  meningitis,  the  mononuclear  cells  predomi- 
nate. Diplococcus  intracellularis  meningitidis  is  also  easily  demon- 
strated in  the  exudate  by  microscopic  examination;  cultural  methods 
and  inoculations  into  lower  animals  will  help  to  a  diagnosis  in  doubtful 
cases.  Usually  not  much  difficulty  is  experienced  in  differentiating 
typhoid  fever  and  pneumonia;  but  in  some  cases  with  marked  meningism 
the  differential  diagnosis  may  be  for  the  moment  impossible  without 
resort  to  lumbar  puncture,  and  since  this  is  not  only  a  diagnostic  measure, 
but  also  a  therapeutic  measure  of  value,  it  should  not  be  delayed.  Menin- 
gitis, of  course,  may  complicate  pneumonia  and  typhoid  fever. 

Prognosis. — ^The  mortality  varies  much  in  different  epidemics — from 
25  to  75  per  cent. — and  is  usually  in  direct  ratio  to  the  severity  of  the 
cerebral  symptoms.  Fulminant  cases  may  result  fatally  within  twelve 
hours;  and  ordinary  acute  cases  in  from  four  to  ten  days.  In  favorable 
cases  convalescence  usually  sets  in  at  the  end  of  ten  to  fifteen  days,  but 
it  may  be  much  delayed,  and  death  may  eventually  result,  generally  from 
complications  or  exhaustion,  at  the  end  of  weeks  or  even  months. 

Treatment. — Isolation  and  other  prophylactic  measures  (page  29),  rest 
in  bed,  quiet,  and  a  liquid  and  soft  nutritious  diet  comprise  the  general 
measures  useful  in  the  disease.  Flexner's  antimeningococcic  serum, 
although  still  on  trial,  seems  to  be  more  or  less  of  a  specific.  In  using 
it,  lumbar  puncture  should  be  first  performed,  and  then  30  c.c.  (in 
fulminant  cases,  45  c.c.)  of  the  serum  should  be  injected.  This  should 
be  done  daily  for  four  or  five  days;  more  frequently,  if  the  symptoms 
are  alarming,  and  for  a  longer  period,  if  the  symptoms  persist.  The 
use  of  extract  of  washed  leukocytes  has  been  suggested  by  Hiss.  In 
the  absence  of  a  specific,  treatment  is  largely  symptomatic.     Hydro- 


90  BACTERIAL  INFECTIONS 

therapy  is  of  value  in  most  cases,  and  in  addition  to  a  tub  bath,  should 
the  temperature  be  high,  much  relief  is  afforded  by  an  ice-bag  to  the 
head  and  along  the  spine.  Hot  baths  are  often  grateful  to  the  patient, 
and  seem  to  lead  to  some  improvement  in  the  general  symptoms.  Counter- 
irritation  by  means  of  the  Paquelin  cautery  is  much  preferable  to  blisters. 
Preparations  of  opium  are  useful  in  relieving  the  headache,  the  pains 
in  the  back,  and  the  muscular  contractions,  and  may  often  be  serviceably 
combined  with  atropine  or  the  bromides.  Potassium  iodide,  ergot, 
quinine,  salicylic  acid,  cannabis  indica,  and  mercury  (for  its  antiseptic 
properties)  have  also  been  recommended.  Pilocarpine  has  been  reported 
of  value  by  reason  of  the  leukocytosis  it  induces.  Stimulants  may  be  used 
when  exhaustion  supervenes.  Lumbar  puncture  is  a  very  serviceable 
procedure — not  only  diagnostically  but  therapeutically.  The  withdrawal 
of  20  to  30  c.c.  of  cerebrospinal  fluid  is  often  followed  immediately  by 
relief  of  the  headache  and  the  muscular  contractures,  and  it  is  reasonable 
to  suppose  that  a  certain  amount  of  toxins  is  also  withdrawn.  The  pro- 
cedure may  be  repeated  from  time  to  time.  It  has  been  suggested  to  irri- 
gate the  cerebrospinal  canal  with  physiological  saline  solution;  perhaps 
with  improvement  in  technique  this  may  become  a  well-indicated  thera- 
peutic measure. 

GONOOOCCIO  INFECTION. 

Gonococcic  infection  is  an  acute,  specific,  infectious,  and  highly  con- 
tagious disease  caused  by  Micrococcus  gonorrhoeae  (Neisser),  and  charac- 
terized by  Menorrhagia  and  sometimes  by  general  systemic  infection. 

Etiology. — ^The  specific  cause  of  the  disease  is  the  gonococcus,  which, 
although  usually  acquired  in  sexual  intercourse  and  attacking  first  the 
mucous  membrane  of  the  urethra  in  the  male,  and  the  vulva,  vagina, 
and  urethra  in  the  female,  may  nevertheless  attack  any  mucous  membrane, 
such  as  the  conjunctiva,  the  anus,  the  oral  mucous  membrane,  etc. 
While  the  lesions  that  it  provokes  are  often  confined  to  the  genito-urinary 
tract,  it  not  uncommonly  causes  the  most  widespread  local  disease, 
such  as  cystitis,  prostatitis,  vesiculitis,  epididymitis,  orchitis,  etc.,  in  the 
male,  and  endocervicitis,  metritis,  salpingitis,  ovaritis,  peritonitis,  etc., 
in  the  female;  it  is  one  of  the  most  prolific  causes  of  continued  ill-health 
in  both  sexes,  but  especially  in  women  the  innocent  victims  of  uncured, 
more  or  less  quiescent,  antemarital  infection  in  their  husbands;  and 
it  sometimes  gives  rise  to  general  infection.  The  general  manifesta- 
tions of  the  local  infection  are  due,  in  the  great  majority  of  cases,  to 
toxemia;  occasionally,  however,  to  gonococcic  bacteremia.  Although 
arthritis,  endocarditis,  pericarditis,  myocarditis,  myelitis,  keratitis, 
iritis,  and  panophthalmitis,  etc.,  have  been  reported,  special  impor- 
tance in  the  present  connection  attaches  to:  (1)  Gonococcic  bacteremia; 
(2)  gonococcic  endocarditis;  and  (3)  gonococcic  synovitis  and  arthritis. 

Symptoms. — Gonococcic  bacteremia  (septicemia,  pyemia)  has  occasion- 
ally been  observed  in  association  with  a  focus  of  suppuration  in  the 


GONOCOCCIC  INFECTION  91 

genito-urinary  tract,  and  with  gonococcic  endocarditis  and  artliritis. 
The  symptoms  have  been  those  of  profound  intoxication  together  with 
the  manifestations  of  the  local  infection.  The  gonococcus  has  been 
cuhivated  from  the  l)lood. 

Gonococcic  endocarditis  has  been  observed  in  a  few,  but  gradually 
increasing  number  of  cases.  It  has  usually  been  associated  with  (some- 
times preceding,  sometimes  following)  arthritis,  and  the  gonococcus 
has  been  isolated  from  the  blood;  in  other  words,  the  condition  is  a  bac- 
teremia. The  symptoms  do  not  dift'er  from  those  of  endocarditis  due  to 
other  causes.  Pericarditis  and  myocarditis  have  been  observed  in  a  few 
fatal  cases. 

Gonococcic  synovitis  and  arthritis  develop  usually  when  the  acute 
urethritis  is  subsiding,  occasionally  when  it  has  become  chronic.  It  is 
somewhat  more  common  in  men  than  in  women.  It  may  involve  one 
or  several  joints;  more  than  one  are  more  frequently  involved  than  is 
generally  supposed.  The  knee  (men),  wrist  (women),  and  ankle  are 
most  likely  to  be  attacked,  but  the  smaller  joints  are  not  infrequently 
affected.  Irregular  fugitive  pains  and  possibly  some  tenderness  are  com- 
mon during  many  attacks  of  gonococcic  urethritis,  but  they  are  doubtless 
expressions  of  the  toxemia  and  they  soon  subside.  In  other  cases  the 
more  common  manifestations  of  synovitis  develop — extreme  pain, 
tenderness,  swelling,  and  inability  to  move  the  joint.  Slight  fever  may 
be  present  for  several  days,  but  in  most  cases  (in  the  absence  of  suppura- 
tion) it  soon  subsides,  and  the  general  symptoms  are  inconspicuous  as 
contrasted  with  the  local.  The  effusion  is  within  and  without  the 
joint,  and  may  extend  along  the  fascise  and  the  tendons  and  involve 
the  bursse.  It  is  usually  serous  or  serofibrinous  in  character.  By 
aspiration  and  culture  methods  the  gonococcus  may  be  recovered,  but  a 
mixed  infection  is  not  unknown.  Occasionally  suppuration  results 
(suppurative  synovitis,  empyema  or  phlegmon  of  the  joint)  and  may 
result  in  widespread  destruction  of  the  articulating  surfaces.  Mild 
infections  may  result  in  recovery,  but  permanent  stiffness  (fibrous  anky- 
losis) due  to  chronic  inflammation  of  the  articular  and  periarticular 
structures  is  much  more  common.  Occasionally  a  chronic  hydrops 
(hydrarthrosis)  ensues.  Bony  ankylosis  may  result  from  the  more 
destructive  infections.  Exostosis,  especially  of  the  os  calcis,  is  not  un- 
common, and  gives  rise  to  local  pain,  tenderness,  and  a  "  tiptoeing 
gait''  (one  form  of  "painful  heel"). 

Diagnosis. — Gonococcic  synovitis  and  arthritis  may  be  distinguished 
from  rheumatic  fever  (to  which  it  is  in  no  way  related)  by  the  history 
of  urethritis,  severity  of  the  local  lesions,  relative  meagreness  of  the 
general  symptoms,  persistence  of  the  articular  lesions  and  their  non- 
response  to  the  salicylates,  and  the  more  likely  involvement  of  the  tem- 
poromaxillary,  sternoclavicular,  sacroiliac,  pubic,  and  intravcrtebral 
joints. 

Treatment. — The  urethritis,  whether  acute  or  chroin'c,  should  receive 
attention.      The  salicylates  and  potassium   iodide  are  of  very  little,  if 


92  BACTERIAL  INFECTIONS 

any,  service.  Some  good  seems  to  attend  the  use  of  syrup  of  iron  iodide, 
10  to  60  minims  (0.6  to  4  c.c.)  three  times  a  day.  In  most  cases  tonics 
are  called  for  sooner  or  later,  in  which  event  iron,  quinine,  strychnine, 
arsenic,  and  cod-liver  oil  may  be  valuable.  For  the  relief  of  the  local 
symptoms  nothing  is  as  efficacious  as  absolute  rest  enjoined  by  a  fixed 
dressing.  All  other  measures,  such  as  hot  and  cold  applications,  lead 
water  and  laudanum,  counterirritation,  ointments  of  ichthyol,  bella- 
donna, mercury,  iodine,  etc.,  though  of  value,  are  of  subsidiary  impor- 
tance. If  the  joint  has  become  fixed  in  a  poor  position,  it  must  be  straight- 
ened, under  an  anesthetic,  if  necessary.  If  improvement  is  not  mani- 
fested soon,  the  joint  should  be  opened,  irrigated,  and  subsequently  treated 
aseptically.  Counterirritation  (blisters,  thermocautery),  massage,  passive 
movements,  superheated  dry  air  ("  baking  the  joint"),  and  Bier's  "  passive 
hyperemia"  treatment  are  sometimes  of  value  in  relieving  some  of  the 
chronic  manifestations.  An  antigonococcic  serum  has  been  used,  with 
indifferent  success.  Bacterial  vaccines  seem  to  have  been  of  service  in 
some  cases. 

TUBERCULOSIS. 

{Phthisis;  Consumption;  Scrofula.) 

Tuberculosis  is  a  specific,  infectious,  and  mildly  contagious  disease 
caused  by  Bacillus  tuberculosis  (Koch);  it  is  characterized  anatomically 
by  the  development  of  small  nodules,  so-called  tubercles,  or  a  diffuse 
productive  inflammation,  both  of  which  tend  to  undergo  caseation  and 
softening  or,  less  commonly,  fibrosis  and  calcification;  the  clinical  mani- 
festations vary,  depending  upon  the  type  of  infection  and  the  tissues 
especially  involved. 

Etiology. — ^Tuberculosis  is  an  exceedingly  widespread  disease ;  it  occurs 
in  all  parts  of  the  world,  although  it  is  most  prevalent  in  the  temperate 
zone  and  at  low  rather  than  high  altitudes;  and  it  affects  many  species 
of  animals,  notably  man,  cattle,  fowls,  birds,  domestic  animals,  etc. 
Of  human  subjects,  no  race  is  exempt;  the  negro  and  the  American 
Indian  display  a  high  degree  of  susceptibility,  and  the  Hebrew  appar- 
ently some  relative  immunity.  The  disease  occurs  at  all  ages,  but  there 
seems  to  be  a  special  susceptibility  during  the  first  two  years  of  life 
(perhaps  due  to  milk-borne  infection  or  close  association  with  a  tuber- 
culous mother),  and  during  adolescence  and  early  adult  life  (fifteenth 
to  twentieth  years).  Sex  as  such  is  without  etiological  significance;  the 
frequency  of  the  disease  in  women  may  be  in  part  attributed  to  a  sedentary 
indoor  life,  lack  of  outdoor  exercise,  pregnancy,  and  lactation — which 
reduce  the  resisting  powers.  The  poor  and  the  industrial  workers  are 
especially  subject  to  the  infection;  botii  often  are  provided  with  insuffi- 
cient and  improper  food  and  clothing;  they  live  and  work  in  dark, 
overcrowded,  ill-ventilated,  and  otherwise  insanitary  rooms;  and  they 
are  subject  often  to  prolonged  and  exhausting  labor  and  to  the  inhalation 
of  irritating,  dust-  and  bacilli-laden  atmosphere,  etc.     Other  predisposing 


TUBERCULOSIS  93 

factors  comprise  trauma  (especially  of  the  bones  and  joints);  catarrhal 
inflammation  of  the  respiratory  tract  (often  tuberculous  from  the  begin- 
ning); infectious  diseases  like  pneumonia  (often  tuberculous  from  the 
beginning),  influenza,  pertussis,  measles,  typhoid  fever,  syphilis,  etc.; 
debilitating  diseases,  such  as  diabetes,  carcinoma,  etc.;  aneurysm  and 
compression  of  the  lung,  and  chronic  diseases  of  the  heart  associated 
with  anemia  of  the  lungs,  such  as  aortic  valve  disease:  mitral  valve 
disease,  in  consequence  of  the  chronic  pulmonary  congestion  that  it 
induces,  seems  to  afford  some  immunity  to  tuberculosis  of  the  lungs. 
Some  persons  seem  to  possess  a  more  or  less  efficient  natural  immunity, 
some  of  these  being  descendants  of  tuberculous  ancestors.  One  attack 
of  the  disease  does  not  confer  immunity,  at  least  not  a  lasting  immunity, 
since  recurrences  or  relapses  are  the  rule. 

The  exciting  cause  of  the  disease  is  Bacillus  tuberculosis,  of  which 
four  types  may  be  distinguished — the  human,  the  bovine,  the  avian,  and 
the  piscian.  These,  perhaps,  originally  comprised  a  single  type,  but 
owing  to  environmental  conditions  have  developed  special  individual 
characteristics.  The  human  and  the  bovine  types  are  intercommunicable, 
but  the  avian  and  the  piscian  types  appear  to  be  either  incapable  of 
producing  tuberculosis  in  man  or  capable  of  producing  it  only  in  a  mild 
form.  Raw  has  recently  suggested  that  in  the  human  subject  the  human 
type  of  the  bacillus  affects  the  lungs,  the  intestines,  and  the  abdominal 
viscera,  while  the  bovine  type  affects  the  lymph  nodes,  the  peritoneum, 
the  meninges,  the  bones  and  joints,  and  probably  the  skin — an  opinion 
that  has  not  yet  been  confirmed.  Infection  is  transmitted  largely  through 
the  medium  of  infected  air  or  infected  food;  but  it  may  be  transmitted 
also  by  direct  contact  or  inoculation,  and  perhaps  by  a  third  person,  by 
fomites,  and  by  domestic  animals.  The  air  becomes  infected  through 
the  drying  and  subsequent  dispersion  of  bacilli-laden  sputum,  and 
through  the  projection  into  the  atmosphere  by  coughing  of  minute, 
invisible,  droplets  of  infected  sputum  and  saliva.  Food,  especiallv 
milk  and  butter,  becomes  contaminated  by  tuberculosis  especially  of 
the  udders  of  cattle,  or  by  being  incautiously  handled  by  tuberculous 
subjects;  the  meat  from  tuberculous  cattle  also  may  be  infected  by 
widespread  tuberculosis  of  the  animal;  and  the  milk,  meat,  butter,  and 
other  foodstuffs  may  become  infected  by  flies  and  other  insects  that  have 
walked  on  or  fed  upon  tuberculous  sputum.  Infection  may  be  acquired: 
(1)  By  inhalation — which  is  doubtless  the  most  common  mode  of  infec- 
tion. The  bacilli  probably  gain  access  to  the  tissues  througli  the  walls 
of  the  l)ronchi  or  bronchioles,  and  set  up  a  primary  pulmonary  tuber- 
culosis. (2)  By  ingestion — probably  the  second  most  common  mode 
of  infection.  The  bacilli  carried  in  foodstuffs  may  penetrate  the  in- 
testinal mucosa  without  producing  discoverable  lesions;  thence  they 
gain  access  to  the  mesenteric  lymph  nodes,  where  they  may  set  up  tuber- 
culous lesions;  or,  according  to  some  observers,  they  invade  the  thoracic 
lymphatics  and  from  these  subsequently  involve  the  lung,  giving  rise  in 
this  manner  to  pulmonary  tuberculosis.     (3)  By  way  of  the  tonsils  and 


94  BACTERIAL  INFECTIONS 

other  lymphatics  of  the  oral  and  pharyngeal  cavity  (such  as  carious  teeth, 
etc.).  Tuberculosis  of  the  cervical  lymph  nodes  ensues,  and  from  these 
foci,  dissemination  may  occur  to  other  parts  of  the  body,  especially  the 
lungs.  (4)  Direct  inoculation  into  the  skin  through  an  abrasion,  as  may 
occur  at  dissections,  operations,  necropsies,  etc.;  the  ensuing  lesion  is 
often  spoken  of  as  an  anatomical  tubercle.  (5)  By  direct  inoculation 
of  the  genitalia  in  sexual  intercourse — a  rare  mode  of  infection,  but  per- 
haps responsible  for  some  cases  of  tuberculosis  of  the  uterus  and  Fallo- 
pian tubes;  rarely  of  other  parts  of  the  genitalia  in  both  sexes.  (6)  By 
way  of  the  placenta — the  foetus  becoming  infected  by  a  tuberculous 
mother.  This  so-called  congenital  tuberculosis  is  very  rare  in  the 
human  subject;  it  seems  to  be  more  common  in  certain  of  the  lower 
animals,  especially  cattle. 

Infection  having  occurred,  the  bacilli:  may  be  disseminated  more  or 
less  widely  throughout  the  body:  (1)  By  way  of  the  lymphatics.  This 
is  the  commonest  mode  of  dissemination,  especially  in  all  forms  of  tuber- 
culosis in  children,  and  in  the  subacute  and  chronic  pulmonary,  intestinal, 
and  other  types  of  the  disease  in  adults.  (2)  By  way  of  the  bloodvessels. 
This  is  the  mode  of  dissemination  in  miliary  tuberculosis,  the  bacilli 
gaining  access  to  the  vascular  channels  through  rupture  thereinto  of  a 
tuberculous  focus,  most  commonly  the  rupture  of  a  tuberculous  bron- 
chial lymph  node  into  a  pulmonary  vein.  (3)  By  way  of  a  mucous 
surface.  This  is  a  common  mode  of  extension  of  the  lesions  in  pul- 
monary tuberculosis,  infectious  material  (sputum)  being  discharged  into 
a  bronchus  and  then  aspirated  into  another  bronchus  that  leads  to  an 
uninvolved  portion  of  the  lung;  certain  intestinal  ulcers  also  perhaps 
exemplify  this  mode  of  dissemination,  sputum  being  swallowed  and 
infecting  the  intestinal  mucosa. 

Pathology. — Although  no  organ  of  the  body  is  exempt  from  tubercu- 
losis, the  incidence  of  involvement  varies  considerably.  In  children, 
the  lymph  nodes,  bones,  and  joints  are  most  commonly  involved;  in 
adults,  the  lungs,  intestines,  urinary  organs,  serous  membranes,  etc. 
The  lesions  consist  of  two  main  types — tubercle  formation  and  a  diffuse 
productive  inflammation.  The  characteristic  lesion  is  the  tubercle, 
which  in  its  earliest  stage,  the  so-called  miliary  tubercle,  consists  of  a 
o-rayish,  somewhat  translucent  nodule,  a  millimeter  or  less  in  diameter 
(the  size  of  a  millet  seed);  it  is  firmer  than  the  surrounding  tissue,  projects 
slightly  from  the  general  level  of  the  cut  surface  of  an  organ,  and  may  be 
delimited  by  a  narrow  zone  of  reactive  congestion.  In  the  course  of 
time  these  miliary,  or  gray,  tubercles  increase  in  size  by  peripheral 
extension,  and  concurrently  therewith  their  centres  become  yellowish  in 
color  and  soft — the  so-called  yellow,  or  caseous  tubercle.  In  consequence 
of  the  coalescence  of  neighboring  tubercles,  large  tu))erculous  masses 
form  and  may  attain  the  size  of  a  hen's  egg  (the  so-called  solitary  tubercle, 
common  in  the  brain  and  meninges);  and  in  consequence  of  central 
caseation  and  liquefaction  necrosis,  a  so-called  tuberculous  (or  cold) 
"abscess"  (consisting,  however,  only  of  more  or  less  fluid  or  inspissated 


TUBERCULOSIS  95 

granular  debris)  results;  this  being  discharged  externally  leaves  a  cavity 
(especially  common  in  the  lungs),  or  one  or  several  sinuses  (especially 
common  in  connection  with  bones  and  joints).  In  the  neighborhood  of 
coalesced  tubercles,  small  gray  or  yellowish  tubercles  are  usually  en- 
countered, the  result  in  most  cases  of  lymphatic  extension  (so-called 
mother  and  daughter  tubercles).  The  much  rarer  diffuse  productive 
inflammation  may  occur  in  any  organ,  but  is  most  common  in  the  lungs 
and  the  lymph  nodes.  It  may  or  may  not  be  associated  with  the  forma- 
tion of  definite  tubercles.  For  instance,  the  inhalation  of  large  numbers 
of  virulent  bacilli  by  susceptible  individuals  may  lead  to  the  rapid 
development  of  tuberculous  pneumonia,  which  exhibits  many  clinical 
and  pathological  analogies  with  ordinary  pneumococcic  infection  of  the 
lung.  In  the  early  stages,  however,  the  lung  has  a  more  gelatinous 
appearance,  due  to  certain  peculiarities  of  the  inflammatory  oedema; 
later  it  becomes  cheesy  in  character,  and  often  the  seat  of  widespread 
softening  and  excavation. 

The  first  effect  of  tubercle  bacilli  settled  and  multiplying  in  the  tissues 
appears  to  be  irritative  rather  than  degenerative — proliferation  rather 
than  death  of  the  cells.  The  earliest  lesions  consist  of  the  development 
of  large,  ovoid,  or  polygonal  cells  with  ovoid  or  elliptical,  vesicular  nuclei, 
and  an  abundant  cytoplasm,  harboring  usually  few  or  many  tubercle 
bacilli.  These  cells,  spoken  of  as  epithelioid  or  endothelioid,  on  account 
of  obvious  resemblances,  are  derived  from  proliferation  of  the  endothe- 
lium of  capillary  bloodvessels  and  lymphatics,  as  well  as  other  fixed 
connective  tissue  cells.  About  this  focus  of  epithelioid  cells  (so-called 
epithelioid  tubercle)  leukocytes  collect  in  greater  or  less  numbers :  at  first 
many  polynuclear  cells,  but  soon  mononuclear  cells  predominate  (so- 
called  lymphoid  tubercle).  This  cellular  accumulation,  which  does  not 
differ  from  the  small  round-cell  accumulations  of  inflammation,  com- 
prises lymphocytes  from  the  surrounding  vascular  and  lymphatic  channels, 
as  well  as  proliferated  fixed  connective  cells;  that  is,  the  chemotactic  influ- 
ence of  the  tubercle  toxin  seems  to  be  lymphocytic  rather  than  poly- 
nuclear leukocytic.  About  this  time,  the  capillaries  of  the  tuberculous 
focus  become  occluded,  and  since  new  capillaries  are  not  formed,  the 
tubercle  soon  becomes  both  extravascular  and  avascular.  In  its  early 
stages  the  tubercle  may  consist  only  of  these  epithelioid  and  lymphoid 
cells,  in  varying  .proportion,  and  a  delicate  reticulum,  doubtless  the 
remains  of  stretched  and  otherwise  altered  fibers  of  the  fixed  connective 
tissue.  In  many  cases,  however,  so-called  giant  cells  also  are  encoun- 
tered: large,  irregular  cells,  with  many  nuclei  arranged  peripherally  or 
toward  one  pole,  and  containing  many  tubercle  bacilli.  These  result 
from  fusion  of  neighboring  epithelioid  cells  or  from  nuclear  proliferation 
(partly  amitotic)  without  coincident  cytoplasmic  division.  The  appear- 
ance within  these  giant  cells  of  a  hyaline  or  granular  centre,  as  well  as 
certain  peripheral  extensions,  suggesting  j)erhaps  fusion  of  adjacent 
epithelioid  cells,  indicates  that  the  giant  cell  is  the  first  retrograde 
change  within  the  tubercle.     Soon,  however,  other  evidences  of  necrosis 


96  BACTERIAL  INFECTIONS 

supervene — the  result  of  the  direct  action  of  the  tubercle  toxin  as  well 
as  the  avascularity:  the  nuclei  of  the  central  epithelioid  cells  undergo 
various  retrograde  changes  (hyperchromatosis,  karyolysis,  karyorrhexis, 
pyknosis),  the  cytoplasm  becomes  granular  (ground-glass  appearance), 
and  the  cell  outline  becomes  indistinct;  ultimately  all  cellular  structure 
disappears,  and  the  central  portion  of  the  tubercle  becomes  converted 
into  a  granular  cheesy  mass.  This  necrosis  increases  by  peripheral 
extension,  so  that  ultimately  the  tubercle  consists  of  a  central  necrotic 
area,  and  more  or  less  ill-defined  zones  of  epithelioid  cells  and  giant  cells, 
and  of  round-cell  infiltration.  In  some  cases,  in  consequence  of  immu- 
nizing processes,  caseation  becomes  retarded  or  arrested,  the  peripheral 
fibroblasts  are  enabled  to  build  up  more  or  less  efficient  new  connective 
tissue,  which  may  or  may  not  contain  tubercles,  and  ultimately  the 
tuberculous  focus  may  be  surrounded,  encapsulated,  or  pervaded  by 
fibrous  connective  tissue  (fibrocaseous  tubercle).  This  fibrosis  may 
progress  until  the  tuberculous  focus  has  been  completely  absorbed,  and 
cure  ensues;  more  commonly,  perhaps,  more  or  less  caseous  material 
remains  within  the  connective  tissue  capsule,  and  the  capsule  itself  may 
become  calcified  (quiescent,  inactive  tuberculosis).  In  the  event  of 
progressive  caseation,  secondary  infections  are  quite  likely  to  ensue, 
especially  in  the  lungs — infections  with  the  pneumococcus,  staphylococcus, 
streptococcus,  influenza  bacillus,  Micrococcus  tetragenus,  etc.  The 
general  toxemia  that  results  from  the  absorption  of  the  tubercle  toxin 
leads  to  fever,  emaciation,  amyloid  and  fatty  degeneration,  etc. ;  but  some 
of  the  general  manifestations,  such  as  the  so-called  hectic  fever,  are  due 
in  part  to  the  toxemia  of  the  secondary  infections. 

Acute  Miliary  Tuberculosis. 

Etiology. — In  addition  to  the  general  etiological  factors,  already  men- 
tioned, special  importance  attaches  to  the  predisposing  influence  in  mil- 
iary tuberculosis  of  :  (1)  Childhood  and  youth,  perhaps  accounted  for  by 
the  great  activity  of  the  lymphatic  system,  especially  its  active  absorp- 
tion and  conduction;  (2)  localized  chronic  pulmonary  tuberculosis,  in 
which  the  fatal  termination  is  frequently  determined  by  dissemination 
of  the  process  (miliary  tuberculosis) — in  the  lungs  or  more  or  less  widely 
throughout  the  body;  (3)  other  acute  infections,  such  as  pertussis, 
measles,  typhoid  fever,  etc.,  which  are  not  infrequently  followed  by 
miliary  tuberculosis;  (4)  trauma,  the  mechanical  effect  of  which  may  be  to 
permit  the  entrance  of  tubercle  bacilli  into  the  blood  stream,  or  to  activate 
a  quiescent  tuberculous  focus  which  later  may  lead  to  dissemination  of 
the  infection;  (5)  pregnancy,  the  puerperium,  and  lactation,  which  may 
reduce  the  resisting  powers;  and  (6)  debilitating  diseases,  like  diabetes, 
cirrhosis  of  the  liver,  chronic  nephritis,  etc.,  in  which  the  lethal  issue  is 
often  due  to  miliary  (and  other  forms  of)  tuberculosis. 

Pathology. — ^Acute  miliary  tuberculosis  may  be  confined  to  one  or 
several  organs,  or  it  may  be  widespread  through  the  body.     The  infection 


ACUTE  MILIARY   TUBERCULOSIS  97 

is  transmitted  by  the  blood  stream^  to  which  the  bacilH  gain  access  in 
consequence  of,  (1)  the  irruption  of  a  tuberculous  focus  into  the  vascular 
stream,  or  (2)  tuberculous  disease  of  the  wall  of  a  vein,  artery,  or  lymph 
vessel.  The  characteristic  lesion  consists  of  the  miliary  or  gray  tubercle; 
but  in  some  cases,  of  comparatively  slow  progression  or  moderately  long- 
duration,  more  or  less  caseation,  the  so-called  yellow  tubercle  develops. 
These  tubercles,  especially  the  miliary  or  gray  tubercle,  may  be  found 
in  any  organ  or  tissue  of  the  body,  but  they  are  most  common  in  the  lungs, 
liver,  spleen,  kidneys,  intestine,  meninges,  etc.  If,  as  is  common,  there 
is  primary  disease  of  the  lungs  or  the  peribronchial  lymph  nodes,  the 
bacilli  may  gain  entrance  into  the  pulmonary  veins,  and  be  thence  trans- 
mitted to  the  heart  and  the  systemic  circulation.  In  other  cases,  the 
bacilli  may  gain  the  blood  stream  by  way  of  the  thoracic  duct.  In  cases 
of  disseminated  infection,  tuberculous  arteritis,  phlebitis,  and  lymphan- 
gitis have  been  found,  but  it  is  not  always  possible  to  determine  whether 
these  vascular  lesions  are  the  result  or  the  cause  of  the  generalized  disease; 
older  lesions  in  the  vessel  walls,  however,  suggest  that  they  are  the  ante- 
cedent process.  Tubercles  have  been  found  in  the  walls  of  the  thoracic 
duct,  the  pulmonary  veins,  the  jugular  veins,  the  aorta,  and  certain 
smaller  arteries,  etc.  In  the  lungs  miliary  tubercles  are  usually  present 
in  greatest  numbers,  and  are  likely  to  be  most  widespread  in  distribution ; 
they  may  develop  in  the  alveolar  walls  or  in  the  peribronchial  or  peri- 
vascular tissues.  The  liver  is  almost  always  affected  in  generalized 
miliary  tuberculosis;  two  sources  of  infection  are  possible — the  portal 
and  the  general  arterial  circulatory  system;  the  tubercles  may  be  found 
in  the  intralobular  or  interlobular  tissue,  and  there  may  be  also  some 
hyperplasia  of  the  connective  tissue  and  proliferation  of  the  biliary  ducts. 
In  the  spleen  the  tubercles  may  be  distributed  regularly  or  irregularly. 
In  the  walls  of  the  intestine  tubercles  are  common,  especially  in  the 
submucous  and  serous  coats,  and  they  are  usually  associated  with  adja- 
cent ulceration.  Infection  may  occur  through  the  lumen  of  the  gut  or  by 
way  of  the  blood  stream.  In'  the  kidneys,  which  are  commonly  involved, 
the  tubercles  are  most  frequently  seen  in  the  cortex.  The  serous  mem- 
branes, notably  the  cerebrospinal  meninges,  the  peritoneum,  the  pleurae, 
and  the  pericardium,  are  commonly  involved;  occasionally  also  the  endo- 
cardium. The  tubercles  develop  also  in  the  bone  marrow,  the  choroid 
coat  of  the  eye,  etc.,  but  they  seem  to  be  comparatively  uncommon  in  the 
pancreas,  thyroid  body,  the  myocardium,  the  stomach,  the  uterus,  etc. 

Symptoms. — ^The  symptoms  vary  considerably  in  different  cases.  In 
the  one  series  of  cases,  following  a  more  or  less  obvious  tuberculous  focus 
somewhere  in  the  body  (lungs,  lymph  nodes,  testicles,  bones,  joints,  etc.), 
evidences  of  general  involvement  of  the  body  develop — the  so-called 
general,  typhoid,  or  toxic  form;  in  another  series,  the  major  symptoms 
are  referable  to  the  lungs — the  so-called  pulmonary  form;  and  in  still 
another  series,  the  chief  phenomena  are  cerebral — the  so-called  menin- 
geal form;  but  in  most  cases  the  lesions  are  more  or  less  widespread, 
7 


98  BACTERIAL  INFECTIONS 

although  the  predominant  symptoms  may  be  referable  to  one  or 
another  system  of  organs. 

In  cases  without  an  obvious  antecedent  tuberculous  focus  somewhere 
in  the  body,  the  first  noteworthy  symptoms  consist,  as  a  rule,  of  general 
failure  of  the  health,  weakness,  anorexia,  and  fever.  The  fever  may  be 
continuous  in  type,  or  from  time  to  time  remittent. 

In  pulmonary  infection,  the  sudden  development  of  high  tempera- 
ture running  continuously  over  an  extended  period  is  always  suggestive 
of  the  development  of  miliary  tuberculosis.  The  irruption  of  the  in- 
fectious material  into  the  blood  doubtless  marks  the  inception  of  the 
pyretic  condition.  The  temperature  may  reach  104°  or  105°  F. ;  there 
is  usually  a  drop  of  1°  or  2°  in  the  morning  temperature,  but  now  and 
then  this  may  be  reversed,  the  evening  temperature  being  the  lower, 
which  by  some  observers  has  been  held  to  be  diagnostic  of  the  disease. 
Although  the  majority  of  cases  present  fever  of  one  or  another  type,  some 
show  a  continuously  subnormal  temperature;  some  of  these  may  be 
interpreted  as  cases  of  cerebral  infection,  in  consequence  of  which 
depression  of  the  thermogenic  centres  has  taken  place.  On  the  contrary, 
others  show  no  such  involvement,  the  absence  of  fever  seeming  to  be  an 
expression  of  insensibility  of  the  heat-producing  centres. 

Certain  respiratory  symptoms,  such  as  dyspnoea,  cough,  and  cyanosis, 
are  quite  constant.  Dyspnoea  may  be  intense,  especially  in  children,  a 
respiratory  rate  of  75  to  90  per  minute  not  being  unusual.  This  is  pro- 
duced not  infrequently  without  especial  lung  involvement,  in  which  event 
it  has  been  ascribed  to  a  toxic  condition  of  the  respiratory  centres  and  to 
the  development  of  tubercles  on  the  diaphragm.  Miliary  tubercles  in 
the  pulmonary  tissues  may  be  sufficiently  irritating  to  exert  a  pro- 
nounced effect  upon  the  pneumogastric  nerve.  Cheyne-Stokes  breathing 
is  not  infrequently  observed.  Dyspnoea  and  increase  of  pulse  rate  are 
usually  coincident  in  their  development,  but  not  rarely  dyspnoea  has  the 
precedence.  Cough  is  an  important  symptom,  preceding  not  infre- 
quently the  development  of  dyspnoea.  It  is  probably  due  to  the  toxemia, 
as  well  as  to  the  mechanical  effect  of  the  tubercles  in  the  lungs.  It  is 
variable  in  its  intensity,  some  cases  presenting  a  violent  paroxysmal 
cough  which,  when  associated  with  severe  dyspnoea,  simulates  asthma. 
In  the  early  stages  of  the  affection  there  is  little,  if  any,  expectoration, 
but  now  and  then  small  quantities  of  blood  may  appear.  This  rarely  is 
in  such  quantities  as  to  resemble  the  rusty  sputum  of  croupous  pneu- 
monia. In  the  later  stages,  the  expectoration  is  more  abundant  and 
becomes  mucopurulent  in  character.  This  picture  is  somewhat  altered 
when  there  has  been  an  antecedent  chronic  pulmonary  tuberculosis, 
and  the  acute  generalized  condition  is  a  complication.  Under  these 
circumstances  the  dyspnoea  and  cough  usually  have  existed  for  an  ex- 
tended- period,  and  there  is  usually  an  exaggeration  of  the  symptoms 
upon  the  development  of  the  additional  infection.  Cyanosis  may  be 
extreme,  more  so  than  in  most  other  diseases,  and  is  quite  significant  of 


ACUTE  MILIARY   TUBERCULOSIS  99 

miliary  tuberculosis  of  the  lungs  (eliminating  emphysema  and  pneu- 
monia) . 

The  cardiovascular  system  is  more  or  less  affected.  The  heart  action 
becomes  accelerated,  the  sounds  become  weak,  and  passive  congestion 
and  oedema  of  the  dependent  parts  mark  the  later  stages  of  the  disease. 
The  blood  pressure  is  typically  lowered.  The  pulse  is  quickened, 
averaging  120  to  150  beats  per  minute,  and  at  times  is  dicrotic  in  char- 
acter. The  greatest  acceleration  of  pulse  rate  is  seen  in  children,  while 
in  the  aged  it  may  be  below  100  per  minute. 

Anorexia  is  constant,  and  nausea  and  vomiting  are  often  present, 
especially  in  meningeal  infection.  Abdominal  tenderness  and  meteor- 
isra  are  at  times  noted,  especially  in  the  presence  of  peritonitis.  The 
patient  is  usually  constipated,  though  diarrhoea  may  occur  from  time  to 
time,  and  be  associated  with  hemorrhage,  with  or  without  intestinal 
ulceration.  The  amount  of  urine  excreted  is  usually  small,  the  result 
in  part  of  profuse  sweating,  especially  at  night.  In  practically  all  cases 
there  is  a  low-grade  nephritis  which  accounts  for  a  slight  albuminuria. 
Peptonuria  and  excessive  excretion  of  urates  often  accompany  the  disease. 

The  skin  generally  is  pale,  but  in  the  peripheral  portion  of  the  body, 
as  the  fingers  and  toes,  more  or  less,  sometimes  extreme,  cyanosis  is  evi- 
dent. Eruptions  of  several  types  are  sometimes  seen,  such  as  herpes, 
petechise,  miliaria,  sudamina,  etc.  Miliary  tubercles  are  rare  cutaneous 
lesions.  Profuse  sweating  occurs  in  practically  all  cases,  and  is  due  to 
a  toxic  efifect  upon  the  nervous  system.  This  generally  appears  at  night 
and  is  coincident  with  a  fall  of  temperature. 

Certain  nervous  symptoms  are  seen  in  almost  all  cases  of  generalized 
miliary  tuberculosis  without  meningeal  involvement,  such  as  headache, 
vertigo,  hebetude,  and  somnolence;  they  are  referable  to  the  toxemia. 
The  headache  may  be  mild  or  severe,  frontal  or  vertical  in  type.  It  is 
usually  most  marked  during  the  periods  of  increment  of  fever.  Vertigo 
is  usually  not  so  conspicuous  unless  there  is  meningeal  infection.  Hebe- 
tude and  somnolence  are  often  marked  in  the  later  stages.  When 
meningeal  infection  is  present  the  nervous  symptoms  are  intense  and 
tend  to  overshadow  the  general  symptoms,  such  as  cough,  dyspnoea, 
profuse  sweating,  etc.  Convulsions,  paralyses,  vomiting,  painful  con- 
tracture of  the  posterior  cervical  muscles,  strabismus,  contraction  or 
dilatation  of  the  pupils,  and  flexion-contracture  of  the  knee  (Kernig's 
sign)  may  occur.  Delirium,  coma,  and  death  often  terminate  the  condi- 
tion.    Tubercles  may  develop  in  the  choroid  coat,  usually  of  both  eyes. 

Physical  Signs. — The  physical  signs,  as  a  rule,  are  merely  those  of 
bronchitis,  although,  of  course,  in  some  cases  they  are  modified  by  the 
signs  of  antecedent  pulmonary  tuberculosis,  such  as  solidification  or 
cavity  formation.  The  percussion  note  may  be  somewhat  hyperresonant 
— from  infiation  of  the  lungs.  The  breath  sounds  are  harsh  and  the 
expiration  prolonged;  the  rales  may  be  fine  crackling  or  bubbling,  or 
sibilant  and  sonorous;  frictions  may  be  heard  (pleural  tubercles).  In 
the  course  of  time,  a  soft  systolic  murmur  may  become  audible  at  the 


100  BACTERIAL  INFECTIONS 

apex  of  the  heart,  and  the  pulmonary  second  sound  may  become  accen- 
tuated (congestion  of  the  hmgs).  The  liver  and  the  spleen  are  some- 
times moderately  enlarged  from  congestion  and  the  presence  of  tubercles; 
they  are  rarely  tender.  Meteorism,  abdominal  tenderness,  and  rigidity 
are  often  seen  in  involvement  of  the  peritoneum. 

Diagnosis. — The  pulmonary  form  of  miliary  tuberculosis  is  usually 
readily  recognized  from  the  detection  of  an  antecedent  tuberculous 
focus  in  the  lungs  or  elsewhere,  the  presence  of  cough,  dyspnoea,  marked 
cyanosis,  the  physical  signs  of  bronchitis,  and  tubercle  bacilli  in  the 
sputum  (which,  however,  may  be  missed  until  late  in  the  course  of  the 
disease).  Cerebral  symptoms  suggest  meningeal  involvement,  which 
may  be  determined  definitely  by  finding  tubercle  bacilli  and  an  excess 
of  lymphocytes  in  the  cerebrospinal  fluid,  or  by  detecting  choroid  tuber- 
cles. The  general,  toxic,  or  typhoid  form  resembles  and  is  commonly 
mistaken  for  typhoid  fever,  but  its  likelihood  is  suggested  by  absence 
of  the  characteristic  t}^hoid  fever  curve,  of  abdominal  symptoms,  of 
erythematous  rose-spots,  of  leukopenia,  and  of  the  Gruber-Widal  reac- 
tion, and  by  the  presence  of  increased  pulse  rate,  of  dyspnoea,  of  cyanosis, 
of  occasionally  bloody  sputum,  of  choroid  tubercles,  and  of  tubercle 
bacilli  in  the  cerebrospinal  fluid  and  rarely  in  the  blood. 

Prognosis. — ^The  outlook  is  extremely  grave;  so  far  as  is  known  the 
termination  is  invariably  fatal  in  from  a  few  hours  (apparently)  to 
several  weeks  or  several  months.  The  average  duration  of  the  general 
or  typhoid  cases  is  about  four  weeks;  that  of  the  meningeal  cases  some- 
what less. 

Tuberculosis  of  the  Lymphatic  System. 

Lymph  Nodes. — Etiology. — ^Tuberculosis  of  the  lymph  nodes  (scrof- 
ula) is  very  common  in  children,  especially  prior  to  the  tenth  year 
of  age,  and  in  the  female  sex;  but  it  may  occur  in  both  sexes  and  at 
all  ages.  The  process  may  be  widespread  or  circumscribed,  especially 
to  the  cervical,  bronchial,  or  mesenteric  lymph  nodes.  In  the  cervical 
cases  the  infection  occurs  by  way  of  the  tonsils,  carious  teeth,  and  the 
cutaneous  and  mucous  surfaces  of  the  head  and  neck  and  related  cavities 
(nose,  mouth,  pharynx,  larynx,  etc.).  The  bronchial  nodes  are  involved 
in  all  cases  of  pulmonary  infection,  in  adults  as  well  as  in  children;  the 
infection  may  be  bronchogenic,  or,  especially  in  children,  it  may  occur 
by  way  of  the  intestine,  the  bacilli  penetrating  the  mucosa  and  traversing 
without  infecting  the  mesenteric  and  other  abdominal  lymph  nodes. 
Some  writers  maintain  that  in  many  of  these  cases  infection  occurs 
during  intra-uterine  life,  and  that  there  is  a  variable  period  of  latency  or 
quiescence  after  birth.  The  mesenteric  and  retroperitoneal  nodes  may 
become  infected  in  consequence  of  infected  food,  especially  milk  and 
butter;  the  disorder  is  especially  common  in  children  (tabes  mesenterica). 
In  adults  mesenteric  involvement  is  commonly  secondary  to  intestinal 
ulceration. 


TUBERCULOSIS  OP  THE  LYMPHATIC  SYSTEM  101 

Pathology. — The  lesions  consist  of  tubercle  formation,  at  first  gray 
or  miliary  tubercles,  and  later  yellow  or  caseous  tubercles;  or  of  diffuse 
productive  inflammation.  The  diseased  lymph  nodes  vary  in  size  from 
that  of  a  pea  to  that  of  a  walnut  or  thereabout.  Usually  one  node  after 
another  in  a  chain  becomes  diseased.  At  first  they  are  firm  and  flesh-like, 
but  generally,  especially  in  the  neck,  they  undergo  caseation,  softening, 
and  may  discharge  externally.  Like  changes  may  occur  in  other  situa- 
tions. On  the  other  hand,  there  is  some  considerable  tendency  to  spon- 
taneous healing,  although  it  may  be  long  delayed;  but  fibrosis  and  calci- 
fication often  eventually  ensue,  especially  in  the  bronchial  and  mesenteric 
nodes.  In  many  of  these,  notably  the  bronchial  nodes,  the  tuberculous 
process  is  merely  latent  or  quiescent,  and  at  a  favorable  opportunity 
may  serve  as  the  source  of  a  more  or  less  widespread  infection. 

Symptoms. — On  account  of  their  comparatively  superficial  position, 
tuberculosis  of  the  cervical  lymph  nodes  is  readily  recognized.  Node 
after  node,  as  a  rule,  gradually  increases  in  size,  until  the  whole  chain 
may  be  involved.  Usually  there  is  little,  if  any,  pain,  especially  in  the 
early  stages ;  tenderness,  as  a  rule,  is  slight,  but  from  time  to  time  an  acute 
exacerbation  of  the  condition  may  supervene,  and  lead  to  increased 
tenderness,  some  pain,  and  perhaps  redness  of  the  overlying  skin:  this 
is  likely  to  be  associated  with  an  acute  infection  of  the  upper  respira- 
tory tract  (coryza,  laryngitis,  bronchitis).  The  enlarged  lymph  nodes 
manifest  a  marked  tendency  toward  fusion  of  adjacent  nodes,  caseation 
and  softening,  adhesion  with  the  overlying  skin,  and  the  eventual  dis- 
charge externally  of  the  caseous  material;  sinuses  may  persist  for  a  long 
time,  and  may  ultimately  heal  with  more  or  less  disfiguring  scars.  In 
some  cases,  however,  the  nodes  having  reached  the  size  of  a  bean  or 
cherry,  gradually  decrease  in  size  and  become  firm  and  hard ;  the  process 
becomes  quiescent,  arrested,  or  healed.  Tuberculosis  of  the  bronchial 
nodes  may  give  rise  to  no  symptoms;  it  is  an  extraordinarily  common, 
almost  constant,  condition  at  the  necropsy.  Sometimes,  however,  suffi- 
cient enlargement  occurs  to  cause  cough  (which  may  simulate  that  of 
pertussis),  dyspnoea,  secondary  anemia,  and  more  or  less  impairment 
of  the  general  health.  The  superficial  veins  of  the  chest,  neck,  and  head 
may  become  distended  from  interference  with  the  venous  circulation  in 
the  thorax;  there  may  be  relative  dulness  over  and  to  both  sides  of  the 
fifth  and  sixth  vertebrae  (de  la  Camp's  sign)  and  perhaps  tenderness 
in  the  interscapular  region  (Petruschky's  spinalgia);  unilateral  restriction 
of  the  respiratory  excursions  (Grancher's  sign)  may  l)e  present;  and  in 
some  cases  if  the  head  is  strongly  flexed  backward  a  murnnu"  may  be- 
come audible  over  the  sternum  or  in  the  suprasternal  fossa  (Eustace 
Smith's  sign),  supposed  to  result  from  compression  of  the  aorta  by  the 
enlarged  lymph  nodes.  The  axillary  and  inguinal  nodes  present  changes 
analogous  to  those  of  the  cervical.  In  localized  tuberculosis  of  the  lym]>h 
nodes,  constitutional  disturbances  are  commonly  slight,  and  consist  of 
occasional  slight  fever,  increased  pulse-rate,  and  perhaps  some  loss  of 
flesh  and  strength;  in  the  event  of  softening,  secondary  infection,  and 


102  BACTERIAL  INFECTION^ 

generalization  of  the  process,  these  general  manifestations  are  likely  to 
become  marked.  In  involvement  of  the  mesenteric  nodes  (tabes  mes- 
enterica),  loss  of  flesh  and  strength,  secondary  anemia,  and  debility 
usually  become  aggravated;  the  abdomen  commonly  becomes  distended; 
there  may  be  considerable  diarrhoea;  and  the  enlarged  nodes  may  be 
palpable  through  the  abdominal  wall.  In  a  few  cases,  tuberculosis  of 
the  peritoneum  becomes  associated. 

Diagnosis. — Tuberculosis  must  be  distinguished  from  other  forms  of 
enlarged  lymph  nodes,  especially  syphilis,  leukemia,  benign  and  malig- 
nant lymphoma,  and  Hodgkin's  disease. 

Prognosis. — Tuberculosis  of  the  lymph  nodes  is  a  chronic  disorder, 
with  a  general  tendency  toward  spontaneous  recovery — which,  however, 
may  be  delayed  by  softening  and  suppuration.  Death  may  ensue  if  the 
process  becomes  generalized  or  the  general  health  seriously  impaired. 
The  more  or  less  quiescent  processes  common  in  the  bronchial  nodes 
often,  when  the  subject  loses  his  resisting  power,  are  the  source  whence 
pulmonary  and  more  widespread  tuberculosis  takes  its  origin. 

Treatment. — In  addition  to  the  general  measures  to  be  presently  men- 
tioned, enlarged,  but  especially  enlarging  and  softened,  lymph  nodes 
should  be  removed  surgically,  care  being  exercised  not  to  handle  roughly 
or  rupture  the  softened  nodes  and  thus  favor  dissemination  of  the  process 
or  its  local  implantation  in  tissues  unaffected. 

Spleen. — Infection  of  the  spleen  is  usually  hematogenic.  The  common 
lesion  is  the  miliary  or  the  caseous  tubercle,  although,  especially  in  chil- 
dren, larger  caseous  masses  may  develop;  these  may  become  calcified. 
The  organ  becomes  only  slightly  enlarged.  In  chronic  suppurating  tuber- 
culosis (secondary  infections),  especially  of  the  bones,  amyloid  disease 
of  the  spleen  is  likely  to  develop  and  give  rise  to  notable  enlargement 
of  the  organ,  which  may  be  readily  detected  upon  physical  examination. 

Bone  Marrow. — Miliary  tuberculosis  of  the  bone  marrow  occurs  in 
practically  all  cases  of  generalized  miliary  tuberculosis,  and  in  some 
cases  in  which  otherwise  only  the  lungs  appear  to  be  involved.  The 
infection  is  hematogenic.  In  advanced  tuberculosis  of  other  organs,  the 
bone  marrow  is  frequently  soft  and  gelatinous.  The  bone  marrow  may 
also  become  involved  by  extension  of  tuberculosis  of  the  epiphysis  or 
other  parts  of  the  bone,  whereupon  caseous  masses  are  likely  to  develop. 

Serous  Membranes. — Pleura. — Tuberculosis  of  the  pleura  rarely 
perhaps  may  be  primary,  though  this  is  doubtful;  usually  it  is  secondary 
to  disease  of  the  lungs  or  bronchial  lymph  nodes,  or  it  may  follow  dis- 
ease of  the  vertebrae,  pericardium,  peritoneum,  etc.  It  may  occur  in  an 
acute  or  a  chronic  form.  The  acute  cases  are  represented  by  the  majority 
of  the  cases  of  ordinary  serofibrinous  pleuritis  (which  upon  good  evidence 
are  properly  viewed  as  tuberculous,  although  this  may  be  demonstrable 
only  upon  finding  tubercle  bacilli  in  the  exudate,  by  cultural  experiments 
or  animal  inoculations,  or  by  demonstrating  lymphocytosis  of  the  exu- 
date); in  other  cases,  miliary  tubercles  may  be  present — usually  asso- 
ciated with  generalized  miliary  tuberculosis.     In  the  chronic  cases,  the 


TUBERCULOSIS   OF   THE  LYMPHATIC  SYSTEM  103 

pleura  may  be  greatly  thickened  with  fibrous  or  fibrocaseous  tissue;  or 
dense  adhesions  may  bind  together  the  two  serous  surfaces  so  that  the 
pleural  sac  is  obliterated;  or  rarely  large  caseous  masses,  analogous  to 
the  "pearl  disease"  of  cattle,  may  develop.  Rupture  into  the  pleural 
sac  of  a  tuberculous  cavity  and  the  establishment  of  a  communication 
between  the  respiratory  tract  and  the  pleura  is  the  commonest  mode  of 
development  of  pneumothorax  or  pyopneumothorax.  These  conditions 
are  discussed  in  detail  under  diseases  of  the  respiratory  system. 

Pericardium. — Tuberculosis  of  the  pericardium  is  less  common  than 
that  of  other  serous  membranes;  but  it  is  more  common  than  tuberculosis 
of  the  myocardium  or  endocardium.  The  infection  is  usually  lympho- 
genic— from  the  bronchial  lymph  nodes;  but  it  may  be  due  to  extension 
from  the  pleura  or  the  mediastinal  or  other  neighboring  tissues;  and  it 
is  rarely  the  result  of  hemogenic  infection.  The  process  may  appear 
as:  (1)  The  ordinary  serofibrinous  pericarditis,  which  like  the  similar 
process  in  the  pleura  is  usually  tuberculous;  (2)  miliary  tubercles- -due 
to  hemogenic  infection;  (3)  large  caseous  masses — commonly  lympho- 
genic infection;  and  (4)  dense  fibrous  or  fibrocaseous  adhesions 
binding  together  the  two  serous  surfaces  and  more  or  less  completely 
obliterating  the  pericardial  sac.  These  conditions  are  discussed  in  more 
detail  under  diseases  of  the  pericardium. 

Peritoneum. — Cases  of  primary  tuberculosis  of  the  peritoneum  have 
been  reported,  but  it  is  exceedingly  doubtful  if  this  ever  occurs.  The 
process  is  usually  secondary  to  tuberculosis  of  the  pleura,  pericardium, 
mesenteric  nodes,  intestines,  genitalia,  especially  in  the  female  (the 
Fallopian  tubes,  etc.);  and  it  may  be  part  of  a  generalized  miliary  tuber- 
culosis. The  infection  may  occur  by  direct  extension,  by  continuity 
or  contiguity  of  tissue;  or  it  may  be  lymphogenic  or  hemogenic.  The 
lesions  may  consist  of  miliary  tubercles,  of  larger  caseous  masses,  or 
of  adhesions. 

In  the  miliary  type  the  tubercles  are  found  disseminated  more  or  less 
generally  over  the  peritoneum;  they  are  commonly  most  numerous  over 
tlie  intestines,  but  they  may  be  seen  over  the  spleen,  liver,  stomach,  pelvic 
organs,  and  parietal  peritoneum.  Those  miliary  tubercles,  which  are 
found  upon  the  serous  surface  of  intestinal  ulcers  and  not  otherwise  in 
the  peritoneum,  are  commonly  not  considered  as  manifestations  of  tuber- 
culous peritonitis.  A  large  serous  exudate  is  usually  the  characteristic 
feature;  in  some  cases  the  fluid  is  hemorrhagic  in  character.  The 
caseous  or  ulcerative  type  is  a  chronic  condition,  and  may  be  the  result 
of  any  of  the  sources  of  infection  except  the  blood  channels.  In  this  type 
large  cheesy  masses  develop,  a  plastic  exudate  is  thrown  out  and  gives 
rise  to  more  or  less  adhesion  of  the  abdominal  organs.  The  omentum 
shares  in  the  condition,  and  large  caseous  masses  may  develop  therein. 
The  adhesive  type  is  even  more  chronic,  and  is  characterized  by  the 
development  of  dense  fibrous  adhesions  between  the  various  organs. 
There  is  sometimes  an  absence  of  exudate,  whence  the  condition  is  spoken 
of  as  dry  peritonitis;  often  there  are  sacculations  with  more  or  less  fluid. 


104  BACTERIAL  INFECTIONS 

Symptoms. — Miliary  tuberculosis  of  the  peritoneum  presents  the 
usual  symptoms  of  acute  generalized  miliary  tuberculosis,  such  as  fever, 
increased  pulse  and  respiratory  rate,  headache,  loss  of  appetite,  and 
progressive  emaciation.  Certain  localizing  symptoms,  however,  may 
be  observed,  such  as  abdominal  pain  and  tenderness,  distention,  t}Tii- 
panites,  and  ascites.  The  bowels  may  be  constipated  or  loose.  The 
onset  of  symptoms  is  usually  gradual,  though  in  some  cases  it  is  abrupt. 
The  course  is  commonly  not  prolonged  beyond  one  or  two  months.  In 
chronic  caseous  peritonitis  the  onset  is  much  more  gradual.  The  patient 
slowly  fails  in  health,  emaciates,  and  develops  moderate  fever.  After 
a  time  abdominal  pain  is  complained  of  and  tenderness  and  distention 
are  noted.  Nausea  and  vomiting  usually  appear  late  in  the  disease. 
Owing  to  the  wasting  of  the  abdominal  tissues  and  to  the  obstruction 
offered  to  the  circulation  in  the  intra-abdominal  vessels,  the  superficial 
abdominal  veins  become  prominent.  Inflammatory  changes  about  the 
umbilicus  with  a  discharge  of  purulent  or  fecal  matter  may  occur.  Pal- 
pation reveals  a  doughiness  of  the  abdomen,  marked  here  and  there  by 
rather  firm  tumor-like  masses,  which  have  been  found  to  be  made  up  of 
intestinal  coils  and  omentum,  sometimes  enclosing  sacculated  fluid. 
The  course  of  the  disease  may  be  prolonged  over  many  months  and  may 
develop  into  the  adhesive  type.  In  the  caseous  type  there  are  usually 
symptoms  referable  to  infection  of  other  parts  of  the  body,  as,  for  example, 
the  lungs  and  intestines.  In  many  instances  the  adhesive  type  is  second- 
ary to  the  miliary  or  caseous,  but  some  cases  are  doubtless  primary  in 
character.  The  symptoms  are  much  like  those  just  mentioned,  except 
that  there  may  be  no  evidences  of  abdominal  distention  and  ascites;  on 
the  contrary,  the  abdominal  walls  are  likely  to  be  retracted.  Pain 
and  tenderness  are  moderate,  and  constipation  is  usually  marked. 
Tuberculosis  of  the  peritoneum  is  not  infrequently  associated  with  hepatic 
cirrhosis,  which  is  usually  the  primary  condition. 

Diagnosis. — ^The  diagnosis  of  peritoneal  tuberculosis  is  often  difii- 
cult.  In  cases  of  acute  generalized  disease,  which  present  abdominal 
tenderness,  distention,  and  ascites,  the  diagnosis  is  suggested,  though 
not  infrequently  the  condition  has  been  mistaken  for  typhoid  fever;  in 
the  chronic  caseous  and  fibrous  types  the  symptoms  and  physical  signs 
may  lead  to  confusion  with  simple  peritonitis.  The  fever  is  likely  to 
be  more  irregular  in  tuberculosis  than  in  typhoid  fever,  and  it  does  not 
show  the  lysis  which  is  characteristic  of  the  latter  aft'ection.  Abdominal 
tenderness  is  more  commonly  general  in  tuberculosis  of  the  peritoneum, 
while  in  typhoid  fever  it  is  likely  to  be  confined  to  the  cecal  region.  The 
redness  and  induration  of  the  tissues  about  the  umbilicus  with  the  dis- 
charge of  purulent  or  fecal  material  therefrom  is  diagnostic  of  tubercu- 
lous peritonitis.  Palpation  and  percussion  of  the  abdomen  usually 
reveal  masses  of  omental  and  intestinal  tissues.  In  many  instances  it 
may  be  very  difficult  to  difterentiate  the  simple  from  the  tuberculous 
type  of  peritonitis.  Fluid  may  be  withdrawn  from  the  abdomen,  but  it 
usuallv  does  not  show  the  presence  of  tubercle  ])acilli;  but  may  reveal 


TUBERCULOSIS  OF  THE  LYMPHATIC  SYSTEM  105 

lymphocytosis.  Animal  inoculation  of  this  fluid,  however,  may  reveal 
the  character  of  the  disease.  The  detection  of  tuberculous  foci  in  other 
parts  of  the  body  may  be  of  great  assistance  in  the  diagnosis  of  the  peri- 
toneal condition. 

Prognosis. — ^The  prognosis  depends  largely  upon  the  degree  of  infec- 
tion of  other  parts  of  the  body,  as  for  example,  if  the  intestines  and  lungs 
are  markedly  diseased  the  outlook  is  grave.  Aside  from  this,  tuberculosis 
of  the  peritoneum  not  infrequently  becomes  spontaneously  arrested,  its 
specific  character  disappearing  and  dense  fibrous  adhesions  developing. 
Cases  of  miliary  tuberculosis  of  the  peritoneum  are  generally  fatal,  but 
those  of  the  caseous  and  adhesive  types  may  undergo  a  certain  degree  of 
resolution.  The  more  there  is  of  fibrous  tissue  and  the  less  of  caseation 
the  greater  is  the  probability  of  recovery  from  the  immediate  effects  of 
the  disease.  The  development  of  fibrous  adhesions  may  cause  consider- 
able disturbance  in  the  functions  of  the  abdominal  organs;  and  relapses 
are  not  uncommon  in  those  cases,  which  seem  to  be  tending  toward 
recovery.  In  such  an  event  death  not  infrequently  occurs.  Tuberculosis 
of  the  peritoneum  usually  warrants  a  more  favorable  prognosis  than 
tuberculosis  of  the  meninges,  and  oftentimes  of  the  pleura. 

Treatment. — In  addition  to  the  general  measures,  to  be  presently 
mentioned,  operative  procedures  are  often  of  much  service,  although  they 
should  not  be  lightly  undertaken,  since  many  cases  after  the  lapse  of 
several  months  tend  to  spontaneous  recovery.  Recovery  also  sometimes 
follows  repeated  tappings.  Yeo  speaks  highly  of  iodoform,  ^  grain  (0.03 
gram)  in  cod-liver  oil,  2  drams  (8  c.c.)  thrice  daily;  and  inunctions  of 
the  abdomen  twice  daily  with  a  mixture  of  equal  parts  of  iodoform 
ointment  and  cod-liver  oil.  Coeliotomy  with  or  without  peritoneal  irri- 
gation with  physiological  saline  solution  or  mild  antiseptic  solutions,  or 
the  use  of  iodoform  or  other  dusting  powders,  is  much  superior  to  simple 
paracentesis.  Although  the  operation  is  frequently  followed  by  excellent 
results — cure  in  from  one-half  to  three-fourths  of  the  cases — its  mode  of 
action  is  not  definitely  known:  the  access  of  sunlight  and  air,  the  trau- 
matism of  the  operative  manipulations,  the  access  of  fresh  blood  serum 
with  augmented  antitoxic  or  bactericidal  properties  permitted  by  removal 
of  the  peritoneal  fluid,  etc.,  have  been  credited  with  the  curative  properties. 

Tuberculosis  of  Several  Serous  Membranes;  Multiple  Serositis;  Polyor- 
rhomenitis. — The  pleurae,  pericardium,  and  peritoneum  may  be  involved 
concurrently  in  tuberculosis,  the  infection  developing  simultaneously  or 
sequentially  in  two  or  more  of  the  serous  membranes;  and  the  lesions 
may  be  equal  or-  disproportionately  more  marked  in  the  one  than  in  the 
others.  They  may  consist  of  miliary  tubercles,  of  larger  caseous  masses 
with  more  or  less  fluid  exudation,  or  of  fibrous  or  fibrocaseous  thicken- 
ings and  adhesions  with  varying  amounts  of  fluid,  sometimes  very  little, 
sometimes  considerable.  The  condition  is  discussed  in  more  detail  under 
diseases  of  the  peritoneum. 


106  BACTERIAL  INFECTIONS 


Tuberculosis  of  the  Circulatory  System. 

Heart. — Tuberculosis  of  the  myocardium  is  rare;  it  is  always  sec- 
ondary to  a  focus  elsewhere  in  the  body.  Four  forms  are  recognized: 
(1)  Miliary  tubercles,  (2)  large  caseous  tubercles,  (3)  diffuse  tuberculous 
infiltration,  and  (4)  generalized  fibrosis.  The  first  three  types  are  usually 
recognized  grossly,  but  the  fourth  may  be  evident  only  upon  micro- 
scopic examination.  The  heart  muscle  may  be  involved  secondarily 
to  the  pericardium.  The  auricular  and  ventricular  walls  are  involved 
apparently  with  equal  frequency.  The  lesions  of  the  first  type  are 
ascribed  to  blood  infection,  and  the  second  to  dissemination  through  the 
lymphatics.  There  are  no  symptoms  by  which  the  disease  can  be 
diagnosticated;  rapid  and  irregular  heart  action  and  sudden  death  have 
been  noted  in  certain  cases,  but  there  are  no  symptoms  which  may  not 
be  referable  to  simple  myocarditis.  Tuberculosis  of  the  endocardium 
may  appear  as  valvular  vegetations,  miliary  tubercles  over  the  mural 
endocardium,  or  diffuse  sclerosis  of  the  endocardium.  The  affection  is 
rare,  though  somewhat  more  frequent  than  myocardial  tuberculosis. 
It  is  always  associated  with  acute  generalized  miliary  tuberculosis,  and 
the  infection  naturally  reaches  the  parts  through  the  blood  stream. 
Cardiac  thrombi  have  been  found  to  contain  tubercle  bacilli  without 
endocardial  lesions  being  present.  There  are  no  symptoms  diagnostic 
of  the  disease;  if  the  valves  are  affected  a  murmur  may  be  heard,  but 
this  may  be  ascribed  to  a  simple  endocarditis. 

Bloodvessels. — ^The  bloodvessels  are  sometimes  the  seat  of  tuber- 
culosis. The  aorta  is  rarely  involved  as  a  result  of  extension  from  a 
caseous  bronchial  or  mediastinal  lymph  node;  the  pulmonary  veins  may 
contain  tubercles  in  their  walls,  especially  in  pulmonary  tuberculosis; 
and  the  small  arteries  or  veins  or  the  capillaries  throughout  the  body 
may  reveal  miliary  tubercles,  especially  in  miliary  tuberculosis.  Mili- 
ary tuberculosis  itself  is  the  result  of  the  irruption  into  a  bloodvessel  of 
a  tuberculous  focus  somewhere  in  the  body.  In  cavity  formation  in 
the  lung,  larger  or  smaller  vessels  are  not  uncommonly  relatively  un- 
affected, even  after  extensive  disease  of  the  other  pulmonary  tissues;  but 
eventually,  from  primary  involvement  of  the  adventitia,  the  wall  becomes 
weakened,  bulges  (that  is,  a  small  aneurysm  develops),  and  may  finally 
rupture  and  give  rise  to  a  more  or  less  copious  hemorrhage. 

Tuberculosis  of  the  Respiratory  System". 

Nose. — ^Tuberculosis  of  the  nasal  mucous  meml)rane  is  usually 
secondary  to  a  lesion  of  the  lungs  or  larynx,  but  a  primary  focus  may 
be  the  result  of  infection  by  means  of  a  contaminated  hanflkerchief  or 
finger.  The  disease  may  appear  in  one  of  two  forms,  as  an  ulcer  or 
as  a  tumor-like  mass  (tuberculoma).  Both  are  rare  and  practically  of 
equal  frequency.     Lupus  involving  the  face  may  by  continuity  of  struc- 


TUBERCULOSIS  OF  THE  RESPIRATORY  SYSTEM  107 

ture  invade  the  nose.  Aside  from  constitutional  treatment,  such  agents 
may  be  employed  as  are  capable  of  destroying  the  infected  tissues,  the 
curette  and  the  galvanocautery. 

Larynx. — Primary  laryngeal  tuberculosis  is  very  rare;  many  writers 
doubt  its  existence.  Statistics  show  that  it  complicates  pulmonary 
tuberculosis  in  25  to  30  per  cent,  of  the  cases.  It  may  appear  early  in 
the  course  of  the  lung  disease,  but  more  frequently  it  is  seen  at  a  later 
period.  Infection  may  occur  through  the  respiratory  tract,  the  blood, 
or  the  lymph.  If  the  condition  is  primary,  the  infectious  material  has 
found  its  way  to  the  part  through  the  inspired  air.  In  the  majority  of 
cases  of  secondary  laryngeal  infection,  those  attending  pulmonary  dis- 
ease, the  sputum  probably  serves  as  the  infectious  medium.  The  fre- 
quency of  involvement  of  the  posterior  surface  of  the  larynx  suggests  the 
probability  of  sputum  infection,  especially  in  bedridden  patients.  The 
blood  may  be  the  carrier  of  infection  in  cases  of  generalized  miliary 
tuberculosis,  while  the  lymph  may  act  in  a  similar  capacity  when  there 
is  tuberculosis  of  adjacent  structures.  Any  portion  of  the  larynx  may 
become  affected.  Some  statistics  show  that  the  vocal  cords  are  more 
frequently  diseased  than  other  parts;  others  show  that  the  epiglottis  is 
the  commonest  seat.  The  disease  appears  primarily  as  a  miliary  tuber- 
culosis of  the  subepithelial  tissues;  after  a  time  coalescence  of  the  lesions 
occurs  with  more  or  less  erosion  of  the  superficial  structures,  and  ulcera- 
tion results.  These  lesions  usually  have  a  rough,  worm-eaten  appear- 
ance and  are  situated  rather  superficially.  On  the  contrary,  tumor 
masses  (tuberculomas)  may  appear,  and  project  into  the  lumen  of  the 
larynx. 

Symptoms. — The  chief  symptoms  are  hoarseness,  pain,  difficulty  in 
swallowing,  and  cough.  Hoarseness  is  usually  the  earliest  symptom,  and 
gradually  progresses  to  almost  complete  aphonia,  which  develops  in  conse- 
quence of  oedema  or  destruction  of  the  vocal  cords.  Pain,  which  usually 
does  not  appear  until  late  in  the  disease,  may  be  moderate  or  severe, 
spontaneous  or  produced  only  upon  swallowing.  In  the  majority  of 
eases  cough  is  produced  by  the  pulmonary  lesions,  although  irritation  of 
the  laryngeal  nerves  alone  may  incite  cough. 

Diagnosis. — The  diagnosis  is  readily  made  in  most  cases  by  a  direct 
examination  of  the  parts;  but  syphilitic  and  malignant  ulceration  must 
be  excluded.  The  worm-eaten  and  superficial  character  of  the  ulcers 
and  the  pallor  of  the  tissues  are  characteristic  of  tuberculosis;  in  syphilis 
the  destruction  of  the  part  is  much  more  rapid,  there  are  evidences  of 
inflammation  in  the  surrounding  tissues,  and  the  ulceration,  which  is 
usually  solitary,  is  likely  to  be  deep.  Malignancy  characteristically 
appears  later  in  life  than  does  tuberculosis  and  syphilis;  the  lesions  are 
primarily  unilateral  in  position;  and  marked  oedema  and  inflammatory 
changes  about  the  ulcer  are  usually  found. 

Prognosis. — The  prognosis  depends  upon  the  extent  of  laryngeal  and 
pulmonary  involvement.  A  larger  percentage  of  cures  is  now  effected 
than  formerly,  owing  to  perfected  methods  of  local  treatment. 


108  BACTERIAL  INFECTIONS 

Treatment. — Constitutional  as  well  as  local  measures  are  important 
in  the  treatment  of  this  condition.  Much  can  be  done  for  the  early 
cases  of  laryngeal  disease,  but  in  those  in  which  extensive  destruction  of 
the  tissues  has  occurred  nothing  but  a  fatal  issue  is  to  be  expected. 
Subjects  who  experience  severe  pains  upon  swallowing  die  not  infre- 
quently of  inanition.  The  most  efficient  treatment  is  that  of  tubercu- 
losis in  general  (to  be  presently  mentioned)  and  the  judicious  admin- 
istration of  such  drugs  as  strychnine,  nux  vomica,  pepsin,  creosote, 
and  ammonium  chloride,  etc.  Creosote  is  of  value  if  mixed  infec- 
tion is  present  in  the  lungs  (shown  by  cavitation  and  free  expecto- 
ration of  purulent  material).  Ammonium  chloride  (by  its  stimulating 
properties)  is  of  service  in  order  to  alleviate  the  marked  dryness  of 
the  mucous  membrane.  The  local  treatment  should  consist  of  the 
application  of  lactic  acid,  in  a  20  to  80  per  cent,  solution,  to  the  ulcers. 
Methylene  blue  in  2  to  4  per  cent,  solution,  or  the  colloidal  silver 
salts  in  20  to  30  per  cent,  solution,  may  be  effective.  The  curette  may 
also  be  of  service.  If  the  condition  is  far  advanced  and  the  patient 
suffers  to  a  marked  degree,  sedative  applications  may  be  employed,  such 
as  cocaine,  boric  acid,  morphine,  iodoform,  orthoform  lozenges,  etc. 

Trachea  and  Bronchi.— Tuberculous  ulceration  of  the  trachea 
and  bronchi  is  not  infrequently  seen  in  cases  of  pulmonary  and  laryn- 
geal infection.  The  ulcers  are  usually  small  and  multiple.  The  bron- 
chial lesions  are  more  frequently  seen  in  the  chronic  than  in  the  acute 
form  of  pulmonary  tuberculosis.  The  ulcers  resemble  those  of  the 
larynx  in  being  rather  superficial  and  worm-eaten  in  appearance.  Infec- 
tion in  most  cases  is  aerogenous  or  bronchogenic  in  character. 

Lungs. — Etiology. — ^Pulmonary  tuberculosis  is  the  commonest  mani- 
festation of  the  disease.  Two  pathways  of  infection  are  postulated: 
the  respiratory  and  the  alimentary;  but  the  former  is  the  more  generally 
accepted.  The  respiratory  or  aerogenous  theory  presupposes  the  aspira- 
tion of  infectious  material  into  the  .lower  respiratory  tract,  where  it 
becomes  deposited  upon  the  mucous  surfaces.  Direct  penetration  of  the 
bacilli  to  the  alveoli  is  questionable;  it  seems  probable  that  they  find 
lodgment  upon  the  mucosa  of  the  small  bronchi  and  bronchioles, 
whence  they  are  carried  either  by  the  lymph  or  by  phagocytes  through 
the  mucous  membrane  to  the  peribronchial  lymph  spaces  in  which  the 
primary  tubercles  develop.  From  these  areas  dissemination  occurs  to 
other  parts  of  the  lungs.  The  alimentary  theory  presupposes  that  the 
ingestion  of  infectious  material  is  followed  by  the  penetration  of  the 
intestinal  walls  by  the  tubercle  bacilli  and  by  their  convection  to  the 
mesenteric  nodes;  thence  they  pass  to  the  lungs  by  way  of  the  thoracic 
duct,  the  left  subclavian  vein,  the  superior  vena  cava,  the  heart,  and  the 
pulmonary  artery;  capillary  embolism  occurs  in  the  lungs  and  miliary 
tubercles  develop.  The  majority  of  cases  of  pulmonary  tuberculosis 
is  due  to  respiratory  infection,  but  a  certain  number  may  be  the  result 
of  alimentary  infection,  especially  in  children,  to  whom  milk  may  be  a 
frequent  carrier  of  the  bacilli.    The  most  important  source  of  pulmonary 


TUBERCULOSIS  OF  THE  RESPIRATORY  SYSTEM  109 

tuberculosis  is  the  inhalation  of  tubercle  bacilli  brought  about  by  the 
inspissation  and  pulverization  of  sputum  from  a  tuberculous  patient. 

Pathology. — Tuberculosis  of  the  lungs  may  develop  in  one  of  four 
forms:  (1)  Acute  miliary  tuberculosis  (which  has  already  been  dis- 
cussed); (2)  acute  pneumonic  tuberculosis;  (3)  chronic  ulcerative  tuber- 
culosis; and  (4)  chronic  fibroid  tuberculosis. 

Acute  Pneumoxic  Tuberculosis. — Acute  pneumonic  tuberculosis 
occurs  in  two  subtypes — the  so-called  pneumonic  and  the  bronchopneu- 
monic.  The  so-called  pneumonic  form  is  most  common  in  adults,  and 
usually  involves  a  lobe  or  an  entire  lung.  In  general  the  appearances 
are  much  like  those  of  pneumococcic  infection  of  the  lung  (croupous 
pneumonia);  but  in  the  early  stages  there  is  more  fluid  exudation  that 
gives  rise  to  a  peculiar  gelatinous  appearance,  and  there  is  likely  to  be 
less  fibrinous  exudation  and  more  desquamative  changes.  Definite 
tubercle  formation  may  or  may  not  be  present;  in  some  cases  the  entire 
exudation  consists  of  the  ordinary  inflammatory  products  with  marked 
proliferation  of  the  alveolar  epithelium,  all  of  which  proceeds  soon  to 
extensive  caseation  and  softening;  in  other  cases,  amidst  the  widespread 
caseation  tubercles  also  may  be  found.  The  bronchopneumonic  form 
is  most  common  in  children  and  young  adults.  The  lesions  consist  of 
reddish,  later  grayish  or  yellowish  foci  of  bronchopneumonia,  which  by 
fusion  may  lead  to  involvement  of  almost  if  not  quite  all  of  a  lobe  or  an 
entire  lung.  There  is  a  marked  disposition  to  caseation,  and,  if  the 
patient  survives  long  enough,  to  excavation. 

Chronic  Ulcerative  Tuberculosis.— In  advanced  cases  the  lesions 
are  quite  diversified,  consisting  of  gray  and  yellow  tubercles,  foci  of 
bronchopneumonia,  diffuse  tuberculous  infiltration  with  caseation, 
excavations,  fibrous  changes  in  the  lung  and  pleura,  etc.  The  disease 
begins  with  the  development  of  gray  tubercles,  most  commonly  in 
the  apex  of  the  upper  lobe  (most  frequently  the  right),  about  an  inch 
to  an  inch  and  a  half  below  the  extreme  limit  of  the  lung;  that  is,  about 
the  distribution  of  the  posterior  apical  bronchus.  This  has  been  attrib- 
uted to  inefficient  expansion  of  this  region  owing  to  the  proximity  of  the 
clavicle  and  to  a  relatively  poor  blood  supply.  The  process  may  also 
begin  in  the  apex  of  the  lower  lobe  (about  an  inch  below  its  uppermost 
limit,  corresponding  to  the  fifth  thoracic  vertebral  spine).  Wherever  the 
tubercles  first  develop,  they  tend  to  progress  downward;  but  in  some 
cases  the  primary  lesions  are  low  down,  at  the  base  of  one  or  the  other 
lung.  When  advanced  there  may  be  few  or  many  tubercles — of  both  the 
gray  and  the  yellow  variety;  and  they  may  be  confined  to  a  small  section 
of  one  lobe,  or  they  may  be  scattered  throughout  an  entire  lung  or  both 
lungs.  In  cases  of  rather  rapid  coiu'se,  about  a  more  or  less  obviously 
primary  focus  there  maybe  many  young  tubercles,  with  comparatively  little 
caseation :  the  patient  has  been  overwhelmed  by  the  toxemia.  In  more 
chronic  cases  conglomerate  tubercles  form,  and  eventually  undergoing 
caseation  and  softening  and  leading  to  ulceration  of  the  wall  of  a  bronchus, 
discharge  their  softened  contents  externally;  a  so-called  cavity  results. 


110  BACTERIAL  INFECTIONS 

These  cavities  are  most  common  in  or  near  the  apex  (the  seat  of  the  oldest 
lesions);  they  vary  much  in  size  and  in  number,  and  they  are  usually 
surrounded  by  more  or  less  fibrosis,  which  surrounds  also  the  adjacent 
bronchi.  These  destructive  changes  are  commonly  due  to  the  associa- 
tion of  pyogenic  cocci  with  the  tubercle  bacilli;  that  is,  they  are  evidences 
of  mixed  infection.  In  some  cases  there  is  more  or  less  fibrosis  aside 
from  that  about  cavities ;  this  fibrosis  may  partly  or  completely  enclose  a 
tuberculous  focus,  isolating  it  from  the  remainder  of  the  lung;  in  other 
cases  strands  of  fibrous  tissue  pervade  and  may  ultimately  replace  the 
tuberculous  focus — the  process  has  become  healed. 

Chronic  Fibroid  Tuberculosis. — In  addition  to  the  aforementioned 
fibrosis  about  a  tuberculous  focus,  more  or  less  extensive  fibrosis  may 
occur  concurrently  with  an  active  tuberculosis — of  the  chronic  ulcerative 
or  chronic  bronchopneumonic  type;  or  it  may  occur  in  association  with 
chronic  pleural  adhesions.  The  fibrosis  may  be  so  extensive  as  almost 
if  not  quite  completely  to  replace  the  pulmonary  tissue  of  an  entire  lobe 
or  more;  there  may  be  cavity  formation;  and  there  is  usually  dilatation 
of  the  smaller  and  medium-sized  bronchi  (bronchiectasis).  In  all  cases 
of  tuberculosis  of  the  hmg,  of  whatever  variety,  pleural  adhesions  are  the 
rule;  empyema  is  cjuite  common;  and  from  rupture  of  a  tuberculous  cavity 
into  the  pleura  pyopneumothorax  may  develop. 

Symptoms. — ^Acute  Pneumonic  Tuberculosis. — In  the  adult  the 
onset  is  often  quite  like  that  of  ordinary  croupous  pneumonia ;  the  physi- 
cal signs  are  those  of  solidification  of  a  lobe  or  an  entire  lung;  and  the 
course  of  the  disorder  is  not  notably  different  from  that  commonly  seen 
in  pneumococcic  infection  of  the  lung.  Suspicion  of  the  real  nature  of  the 
disorder  commonly  is  not  entertained  until  the  expected  crisis  fails  to 
occur.  The  tuberculous  nature  of  the  infection,  however,  is  sometimes 
suggested  by  antecedent  ill  health  of  the  patient,  an  ill-explained  cough 
lasting  for  several  months,  a  more  or  less  well-defined  tuberculous  lesion 
in  the  lung,  bloody  rather  than  rusty  sputum,  sweating,  emaciation, 
remittent  rather  than  continuous  fever,  slight  leukocytosis,  and  later  the 
detection  of  tubercle  bacilli  in  the  sputum.  The  bronchopneumonic 
type  sometimes  develops  in  a  person  previously  well,  but  it  is  most 
likely  to  occur  in  subjects  in  general  ill  health,  or  in  children  after  measles, 
pertussis,  and  other  infections.  The  symptoms  and  physical  signs,  in 
the  beginning  at  least,  are  quite  like  those  of  bronchopneumonia  develop- 
ing under  other  circumstances  and  due  to  other  microorganisms;  but  at  the 
end  of  ten  days  or  two  weeks  the  patient,  especially  if  a  child,  seems  to 
fail  markedly  in  general  health,  to  become  emaciated,  to  develop  chills, 
sweats,  and  hectic  fever,  and,  if  he  does  not  die  soon,  gradually  presents 
the  common  manifestations  of  chronic  ulcerative  tuberculosis. 

Chronic  Ulcerative  Tuberculosis. — This,  the  common  type  of 
tuberculosis  of  the  lungs,  may  reveal  itself  at  the  onset  in  a  variety  of 
ways.  The  first  symptoms  may  be  those  of  general  ill  health,  with  loss 
of  appetite  and  of  weight,  without  localizing  symptoms;  or  those  of 
anemia,  especially  common  in   young  girls,  and  usually  mistaken  for 


TUBERCULOSIS  OF  THE  RESPIRATORY  SYSTEM  111 

chlorosis;  or  those  of  bronchitis    (a   "cold"   that  does   not  get  well), 
laryngitis,  pleuritis,  hemoptysis,  fistula  in  ano,  etc. 

The  classical  symptom  of  pulmonary  tuberculosis  is  cough,  although 
in  a  few  cases  it  is  absent  until  an  advanced  stage  of  the  disease.  In 
many  cases  it  is  the  first  symptom  that  calls  attention  to  the  pulmonary 
condition.  It  may  be  severe  and  very  harassing  to  the  patient,  but,  on 
the  contrary,  it  is  often  mild  and  disturbs  the  patient  only  upon  arising 
in  the  morning.  In  the  beginning  the  cough  is  dry,  but  as  bronchial 
irritation  increases  and  disintegration  of  the  pulmonary  tissues  develops, 
sputum  appears.  At  first  this  is  mucoid  in  character,  but  when  second- 
ary infection  by  pyococci  takes  place  it  becomes  mucopurulent.  In  an 
advanced  stage,  the  sputum  often  contains  small,  hard,  coin-like  masses, 
by  which  it  is  designated  as  "nummular"  in  character.  Elastic  tissue 
evidencing  the  destruction  of  the  lung  is  often  found,  not  only  in  these 
masses,  but  also  free  in  the  sputum.  Except  in  the  earliest  stage  tubercle 
bacilli  also  are  found;  to  these  late  in  the  disease  other  microorganisms  are 
added,  chiefly  staphylococci,  streptococci,  pneumococci,  and  Micrococcus 
tetragenus.  Early  in  the  disease  the  sputum  usually  contains  more  or 
less  bronchial  and  alveolar  epithelium,  the  latter  having  been  held  at 
one  time  to  be  diagnostic  of  the  disease.  AVhen  a  mixed  infection  is 
present  pus  cells  are  found. 

Hemoptysis  not  infrequently  is  the  first  manifestation.  Usually  only 
a  moderate  amount  of  blood  is  lost,  and  this  is  ascribed  to  pulmonary 
congestion.  In  some  cases  small,  frequently  repeated  hemoptyses 
occur  during  the  course  of  the  disease,  and  for  several  days  following 
such  manifestations  the  sputum  is  blood-streaked.  Later  in  such  cases 
larger  hemoptyses  may  ensue,  but  they  rarely  lead  directly  to  death. 
In  the  latter  stages  the  blood  is  derived  from  eroded  bloodvessels  adja- 
cent to  or  within  cavities.  There  is  a  surprisingly  large  number  of  cases 
in  which  no  hemorrhage  occurs  at  any  time,  not  even  when  large  cavities 
are  present. 

Loss  of  weight  is  an  important  early  sign,  and  in  many  instances 
precedes  the  development  of  cough,  expectoration,  and  hemoptysis. 
If  it  be  associated  with  a  slight  rise  of  temperature  in  the  afternoon 
or  early  evening,  suspicions  should  be  immediately  aroused  as  to  its 
tuberculous  basis.  The  association  of  these  two  symptoms  is  of  vital 
importance  in  the  diagnosis  of  the  disease.  In  the  very  earliest  stage 
the  temperature  may  be  subnormal;  but  usually  when  the  patient 
comes  under  observation,  there  is  a  little  fever,  amounting  usually  to 
1°  or  1.5°  F.,  and  the  temperature  is  likely  to  be  very  unstable.  As 
the  disease  advances  the  temperature  increases,  so  that  finally  it  becomes 
typically  hectic  in  character,  the  morning  temperature  being  subnormal 
and  the  afternoon  temperature  (3  to  6  p.m.  or  thereabout)  reaching 
103°  to  104°  F.  (Fig.  3).  The  highest  temperatures  are  seen  in  acute 
pulmonary  involvement;  the  development  of  an  acute  ])neumonic  process 
in  the  chronic  form  of  tuberculosis  adds  materially  to  the  temperature. 
The  fever  is  referable  to  the  toxemia.     The  pulse  rate  is  also  increased, 


112 


BACTERIAL  INFECTIONS 


even  in  an  early  stage;  later  it  is  usually  increased  proportionately  with 
the  temperature,  and  it  is  characteristically  of  low  tension  and  of  small 
volume.  The  respiratory  rate  is  increased,  and  dyspnoea  may  be  noted 
early  in  the  disease.  As  the  disease  advances,  coincidently  with  the 
development  of  cavities,  the  dyspnoea  may  become  marked.  This,  how- 
ever, is  not  always  dependent  upon  the  amount  of  lung  involvement, 
since  in  early  cases  there  may  be  marked  dyspnoea,  due  doubtless  to  a 
toxic  injfluence  on  the  respiratory  centre.  On  the  contrary,  in  some 
advanced  cases  there  is  remarkably  little  dyspnoea. 


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Intermitting,  hectic  fever  in  pulmonary  tuberculosis.      (Musser.) 


Practically  all  patients  complain  at  one  time  or  another  of  thoracic 
pains.  In  many  these  develop  early,  and  they  may  be  unilateral  or 
bilateral  in  distribution.  They  may  be  a  symptom  of  pleurisy  or  inter- 
costal neuralgia,  and  do  not  necessarily  appear  upon  the  same  side  of  the 
chest  as  the  lesion.  Sometimes  the  pains  are  out  of  all  proportion  to  the 
extent  of  pulmonary  or  pleural  involvement.  They  are  sharp  or  stitch- 
like in  character  and  are  intensified  usually  by  deep  breathing  and  cough- 
ing. They  may  be  felt  in  any  part  of  the  chest,  but  the  points  of  predi- 
lection are  about  the  nipples,  in  the  axillae,  and  near  the  angles  of  the 
scapulae.  Tendreness  of  the  thorax  is  not  an  infrequent  symptom,  and 
it  seems  to  be  independent  of  pleuritic  conditions.  However,  many  cases 
show  tenderness  over  the  pulmonary  lesion.  The  overlying  intercostal 
muscles  may  be  quite  rigid  and  contracted. 

Night  sweats  are  characteristic,  especially  in  the  advanced  stage  of  the 
chronic  form  and  throughout  the  course  of  the  acute  form.  The  sweats 
may  be  moderate  or  severe,  the  latter  being  more  frequently  seen 
in  the  acute  type  of  the  disease.  They  are  probably  the  result  of  a 
depressant  action  of  mixed  toxins  (tuberculous  and  pyococcic)  upon 
the  vasomotor  system. 

Loss  of  appetite  may  be  noted  early;  but  in  some  cases  the  patients  do 


TUBERCULOSIS  OF  THE  RESPIRATORY  SYSTEM  113 

not  present  this  symptom  until  the  disease  is  far  advanced.  Vomiting 
is  a  distressing  symptom  manifested  in  some  cases  and  has  no  connection 
apparently  with  gastric  disease,  but  rather  with  the  cough.  It  is  seen 
more  frequently  in  the  morning  than  at  any  other  time  of  the  day,  and  is 
induced  by  severe  attacks  of  coughing  which  not  infrequently  follow 
breakfast.  It  usually  attends  cavity  formation.  There  is  no  constant 
symptom  referable  to  the  intestinal  tract,  though  the  majority  of  patients 
are  constipated.  If  a  persistent  diarrhoea  is  present,  tuberculosis  of  the 
intestines  may  be  suspected.  Often  the  stools  give  evidence  of  deficient 
biliary  secretion.  From  time  to  time  the  patient  complains  of  abdominal 
pains,  which  are  often  referable  to  constipation  and  biliousness.  As  the 
disease  advances  some  subjects  show  a  decreased  elimination  of  urine 
owing  to  nephritis,  which  is  likely  to  develop  sooner  or  later.  Hoarse- 
ness not  infrequently  appears  in  the  bedridden  patient  in  consequence 
of  a  terminal  laryngeal  infection ;  in  a  few  cases  the  distressing  symptoms 
of  laryngitis  develop  at  an  earlier  period.  From  time  to  time,  even  from 
the  earliest  stage  of  the  disease,  headache  is  complained  of,  and  is  due 
doubtless  to  the  toxic  condition  of  the  brain  centres  or  to  defective 
excretion,  or  both.  Coincidently  with  the  development  of  these  symptoms 
the  patient  gradually  loses  in  strength  and  weight;  in  the  very  chronic 
cases  extreme  emaciation  is  seen,  and  is  associated  with  a  hectic  flush 
of  the  cheeks,  hollow^  s'taring  eyes,  etc. 

In  those  patients  in  whom  tuberculosis  has  assumed  a  very  chronic 
form  incurvation  of  the  nails  and  clubbing  of  the  fingers  and  sometimes 
of  the  toes  develop.  These  require  considerable  time  for  their  develop- 
ment, and  are  probably  dependent  upon  a  toxic  influence  and  peripheral 
passive  congestion.  Such  extremities  are  always  cyanosed  and  cold,  as 
a  result  of  defective  circulation. 

Physical  Signs. — In  advanced  cases  the  disease  may  be  disclosed 
by  a  long,  narrow,  and  flat  chest,  with  an  acute  epigastric  angle,  and 
protruding  scapulae  (alar  or  winged  chest).  In  many  cases,  however, 
these  signs  are  absent  for  a  long  time.  The  earliest  physical  signs  con- 
sist of  deficient  expansion,  lagging  behind  or  depression,  of  one  apex 
(usually  the  right)  anteriorly  or  posteriorly;  increased  tactile  and  vocal 
fremitus;  impaired  percussion  resonance  (sometimes  for  a  time  masked 
by  compensatory  inflation  or  emphysema  of  the  surrounding  portion 
of  the  lung,  which  then  yields  a  vesiculotympanitic  note);  and  weak  or 
harsh,  vesicular  breath  sounds  with  prolongation  of  the  expiration.  In 
the  early  stages  it  is  often  difficult  to  determine  whether  these  signs  are 
more  pronounced  that  the  normal  differences  between  the  two  apices. 
Soon,  however,  fine  crackling  and  perhaps  fine  bubbling  rales  become 
apparent;  and  the  breath  sounds  may  take  on  the  so-called  cogwheel 
character  (which  occurs  also  in  other  conditions).  As  the  disease  ad- 
vances (the  infiltration  of  the  lung  increases)  these  signs  become  more 
marked  and  extend  over  a  wider  area,  and  very  commonly  they  develop 
at  the  other  apex,  or  in  the  apex  of  one  of  the  lower  lobes.  The  percussion 
note  becomes  actually  dull,  and  tactile  and  vocal  fremitus  much  exag- 


114  BACTERIAL  INFECTIONS 

gerated,  the  breath  sounds  bronchovesicular  or  bronchial,  the  rales  much 
more  numerous,  and  to  those  previously  present  coarser  bubbling 
(bronchitic)  rales  are  added.  Pleural  frictions  also  are  frequently 
audible,  but  it  is  often  almost  impossible  to  distinguish  them  from 
rales,  especially  when  rales  are  numerous.  Over  an  area  of  excavation 
(cavity  formation)  the  tactile  and  vocal  fremitus  may  be  much  increased 
unless  the  overlying  pleura  is  much  thickened;  bronchophony  and  pecto- 
riloquy are  likely  to  be  elicited;  the  percussion  note  is  vesiculotympanitic 
or  distinctly  tympanitic,  and  the  so-called  cracked-pot  sound  may  be 
elicited,  if  the  cavity  is  near  the  surface,  is  of  fair  size  (about  two  inches 
or  more  in  diameter),  has  thin  resilient  walls,  and  communicates  with  an 
open  bronchus.  The  occurrence  of  tympany  over  a  previously  dull  area 
following  the  evacuation  of  considerable  sputum  is  quite  significant  of  a 
cavity,  but  other  changes  in  the  percussion  note  may  occur,  although  they 
are  inconstant  and  of  minor  diagnostic  importance:  such  as,  variations 
in  the  note,  depending  upon  whether  the  patient  is  in  the  upright  or  the 
recumbent  position  (Gerhardt's  sign),  which  occurs  over  cavities  of 
unequal  axes,  partly  filled  with  fluid,  and  communicating  with  an  open 
bronchus;  a  louder  and  higher  pitched  tympanitic  note  when  the  patient's 
mouth  is  open  as  contrasted  with  the  note  elicited  when  the  mouth  is 
closed  (Wintrich's  sign);  inspiratory  increase  and  expiratory  decrease  in 
the  loudness  and  pitch  of  the  note  (Friedreich's  sign);  the  breath  sounds 
become  bronchial,  cavernous,  or  amphoric  in  character;  and  coarse 
bubbling  or  gurgling,  sometimes  resonant,  rales  may  be  heard.  Myotatic 
irritability  (myoidoema)  is  quite  common  in  advanced  cases.  Over  the 
diseased  area  the  intercostal  muscles  may  be  rigid ;  and  there  may  be  local 
tenderness,  due  sometimes  to  localized  pleuritis,  sometimes  perhaps 
to  toxic  influences  on  the  nerves.  Percussion  over  an  area  of  excavation, 
especially  in  the  subclavicular  region,  may  lead  to  immediate  cough  and 
expectoration  (Erni's  tapotage  sign).  A  systolic  murmur  is  often  audi- 
ble over  the  subclavian  artery,  and  is  referable  to  pleural  adhesions, 
compressing  or  distorting  the  artery.  Early  in  the  course  of  the  disease 
the  heart  usually  reveals  no  abnormality,  aside  from  accentuation  of  the 
pulmonary  second  sound,  the  result  of  congestion  of  the  lungs;  later  a 
functional  systolic  murmur  commonly  develops,  and  a  systolic  murmur  of 
relative  mitral  insufficiency — from  dilatation;  and  the  area  of  cardiac 
dulness  may  become  increased — which,  however,  is  due  to  retraction  of 
the  borders  of  the  lungs  (especially  the  left)  rather  than  to  enlargement 
of  the  heart.  Cardiopulmonary  murmurs  also  are  common.  The  liver 
and  perhaps  the  spleen  may  be  enlarged — the  liver  from  fatty  infiltration; 
both  organs  from  tuberculosis  or  amyloid  disease. 

Chronic  Fibroid  Tuberculosis. — The  chief  symptoms  consist  of 
cough,  mucopurulent  expectoration,  and  dyspnoea;  the  sputum  may  be 
fetid  in  the  event  of  bronchiectasis — which  is  common.  Recurring  attacks 
of  hemoptysis  are  rather  frequent :  I  have  seen  a  subject  in  whom  these 
occurred  over  a  period  of  more  than  twenty  years,  with  maintenance 
of  good  general  health,  the  weight  being  about  or  nearly  two  hundred 


TUBERCULOSIS  OF  THE  RESPIRATORY  SYSTEM  115 

pounds.  From  time  to  time  there  may  be  attacks  of  more  or  less  fever. 
The  physical  signs  are  those  of  chronic  interstitial  pneumonitis:  distor- 
tion and  insinking  of  the  chest,  with  uncovering  and  perhaps  displace- 
ment of  the  heart;  and  over  the  affected  area  dulness  on  percussion,  in- 
creased tactile  and  vocal  fremitus  (except  in  the  event  of  pleural  adhesions 
which  are  rather  common),  bronchovesicular  or  bronchial  breath  sounds, 
and  fine  or  coarse  bubbling  rales. 

Diagnosis. — Acute  pneumonic  tuberculosis,  since  it  resembles  ordinary 
croupous  pneumonia  in  its  mode  of  onset  and  its  course,  is  commonly 
not  recognized  until  the  expected  crisis  does  not  occur;  but  certain  of 
the  aberrant  phenomena  already  mentioned  may  excite  suspicion  of  the 
tuberculous  nature  of  the  infection  and  sometimes  lead  the  observing 
physician  to  an  early  diagnosis.  Chronic  ulcerative  tuberculosis  is  dis- 
closed by  any  of  the  aforementioned  early  symptoms,  especially  slight 
or  progressive  loss  of  weight;  early  subnormal  temperature,  but  rather 
soon  slight  afternoon  fever;  rapid  and  unstable  pulse;  cough  with  or 
without  slight  expectoration;  even  slight  hemoptysis;  and  the  physical 
signs  of  beginning  infiltration  of  the  lung — usually  one  apex.  One  should 
endeavor  to  make  the  diagnosis  before  tubercle  bacilli  appear  in  the 
sputum;  their  detection  as  well  as  the  presence  of  elastic  fibers  makes 
the  diagnosis  conclusive.  In  the  event  of  doubt  recourse  may  be  had  to 
one  of  the  several  tuberculin  tests  (page  125).  Radiographic  examination 
often  enables  one  to  detect  a  tuberculous  focus  in  the  lung  otherwise 
insusceptible  of  recognition.  In  the  differential  diagnosis  one  must 
exclude  syphilis,  actinomycosis,  streptothricosis,  and  malignant  disease 
of  the  lungs.  Syphilis  of  the  lung  is  rare,  and  the  diagnosis  can  seldom 
be  made  with  certainty;  the  disorder  may  be  suspected  upon  the  develop- 
ment in  a  known  syphilitic  subject  of  the  physical  signs  of  chronic  inter- 
stitial pneumonitis,  with  perhaps  bronchiectasis  of  the  lower  lobe,  and 
the  absence  from  the  sputum  of  tubercle  bacilli;  but  one  must  remember 
that  tuberculosis  of  the  lungs  may  occur  in  a  syphilitic  subject  and  that 
tubercle  bacilli  may  not  be  found  for  some  time;  a  positive  Wassermann 
reaction  may  be  of  some  assistance.  Actinomycosis  and  streptothrical 
infections  are  recognizable  by  the  detection  in  the  sputum  of  the  specific 
infectious  agent.  In  malignant  disease  there  is  usually  little  if  an}-  fever; 
the  physical  signs  are  those  of  irregular  solidification — in  one,  sometimes 
in  both,  lungs;  secondary  anemia  and  cachexia  soon  supervene;  the  spu- 
tum is  often  blood-tinged  or  it  may  be  distinctly  bloody,  and  may  reveal 
tumor  cells,  but  no  tubercle  bacilli.  Chronic  fibroid  tuberculosis  is 
readily  recognized  by  the  physical  signs  of  chronic  interstitial  pneu- 
monitis and  the  presence  of  tubercle  bacilli  in  the  sputum. 

Prognosis. — Acute  pneumonic  tuberculosis  usually  leads  to  death  in 
from  four  to  eight  weeks;  rarely  the  progress  of  the  disorder  becomes 
somewhat  stayed,  and  the  process  may  become  chronic,  but  a  fatal 
termination  seems  inevitable.  Death  in  some  of  the  chronic  forms  of 
pulmonary  tuberculosis  may  be  finally  induced  by  the  acute  pneumonic 
or  bronchopneumonic  process.     In  chronic  ulcerative  tuberculosis  the 


116  BACTERIAL  INFECTIONS 

prognosis  depends  upon  the  extent  of  the  process  when  detected,  the 
resistance  of  the  individual,  his  occupation  and  other  social  environment, 
the  ability  or  lack  of  ability  to  place  himself  under  the  best  hygienic, 
medical,  and  other  conditions,  etc.  A  poor  general  condition,  poverty, 
inappropriate  and  insufficient  food,  exliausting  work,  mental  cares  and 
anxiety,  etc.,  are  potent  deterrents  of  recovery.  In  incipient  and  even 
moderately  advanced  cases,  under  favorable  circumstances  and  the  best 
hygienic  surroundings,  the  outlook  is  good,  if  not  for  recovery,  at  least 
for  comparative  comfort  and  prolongation  of  life.  Chronic  fibroid 
tuberculosis  may  be  a  fortunate  outcome  of  the  chronic  ulcerative  process, 
but  whether  developing  thus  or  otherwise,  it  may  last  for  many  (twenty 
or  more)  years. 

Classification. — The  American  Sanatorium  Association,  approving  a 
committee  report,  suggests  the  use  of  the  following  classification  of 
patients  upon  admission  and  discharge  and  for  ultimate  results;  the 
classification  is  equally  applicable  in  private  practice : 

1.  On  x4lD mission. — ^These  definitions  indicate  the  furthest  extent 
of  the  disease  and  the  greatest  severity  of  symptoms  that  a  patient  can 
present  and  still  belong  to  the  stage  defined.  All  patients  beyond  the 
incipient  stage  fall  under  the  moderately  advanced  stage  unless  the 
physical  signs  and  symptoms  exceed  those  of  the  moderately  advanced 
stage,  when  they  should  be  classified  as  far  advanced. 

Incipient. — Slight  or  no  constitutional  symptoms  (including  particu- 
larly gastric  or  intestinal  disturbance  or  rapid  loss  of  weight);  Slight  or 
no  elevation  of  temperature  or  acceleration  of  pulse  at  any  time  during 
the  twenty-four  hours.  Expectoration  usually  small  in  amount  or 
absent;  tubercle  bacilli  may  be  present  or  absent.  Slight  infiltration 
limited  to  the  apex  of  one  or  both  lungs  or  a  small  part  of  one  lung.  No 
tuberculous  complications. 

Moderately  Advanced. — No  marked  impairment  of  function,  either 
local  or  constitutional.  Localized  consolidation,  moderate  in  extent  with 
little  or  no  evidence  of  cavity  formation;  or  infiltration  more  extensive 
than  under  incipient.     No  serious  complications. 

Far  Advanced. — Marked  impairment  of  function,  local  and  constitu- 
tional. Marked  consolidation  of  an  entire  lobe;  or  disseminated  areas 
of  beginning  cavity  formation;  or  serious  complications. 

Miliary  Tuberculosis. 

2.  On  Discharge. — Apparently  Cured. — All  constitutional  symp- 
toms and  expectoration  with  bacilli  absent  for  a  period  of  three  months 
and  the  physical  signs  to  be  those  of  a  healed  lesion. 

Arrested. — Absence  of  all  constitutional  symptoms;  expectoration 
and  bacilli  may  or  may  not  be  present;  physical  signs  stationary  or 
retrogressiye ;  the  foregoing  conditions  to  have  existed  for  at  least  two 
months  (a  somewhat  arbitrary  period,  intended  to  cover  the  cases,  which 
frequently  occur,  of  patients  who  leave  the  sanatorium  for  various 
reasons,  contrary  to  advice,  after  a  stay  of  a  few  weeks,  although  all 
active  symptoms  may  have  ceased  completely  soon  after  entrance). 


TUBERCULOSIS  OF  THE  DIGESTIVE  SYSTEM  117 

Improved.- — Constitutional  symptoms  lessened  or  entirely  absent; 
physical  signs  improved  or  unchanged;  cough  and  expectoration  with 
bacilli  usually  present. 

Unimproved  or  Progressive. — All  essential  symptoms  and  signs  un- 
abated or  increased. 

Died. 

3.  Ultimate  Results. — Cured. — All  constitutional  symptoms  and 
expectoration  with  bacilli  absent  for  a  period  of  two  years  under  ordi- 
nary conditions  of  life. 

Well. — Patients  who  fulfil  all  the  conditions  required  under  "cured," 
but  about  whose  sputum  no  definite  information  can  be  obtained. 

Arrested,  Improved,  Progressive. — As  above. 

Dead. 

Tuberculosis  of  the  Digestive  System. 

Mouth. — Tuberculous  ulceration  of  the  mouth  and  tongue  is  rare,  and 
is  usually  secondary  to  laryngeal  or  pulmonary  involvement.  The  affec- 
tion simulates  syphilitic  and  malignant  ulceration.  The  tuberculous 
lesion  is  commonly  solitary,  sharply  outlined,  and  pale  in  color,  with 
an  area  of  oedematous  tissue  often  surrounding  it.  It  is  superficially 
located,  at  least  in  its  early  stage.  The  syphilitic  lesion  is  generally  an 
ulcerated  gumma,  and  is  deeply  placed.  The  malignant  (carcinomatous) 
ulcer  occurs  usually  later  in  life,  and  considerable  induration  usually 
appears  about  its  margin.  A  tuberculin  test  may  serve  to  dispel  any 
doubt  in  regard  to  the  diagnosis,  foi  the  ulcerated  tissue  is  likely  to  show 
some  reaction  if  tuberculosis  is  present. 

Tonsils  and  Pharynx. — Tuberculosis  of  the  tonsils  may  be  pri- 
mary or  secondary.  It  is  not  improbable  that  infection  finds  its  way  into 
the  system  in  many  cases  through  these  tissues.  However,  it  seems 
likely  that  the  majority  of  cases  are  secondary  and  are  induced  by  sputum 
from  an  infected  lung.  The  disease  appears  as  caseous  foci  adjacent 
to  the  crypts,  and  is  very  common  in  the  advanced  stage  of  pulmonary 
tuberculosis.  The  pharynx  is  even  less  frequently  the  seat  of  tubercu- 
losis than  is  the  oral  mucous  membrane.  The  miliary  type  is  the 
commonest,  and  this  by  progress  or  confluence  of  the  lesions  may  give 
rise  to  ulceration,  which  may  occur  in  advanced  pulmonary  tuberculosis. 

(Esophagus. — The  oesophagus  is  rarely  the  seat  of  tuberculosis. 
Occasionally  caseous  bronchial  and  tracheal  lymph  nodes  erode  through 
the  oesophageal  wall  and  cause  ulceration  therein.  More  rarely  the 
lesion  develops  in  consequence  of  an  abrasion  of  the  mucosa;  this  has 
been  noted  in  a  few  cases  of  malignant  ulceration,  in  which  tubercles 
have  been  noted  in  the  wall. 

Stomach. — ^Aside  from  the  development  of  tuberculous  masses 
in  the  peritoneal  tissues  of  the  gastric  wall  coincidently  with  tubeil'ulous 
peritonitis,  tuberculosis  of  the  stomach  is  very  rare.  The  usual  mani- 
festation is  ulceration  of  the  mucous  membrane,  which  is  somewhat 
more  frequently  foimd  in  infancy  and  childhood  than  in  later  life.     The 


118  BACTERIAL  INFECTIONS 

lesions  may  be  solitary  or  multiple,  commonly  the  latter,  and  they  are 
superficially  placed.  In  a  few  cases  tuberculosis  has  been  known  to 
become  engrafted  upon  a  previously  existing  simple  ulcer.  There  are 
no  specific  symptoms.     It  may  be  associated  with  intestinal  ulceration. 

Intestines. — The  frequency  of  involvement  of  the  small  intestine 
increases  progressively  toward  the  ileocecal  valve,  since  the  lymphoid 
tissue  is  the  seat  of  predilection  and  this  tissue  is  present  in  abundance 
in  the  ileum.  The  appendix  and  cecum  are  also  commonly  diseased. 
The  remainder  of  the  large  intestine  is  aflfected  more  frequently  than  the 
duodenum  or  jejunum.  The  immunity  of  the  duodenum  to  infection 
has  been  ascribed  to  the  acid  intestinal  contents  and  to  the  rapidity 
of  the  intestinal  current.  The  source  of  intestinal  infection  is  chiefly 
infected  milk  and  butter  and  the  swallowing  of  tuberculous  sputum. 
In  infancy  and  childhood  the  bacilli  seem  capable  of  penetrating  the  walls 
of  the  intestines  without  inducing  any  lesions,  and  they  are  then  carried 
to  the  mesenteric  nodes,  where  a  focus  of  disease  is  set  up.  Such  perme- 
ability of  the  intestinal  mucosa  seems  not  to  obtain  in  adult  life.  Intes- 
tinal ulceration  is  noted  rather  more  frequently  in  the  latter  period  of 
life.  Alimentary  infection  is  not  the  sole  source  of  the  disease,  for  in 
cases  of  acute  generalized  miliary  tuberculosis  the  bacilli  are  carried 
by  the  blood  and  give  rise  to  the  characteristic  tubercles. 

Pathology. — ^The  ulcer  is  the  usual  form  of  intestinal  tuberculosis.  It 
is  probably  produced  by  the  coalescence  of  several  adjacent  foci  and  the 
erosion  of  the  mucous  surface.  The  lesion  has  a  ragged,  punched-out 
appearance,  with  an  elevated  and  somewhat  indurated  margin.  Con- 
gestion of  the  adjacent  tissues  may  or  may  not  be  present.  Typically 
the  ulcer  extends  along  the  gut  in  a  circular  manner;  this  has  been 
ascribed  to  the  infection  following  the  course  of  the  lymphatics.  The 
ulcers  vary  in  size  from  that  of  a  millet  seed  to  a  diameter  of  four  or  five 
inches.  On  the  serous  surface  of  the  bowel  opposite  the  lesions  miliary 
tubercles  are  commonly  found.  It  is  rare  to  find  that  an  ulcer  has 
perforated,  such  an  accident  being  apparently  inhibited  by  an  over- 
growth of  the  tissues  at  its  base,  ^^lien  perforation  occurs  adhesions 
develop  between  the  adjacent  coils  of  intestines,  indicating  a  localized 
peritonitis;  at  times  a  generalized  peritonitis  is  the  consequence.  An 
unusual  form  of  intestinal  tuberculosis  is  that  in  which  marked  hyper- 
plastic changes  take  place  without  notable  caseation  and  ulceration. 
This  may  be  found  in  any  part  of  the  intestine,  but  there  is  a  predilection 
for  the  cecal  tissues;  a  certain  degree  of  stenosis  may  co-exist.  A  rectal 
or  anal  fistula  may  be  the  result  of  infection  of  the  lowermost  portion 
of  the  intestinal  tract.  In  cases  of  pulmonary  tuberculosis  4  to  5  per 
cent,  show  such  fistulse,  which  may  be  clinically  the  primary  lesion. 

Symptoms. — The  symptoms  are  indefinite;  some  patients  have  diar- 
rhoea, while  others  exhibit  no  symptoms  referable  to  the  bowels.  Diar- 
rhoea with  abdominal  pains  and  tenderness  in  a  tuberculous  patient  is 
always  suggestive  of  intestinal  involvement.  Involvement  of  the  colon 
seems  to  be  provocative  of  diarrhoea  more  frequently  than  involvement 


TUBERCULOSIS  OF  THE  DIGESTIVE  SYSTEAI  119 

of  the  small  intestine  only.  Intestinal  infection  complicates  pulmonary 
tuberculosis  in  from  60  to  75  per  cent,  of  the  cases,  especially  in  adults. 

Diagnosis. — It  is  practically  impossible  to  differentiate  intestinal 
tuberculosis  from  simple  enteritis  or  enterocolitis.  Bloody  stools  are 
suggestive  of  ulceration.  If  the  diarrhoea  is  refractory  to  medication, 
the  condition  is  likely  to  be  tuberculous  in  character.  The  finding  of 
tubercle  bacilli  in  the  feces  is  not  necessarily  diagnostic.  In  children 
the  diagnosis  is  made  with  even  greater  difficulty  than  in  adults.  If  a 
fistula  is  present  the  feces  may  show  traces  of  pus. 

Prognosis. — The  prognosis  is  unfavorable,  although  in  some  cases 
cicatrization  and  healing  of  the  ulcers  ensues.  Doubtless  the  condition 
hastens  a  fatal  issue,  on  account  of  the  deterioration  of  the  intestinal 
functions  and  the  increased  toxemia  promoted  by  a  large  ulcerated  and 
infected  surface. 

Liver. — Tuberculosis  of  the  liver  develops  mainly  as  a  result  of  infec- 
tion through  the  hepatic  artery  and  the  portal  vein;  it  is  possible  that 
some  cases  are  referable  to  the  entrance  of  infectious  material  through 
the  lymphatics  from  the  gastrohepatic  nodes  and  through  the  biliary 
channels.  The  commonest  sources  of  infection  are  the  lungs  and 
the  intestines,  coincidently  with  the  development  of  acute  generalized 
miliary  tuberculosis.  The  commonest  type  of  hepatic  involvement 
is  the  miliary,  in  which  the  characteristic  tubercles  are  seen,  not  only  in 
the  parenchyma  of  the  organ,  but  frequently  upon  its  peritoneal  surface. 
The  organ  is  likely  to  be  moderately  enlarged.  Another  type  is  that  in 
which  large  caseous  masses  appear;  these  sometimes  soften  and  give 
rise  to  abscesses  and  cavities.  The  condition  is  very  rare.  A  ques- 
tionable type,  tuberculous  cirrhosis,  has  been  described  in  which  there 
are  no  lesions  except  hyperplastic  changes  in  the  connective  tissue. 
There  are  no  characteristic  symptoms,  except  occasional  jaundice,  in 
miliary  and  caseous  tuberculosis  of  the  liver,  but  upon  examination  the 
organ  may  be  found  moderately  enlarged.  In  chronic  suppurative 
tuberculosis  elsewhere  in  the  body  (bones,  etc.),  amyloid  disease  may  co- 
exist and  the  organ  may  be  considerably  enlarged.  In  a  few  of  the 
rare  cases  of  tuberculous  abscess  the  mass  protrudes  from  the  costal 
margin. 

Pancreas. — Tuberculosis  of  the  pancreas  resembles  that  of  the  liver, 
since  the  miliary  type  is  the  commonest,  though  the  organ  is  much  less 
frequently  involved  than  the  liver.  It  has  been  stated  that  this  condition 
is  a  pathological  curiosity  and  that  involvement  of  the  pancreas  is  one 
of  the  rarest  manifestations  of  tuberculosis.  A  more  thorough  study  in 
recent  years  reveals  the  fact  that  the  organ  is  not  uncommonly  affected, 
and  in  children  as  many  as  44  per  cent,  of  cases  of  generalized  disease 
have  been  found  to  show  tuberculous  pancreatitis.  In  adult  life  the 
condition  is  much  less  frequently  seen.  Cases  of  primary  involvement 
have  been  described,  but  these  lack  substantial  proof.  It  is  probable 
that  every  case  is  secondary  to  some  other  focus  in  the  body,  and  that  in  a 
preponderance  of  these  cases  infection  reaches  the  organ  l)y  way  of  the 


120  BACTERIAL  INFECTIONS 

blood  channels,  that  is,  coincidently  with  a  generalized  miliary  disease. 
There  are  two  other  possible  methods  of  entrance  of  infection — by 
the  lymphatics  and  by  the  pancreatic  ducts.  A  few  cases  have  been 
reported  in  which  large  caseous  foci  were  found  in  the  parenchyma  of 
the  organ,  and  in  which  there  was  associated  involvement  of  the 
adjacent  lymph  nodes.  It  is  likely  that  in  some  of  these  instances  the 
true  condition  was  enlargement  and  caseation  of  the  nodes,  w^th  encroach- 
ment upon  but  no  direct  involvement  of  the  pancreas.  No  authentic 
cases  have  been  described  in  which  infection  took  place  through  the 
ducts  from  the  intestines.  There  are  no  symptoms  indicative  of  pan- 
creatic tuberculosis. 


Tuberculosis  of  the  Genito-urinary  System. 

Male  Genitalia. — Tuberculosis  of  the  testicle  is  not  uncommon 
between  the  ages  of  twenty  and  forty  years.  In  the  majority  of  cases, 
the  process  is  secondary  to  a  focus  elsewhere  (hemogenic  infection),  or 
it  follows  tuberculosis  of  some  other  portion  of  the  genito-urinary  system 
(infection  occurring  along  the  vas  deferens).  The  process  is  usually 
unilateral,  though  it  may  be  bilateral.  It  develops  in  an  insidious  manner 
in  the  epididymis  as  a  small  firm  mass;  later  the  body  of  the  testicle  may 
become  invaded,  and  the  lesions  undergoing  caseation  and  softening 
may  form  a  connection  with  the  overlying  skin  and  discharge  externally, 
leaving  sinuses;  or  the  process  may  extend  along  the  vas  deferens,  infect- 
ing it,  and  later  involving  the  seminal  vesicles,  the  prostate,  the  bladder, 
the  ureters,  the  kidneys,  etc.  The  semen  being  infected  may  lead  to 
tuberculosis  of  the  female  genitalia. 

Female  Genitalia. — ^The  Fallopian  tube  is  more  frequently  tuber- 
culous than  any  other  part  of  the  female  generative  system.  It  has  been 
stated  that  from  8  to  16  per  cent,  of  specimens  removed  at  operation  for 
inflammatory  disease  are  found  to  be  tuberculous.  The  source  of 
infection  may  be  the  blood,  the  peritoneum,  or  the  lower  genital  tract. 
The  disease  is  primarily  one  of  tubercle  formation  within  the  mucosa; 
this  eventually  gives  rise  to  nodular,  caseous  masses  and  general  destruc- 
tion of  the  tubal  and  oftentimes  of  the  ovarian  tissues.  In  many  cases 
of  tuberculous  peritonitis  the  tubes  are  the  nidus  from  which  infection  is 
disseminated.  There  are  no  specific  symptoms  aside  from  those  com- 
mon to  ordinary  tuboovarian  disease.  The  uterus  may  present  evi- 
dences of  tuberculosis  primarily,  as  miliary  tubercles  in  the  endometrium ; 
after  a  time  large  cheesy  masses  may  appear.  Infection  may  occur  from 
the  tubes,  vagina,  or  from  the  circulating  blood ;  tuberculous  semen  may 
be  responsible  for  some  cases.  The  disease  has  been  diagnosticated  by 
curettage  and  the  removal  of  particles  of  the  endometrium  in  which 
tubercles  and  bacilli  have  been  found. 

The  mammary  glands  are  rarely  the  seat  of  tuberculosis.  The  sources 
of  infection  are  adjacent  lymphatic  and  osseous  lesions.  Primarily 
the  condition  is  one  of  miliary  tuberculosis,  followed  by  the  production 


TUBERCULOSIS  OF  THE  GENITO-URlN ARY  SYSTEM       121 

of  caseous  foci,  from  which  sinuses  develop  to  the  cutaneous  surface. 
Multiple  areas  of  ulceration  are  not  infrequently  seen.  The  diagnosis 
is  confirmed  by  histological  examination  of  tissues  or  by  finding  tubercle 
bacilli  in  the  purulent  material. 

Urinary  System. — Renal  tuberculosis  is  present  in  from  40  to  50 
per  cent,  of  cases  of  pulmonary  infection.  Recent  studies  have  shown 
that  the  condition  is  much  commoner  than  was  formerly  considered. 
The  infection  may  be  hemogenic,  lymphogenic,  or  urogenic.  The  com- 
monest type  is  miliary  tuberculosis,  which  is  induced  by  blood  infec- 
tion, as  it  is  in  all  other  organs  of  the  body.  The  lesions  are  bilateral; 
the  cortex  especially  shows  the  presence  of  the  characteristic  tubercles, 
associated  with  which  there  is  usually  moderate  hyperplasia  of  the 
interstitial  tissues.  Disease  of  the  retroperitoneal  nodes  may  extend 
to  the  kidney  (lymphogenic  infection),  in  which  event  the  condition  is 
generally  unilateral.  One  rather  large  caseous  focus  may  mark  the 
disease.  These  two  types  have  no  special  symptomatology;  the  detection 
of  tubercle  bacilli  in  the  urine,  though  of  great  importance,  may  not 
necessarily  signify  renal  tuberculosis,  since  it  has  been  stated  that  tubercle 
bacilli  may  be  excreted  by  tuberculous  subjects  in  whom  the  kidneys 
appear  to  be  unaffected.  Some  of  the  supposed  tubercle  bacilli,  how^ever, 
are  doubtless  smegma  or  other  acid-fast  organisms.  The  kidneys  may 
become  diseased  as  the  result  of  an  infection  from  the  bladder  through 
the  ureters  (urogenous  infection),  the  ureters  often  showing  no  evidences 
of  tuberculosis.  Commonly  the  infection  passes  first  up  one  ureter  and 
then  after  a  variable  period  up  the  other.  Gonorrhoea  has  been  sug- 
gested as  a  predisposing  cause.  The  renal  pelvis  and  calyces  are  first 
affected;  thence  the  medullary  and  cortical  parts  are  attacked.  Often 
there  is  considerable  dilatation  of  the  pelvis,  in  consequence  of  more  or 
less  stenosis  of  the  ureter.  The  condition  is  slowly  progressive,  caseation 
and  widespread  destruction  of  the  tissues  occurring,  so  that  usually  the 
kidney  after  a  time  assumes  a  multiloculated  appearance.  The  walls 
of  the  cavities  are  rough,  ragged,  and  necrotic,  and  it  is  not  unusual  to 
find  the  parenchymatous  tissue  completely  destroyed,  and  the  organ  con- 
siderably .enlarged  (pyonephrosis).  Hematuria,  pyuria,  and  bacilluria 
are  symptoms.  Upon  examination  the  enlarged  organ  or  organs  may  be 
well  outlined,  and  a  certain  amount  of  tenderness  may  be  elicited  over  the 
lumbar  region.  The  condition  is  to  be  differentiated  from  malignant 
disease  of  the  kidney.  The  bladder  may  be  the  seat  of  tuberculosis; 
infection  may  occur  through  the  urethra  by  means  of  infected  instru- 
ments or  coincidently  with  gonorrhoea,  or  by  way  of  the  blood  stream;  or 
in  consequence  of  kidney  involvement;  or  from  the  reproductive  organs 
of  the  male  sex.  As  a  consequence  the  vesical  wall  becomes  invaded 
by  tubercles,  caseous  masses,  or  it  becomes  ulcerated.  The  symptoms 
are  those  of  cystitis,  together  with  pyuria  and  bacilluria.  The  urethra  is 
rarely  the  seat  of  tuberculosis.  The  predisposing  factors  are  gonorrhoea, 
stricture,  and  phimosis.  Infection  may  occur  from  the  use  of  infected 
instruments  or,  especially  in  the  female,  it  may  follow  tuberculosis  of 


122  BACTERIAL  INFECTIONS 

the  lower  genital  tract;  the  condition  is  much  less  likely  due  to  a  descend- 
ing infection. 

Tuberculosis  of  the  Nervous  System. 

Brain. — Tuberculosis  of  the  cerebral  meninges  is  associated  with 
generalized  miliary  disease  in  about  75  per  cent,  of  the  cases,  and  the 
infection,  therefore,  is  chiefly  hemogenic  in  type.  The  disorder  is 
most  frequently  seen  in  childhood,  especially  prior  to  the  sixth  year. 
Meningeal  infection  is  not  an  infrequent  complication  of  tuberculosis 
of  the  reproductive  and  osseous  system;  moreover,  it  has  been  shown  that 
it  may  be  a  sequel  of  operations  for  the  relief  of  bone  and  joint  disease, 
and  that  it  is  not  infrequently  a  sequel  of  measles  and  whooping  cough, 
in  which  it  is  probable  that  the  primary  lesion  is  present  in  the  cervical 
or  bronchial  lymph  nodes.  On  the  contrary,  meningeal  disease  may 
arise  in  consequence  of  lymphatic  dissemination,  or  by  direct  continuity  of 
structure.  Tuberculosis  of  the  eye,  ear,  and  cervical  nodes  may  set  up 
the  condition.  A  few  cases  have  been  reported  in  which  the  infection 
occurred  through  the  cribriform  plate  of  the  ethmoid  bone  from  a  tuber- 
culous rhinitis.  Primary  cases  of  meningeal  tuberculosis  are  of  doubtful 
existence. 

Pathology. — The  disease  usually  appears  as  a  leptomeningitis,  but  in 
some  instances  it  is  a  true  meningo-encephalitis.  The  base  is  more 
commonly  affected  than  the  convexity.  There  are  two  chief  types  of  the 
disease :  one  in  which  miliary  tubercles  are  found,  and  the  other  in  which 
large  caseous  nodules  (so-called  solitary  tubercles)  are  encountered.  The 
condition  may  be  localized  or  diffused  throughout  the  meningeal  surfaces. 
The  miliary  tubercles  may  be  scattered  over  the  serous  membranes; 
with  these  there  is  always  more  or  less  exudate  present,  which  serves 
to  flatten  the  convolutions.  The  lateral  ventricles  are  usually  found  to 
contain  an  excess  of  fluid,  and  this,  likewise,  may  be  seen  in  the  third  and 
fourth  ventricles,  the  condition  being  known  as  internal  hydrocephalus. 
In  the  other  type  one  or  more  large  caseous  nodules  are  present,  usually 
over  the  basal  portions  of  the  brain.  An  excess  of  fluid  in  the  ventricles 
usually  co-exists.  Occasionally  chronic  leptomeningitis  is  manifested  by 
thickening  of  the  membranes,  and  is  associated  with  the  presence  of  a 
few  small  caseous  masses,  the  condition  being  indicative  apparently  of  a 
healing  process.  Similar  lesions  may  be  found  in  the  spinal  cord  and 
its  meninges. 

Symptoms. — When  meningitis  supervenes  in  a  case  of  acute  generalized 
miliary  tuberculosis,  its  attending  symptoms  overshadow  all  those  pre- 
viously existing.  The  onset  may  be  insidious  or  abrupt,  usually  the 
former.  There  may  be  a  period  of  vague  prodromes  tiuring  which 
languor,  irritability,  headache,  vomiting,  and  constipation  may  appear. 
Difficulties  in  speech  are  sometimes  noted  early  in  the  condition.  After 
a  time  certain  characteristic  symptoms  appear,  so  that  the  disease  may 
be  divided  into  three  stages:  (i)  the  stage  of  irritation  which  is  referable 


TUBERCULOSIS  OF  THE  NERVOUS  SYSTEM  123 

to  the  meninges  and  cortex;  (2)  the  stage  of  pressure,  referable  to  the 
effusion  into  the  ventricles;  (3)  the  stage  of  paralysis,  referable  to  in- 
creased pressure  and  extension  of  the  disease  to  the  medulla  oblongata. 
The  symptoms  of  the  first  and  second  stages  usually  overlap.  In  the 
early  stage  the  face  is  commonly  flushed,  and  by  stroking  the  skin 
upon  any  part  of  the  body  the  tache  cerebrale  is  usually  obtained.  The 
pupils  are  dilated  and  photophobia  may  be  marked,  especially  in  adults. 
Headache  is  a  common  symptom,  though  more  frequently  noted  in 
adults  than  in  children,  and  it  is  likely  to  be  frontal  in  the  former  and 
generalized  in  the  latter.  Pains  may  be  complained  of  in  various  parts 
of  the  body,  as  in  the  abdomen,  spine,  knees,  etc.,  and  these  joint  exacer- 
bations may  be  so  severe  that  acute  rheumatism  may  be  simulated.  The 
decubitus  is  characteristic,  the  patient  lying  upon  one  side  with  the  legs 
dravk^n  up,  and  he  resents  any  disturbance.  Incessant  vomiting  may  be 
present;  this  is  of  the  cerebral  type,  sudden,  projectile  in  character, 
unattended  by  nausea,  and  occurs  independently  of  taking  food.  Con- 
stipation is  a  common  symptom  usually  relieved  by  aperients,  but  in 
some  instances  there  seems  to  be  almost  complete  paralysis  of  the  bowel. 
Diarrhoea  may  be  a  symptom;  this  is  likely  to  be  present  if  intestinal 
tuberculosis  is  a  complication.  The  temperature  is  usually  not  very 
high,  but  irregular  in  the  early  stage,  while  in  the  paralytic  stage  it  may 
reach  as  high  as  108°  F.  The  pulse  is  likely  to  be  slow  and  irregular 
in  the  early  stage,  but  later  it  becomes  quickened.  In  the  early  stage 
deep,  slow  respirations  are  observed,  to  be  followed  later  by  those  of 
the  Cheyne-Stokes  type.  Retraction  of  the  head  and  stiffness  of  the 
neck  are  usually  not  marked,  and  in  many  instances  they  are  absent. 
To  a  great  extent  these  symptoms  depend  upon  involvement  of  the 
posterior  basal  portions  of  the  brain.  Convulsions  may  appear  in  any 
one  or  all  of  the  stages  of  tuberculous  meningitis;  those  of  the  second 
stage  are  most  distinctive,  inasmuch  as  they  may  serve  to  determine 
the  locality  of  the  inflammation.'  Paralysis,  coma,  and  death  may 
terminate  the  condition.  The  symptoms  of  the  solitary  tubercle  are 
those  of  brain  tumor. 

Diagnosis. — ^Among  the  diseases  which  may  simulate  tuberculous 
meningitis  are  typhoid  fever,  pneumonia,  brain  tumor,  brain  abscess, 
and  thrombosis  of  the  cerebral  sinuses.  The  probability  of  confusion 
is  greatest  in  the  early  stage  of  the  disease,  for  as  it  progresses  distinctive 
symptoms  appear.  The  temperature  is  typically  lower  in  meningitis 
than  in  typhoid  fever,  and  the  irritability  is  greater.  In  the  former,  the 
abdomen  is  retracted,  while  in  the  latter  it  is  distended  and  tympanitic. 
A  rather  rigid  position  and  a  lateral  decubitus  are  seen  in  meningitis, 
and  a  relaxed  position  and  a  dorsal  decubitus  are  common  to  typhoid 
fever.  The  Widal  reaction  and  the  results  of  a  study  of  fluid  i-emovefl 
by  lumbar  puncture  should  eliminate  any  doubt.  The  temperature, 
decubitus,  and  abdominal  condition  in  pneumonia  more  closely  resemble 
typhoid  fever  than  meningitis.  In  brain  tumor  the  condition  is  j)ro- 
longed  and  the  gradual  paralysis  is  very  difi'erent  from  tliat  of  incuiugids; 


124  BACTERIAL  INFECTIONS 

optic  neuritis  is  likely  to  be  much  more  marked  than  in  meningitis. 
Exacerbations  of  temperature  and  rigors  are  characteristic  of  cerebral 
abscess;  these  are  absent  in  tuberculous  meningitis,  at  least  in  its  early 
stage.  Localized  venous  engorgement  about  the  eyes  and  temples  and 
the  presence  of  hemorrhage  in  the  fundus  of  the  eye  may  serve  in  some 
cases  to  differentiate  thrombosis  of  the  cerebral  sinuses  from  menin- 
geal tuberculosis. 

Prognosis. — The  prognosis  depends  somewhat  upon  the  extent  of  the 
inflammation,  since  if  it  is  localized,  recovery  may  possibly  occur,  but 
as  the  condition  is  usually  generalized,  the  disease  is  looked  upon  as  fatal. 
The  course  of  the  average  fatal  case  is  from  three  to  four  weeks,  ^^'hen 
the  disease  is  generalized  over  the  convexity,  the  duration  is  usually 
much  shorter  than  when  it  has  the  basal  distribution. 

Tuberculosis  of  the  Bones  and  Joints. 

Tuberculosis  of  the  bones  and  joints  occurs  in  various  forms,  such  as 
caries  of  bone,  "white  swelling,"  etc.  One-half  of  the  cases  develop 
prior  to  the  twentieth  year;  the  sexes  are  affected  with  equal  frequency. 
Traumatism  seems  to  have  some  predisposing  influence;  though  the 
bacteria  do  not  necessarily  enter  the  system  through  the  channels  thus 
induced,  the  vitality  of  the  part  is  diminished  by  reason  of  the  injury. 
Infection  gains  entrance  to  the  part  from  a  previously  existing  lesion 
in  the  majority  of  instances  by  the  blood  stream.  In  some  cases  the 
lymph  stream  cannot  be  eliminated  from  consideration.  The  primary 
focus  may  be  situated  in  the  lungs,  genitalia,  or  lymph  nodes.  Though 
primary  cases  of  bone  and  joint  tuberculosis  have  been  described,  it 
is  likely  that,  at  least  in  the  majority  of  the  cases,  a  latent  focus  of  disease 
was  present,  probably  in  a  lymph  node,  as  for  example  in  the  cervdcal 
or  bronchial  groups.  So-called  primary  cases  have  been  observed  to 
follow  infections  such  as  measles,  whooping  cough,  scarlet  fever,  etc. 
According  to  Cornet  the  disease  attacks  the  bones  and  joints  in  the 
following  order  of  frequency:  the  spinal  column,  the  hip-joint,  the  small 
joints  of  the  hands  and  feet,  the  knee-joint,  the  long  bones,  the  ankle- 
joint,  the  tarsus,  and  the  elbow-,  shoulder-,  and  wrist-joints.  The 
sternum,  ribs,  cranial  bones,  and  pelvis  are  rarely  tuberculous. 

Pathology. — Of  the  bony  structures,  the  cancellous  or  spongy  parts  are 
the  seats  of  predilection  in  the  development  of  tuberculosis;  this  is  seen 
especially  in  the  ends  of  the  long  bones  and  in  certain  short  bones.  In 
osseous  tuberculosis  the  epiphysis  is  the  commonest  seat  of  initial  in- 
volvement, while  in  joints  the  synovial  membranes  become  first  infected. 
If  the  diseased  bone  is  incised  longitudinally  there  is  seen,  in  the  early 
stages  of  the  affection,  a  small,  yellowish,  nodular  mass  within  the  can- 
cellous structure  at  the  epiphysis.  Microscopic  examination  reveals 
numerous  tubercles  and  bacilli.  At  a  later  stage  of  the  disease  the 
yellowish  mass  is  found  to  have  softened  and  to  contain  necrotic  particles 
of  bone.     Still  later,  if  treatment  has  been  effectual,  more  or  less  fibrosis 


DIAGNOSIS  OF  TUBERCULOSIS  125 

of  the  parts  and  ebumation  of  the  bone  attest  the  fact  that  the  condition 
is  gradually  healing.  Subsequently  much  of  the  fluid  is  lost  and  the 
necrotic  mass  is  of  a  dry,  cheesy  consistency.  On  the  contrary,  gradual 
destruction  of  the  osteal  and  periosteal  tissues  may  occur;  and  the  necrotic 
material  may  be  discharged  through  a  sinus  or  fistula,  which  has  devel- 
oped. At  times  rupture  takes  place  into  the  adjacent  joint.  In  many 
cases,  however,  the  joint  is  primarily  affected  upon  its  synovial  surfaces. 
The  process  has  the  same  general  character  as  heretofore  described;  in 
addition,  in  the  favorable  cases  extreme  fibrosis  gives  rise  to  ankylosis 
or  stiffening  of  the  joint. 

Symptoms. — ^The  symptoms  of  bone  and  joint  tuberculosis  depend 
somewhat  upon  the  point  involved.  The  condition  is  typically  chronic, 
beginning  with  vague  pains  and  tenderness,  together  with  gradual 
increase  in  the  size  of  the  part.  If  a  joint  is  affected,  stiftness 
slowly  develops.  Muscular  spasm  is  often  noted  rather  early  in  the 
disease;  later  there  is  considerable  muscular  atrophy.  The  latter  condi- 
tion serves  to  intensify  the  swollen  appearance  of  the  part.  The  cuta- 
neous tissues  are  usually  pale,  and  coursing  over  the  part  oftentimes 
prominent  veins  are  seen.  If  treatment  is  effectual,  no  further  changes 
may  be  noted,  and  the  condition  is  likely  to  heal.  If  septic  infection 
is  added  to  the  already  existing  tuberculous  lesions,  all  the  symptoms 
become  intensified  and  the  process  often  goes  on  to  sinus  formation', 
the  pus  from  which  contains  many  pyococci,  and  often  but  few,  if 
any,  tubercle  bacilli.  In  spinal  caries  (Pott's  disease),  owing  to  the 
involvement  of  the  bodies  of  the  vertebrae,  the  process  does  not  tend  to 
extend  toward  the  neighboring  .cutaneous  surface,  but  rather  down  the 
sheath  of  the  psoas  muscle,  and  appears  in  the  inguinal  region.  There 
is  always  more  or  less  spinal  deformity  in  Pott's  disease  (kyphosis, 
skoliosis).  In  hip-joint  disease  there  is  a  tendency  toward  shortening 
of  the  alTected  limb. 

Prognosis. — It  is  often  well  to  give  a  guarded  prognosis  in  cases  of  bone 
and  joint  tuberculosis  in  so  far  as  the  local  condition  is  concerned. 
The  possibilities  of  ankylosis  must  be  kept  in  mind,  for  after  considerable 
involvement  of  the  structures  has  taken  place  complete  restoration 
never  occurs.  Severe  cases  may  give  rise  to  widespread  dissemination 
of  the  infection,  and  death  is  the  sequel.  Amyloid  changes  characteris- 
tically take  place  in  the  viscera  (liver,  spleen,  kidneys,  etc.)  in  conse- 
quence of  the  chronic  tuberculous  changes  with  suppuration. 

General  Diagnosis. — In  addition  to  the  aforementioned  diagnostic 
procedures  available  in  the  several  types  and  situations  of  tuberculosis, 
recourse  may  be  had  to  tuberculin  tests;  agglutination  tests  also  have 
been  proposed,  but  they  have  not  proved  satisfactory.  The  tuberculin 
tests  comprise:  (1)  The  von  Pirquet  cutaneous  reaction,  which  consists 
of  preliminary  scarification  and  the  application  to  the  scarified  area  of  a 
drop  of  old  tuberculin — in  a  manner  analogous  to  that  practised  in 
ordinary  vaccination;    a  scarified  but  otherwise  untreated  area  is  used 


126  BACTERIAL  INFECTIONS 

as  a  control.  The  test  is  of  much  value,  especially  in  young  subjects; 
in  adults  the  importance  of  a  slight  reaction  should  not  be  overestimated, 
since  many  adults  are  the  subject  of  more  or  less  quiescent  tuberculosis, 
of  the  bronchial  lymph  nodes,  for  instance;  a  marked  reaction  may  be 
significant  of  reinfection  or  activation  of  a  quiescent  lesion.  (2)  The 
Moro  cutaneous  reaction,  which  consists  of  rubbing  into  the  skin  an 
ointment  of  old  tuberculin  and  lanolin.  The  test  is  of  somewhat  less 
value  than  the  von  Pirquet.  (3)  The  Wolff-Eisner  or  Calmette  con- 
junctival test,  which  consists  in  instilling  into  the  conjunctiva  of  one  eye 
one  drop  of  a  0.5  per  cent,  solution  of  old  tuberculin.  The  ensuing 
reaction  is  sometimes  so  violent  that  the  test  deservedly  has  fallen  into 
disrepute  and  disuse.  (4)  The  hypodermic  test,  which  consists  in  inject- 
ing 2  milligrams  of  old  tuberculin;  the  reaction  consists  in  the  production, 
within  twelve  to  twenty-four  hours,  of  local  irritation,  malaise,  neuro- 
muscular pains  or  soreness,  and  fever  (102°  to  104°).  Should  the  first  in- 
jection prove  unproductive,  the  injections  may  be  increased  to  3,  5,  and  8 
milligrams.  Since  the  introduction  of  the  von  Pirquet  test  the  h^^odermic 
test  has  fallen  into  disuse.  (5)  Material  (sputum,  etc.)  from  a  suspected 
case  may  be  injected  into  a  guinea-pig,  and  the  pig  killed  at  the  end  of 
four  to  six  weeks  (if  it  has  not  died  earlier).  In  the  event  of  the  material 
having  contained  tubercle  bacilli  the  animal  will  be  found  infected. 
(6)  Ebbright  has  suggested  injecting  the  suspected  material  into  a  guinea- 
pig;  at  the  end  of  six  days  injecting  0.25  c.c.  of  old  tuberculin;  and  killing 
the  animal  at  the  end  of  another  twenty-four  hours.  In  the  event  of 
tuberculosis,  the  bacilli  may  be  found  thus  early,  the  view  being  that  the 
large  dose  of  tuberculin  breaks  down  the  body  resistance  and  permits  the 
rapid  multiplication  of  the  tubercle  bacilli.  (7)  Yamamanchi  has 
suggested  injecting  into  a  rabbit  a  few  cubic  centimeters  of  blood  serum 
(or  blister  serum)  from  a  case  of  suspected  tuberculosis,  and  in  a  few 
days  injecting  tuberculin;  the  animal  having  become  sensitized,  experi- 
ences a  severe,  perhaps  fatal,  reaction.  (8)  The  bacilli  may  be  searched 
for  in  the  circulating  blood,  as  suggested  by  Rosenberger;  but  they  are 
not  likely  to  be  found  in  many  cases,  assuredly  not  in  early  or  localized 
infections. 

Prophylaxis. — The  control  of  tuberculosis  may  eventually  be  effected 
by  prophylactic  measures,  of  which  the  following  are  the  most  important: 
(1)  The  education  of  the  public,  by  a  continuation  of  the  present-day 
widespread  antituberculosis  propaganda;  by  disseminating  a  knowledge 
of  the  efficient  means  of  preventing  the  disease — into  municipalities, 
industrial  and  other  associations,  schools,  the  family,  etc.  (2)  Improved 
sanitary  conditions  under  which,  especially  the  poor,  the  industrial 
workers,  etc.,  live  and  work.  (3)  Sanatoriums,  hospitals,  dispensaries,  and 
social  services  for  the  study,  prevention,  and  treatment  of  tuberculosis; 
especially  important  })eing  the  treatment  of  incij^ent  and  far-advanced 
and  hopeless  cases,  and  visiting  the  poor  and  ill-informed  by  trained 
nurses  or  social  workers.  (4)  Supervision  by  the  Public  Health  authori- 
ties, which  should  include  notification  of  the  disease  (in  a  manner  to  avoid 


TREATMENT  OF  TUBERCULOSIS  127 

wounding  the  sensibilities  of  the  patients),  the  destruction  of  sputum, 
the  disinfecting  of  rooms  inhabited  by  tuberculous  patients,  supervision 
of  dairies,  abattoirs,  etc.  (5)  Individual  prophylaxis — which  in  general 
comprises  the  regulations  laid  down  on  page  29.  In  addition,  children 
of  tuberculous  parents  should  have  the  benefit  of  the  best  environmental 
conditions,  and  assuredly  should  not  sleep  in  the  same  rooms  with  their 
diseased  parent  or  parents.  The  ideal  conditions  as  regards  future  health 
suggest  rearing  the  children  apart  from  the  tuberculous  parent — vir- 
tually impossible  of  attainment,  even  were  it  in  every  respect  desirable 
(which  it  is  not).  The  child,  however,  should  be  out-of-doors  as  much  as 
possible,  have  an  abundance  of  good  nutritious  food,  be  well  clad,  and 
afforded  a  sufficiency  of  regulated  exercises.  In  the  event  of  illness, 
especially  catarrhal  disorders  of  the  upper  respiratory  tract,  enlarged 
tonsils,  adenoids,  enlarged  cervical  lymph  nodes,  general  debility,  asthenia 
and  anemia,  etc.,  efficient  treatment  should  be  instantly  undertaken,  and 
tonics,  such  as  iron,  quinine,  strychnine,  arsenic,  cod-liver  oil,  etc., 
should  be  administered. 

Treatment. — The  efficient  management  of  tuberculosis  in  general 
comprises  the  use  of:  (1)  Fresh  air,  nutritious  food,  and  regulated  rest 
and  exercise;  (2)  specific  remedies;  (3)  medicinal  agents,  largely  to 
combat  symptomatic  indications;  and  (4)  certain  additional  measures 
applicable  in  special  forms  of  tuberculosis,  such  as  miliary  tuberculosis, 
acute  pneumonic  tuberculosis,  surgical  tuberculosis,  etc. 

Fresh  Air,  Nutritious  Food,  Rest,  and  Exercise. — Nothing 
transcends  in  importance  fresh  air  and  nutritious  food.  The  benefits 
of  fresh  air  may  be  secured  at  home  in  the  city  or  the  country,  in  sana- 
toriums  near  at  hand,  or  in  certain  mountainous  or  marine  climates.  If 
at  home,  the  patient  should  be  as  much  as  possible  out-of-doors,  and  he 
should  sleep  on  a  balcony  or  with  the  windows  of  his  room  wide  open; 
he  should,  of  course,  be  sufficiently,  but  not  excessively  clothed  (as 
commonly  obtains  among  the  ignorant  classes),  and  he  should  take  the 
precaution  so  to  arrange  his  bed  that  he  is  protected  against  continuous 
draughts,  and  the  rigors  of  storms.  Night  air,  dampness,  rain,  snow,  and 
the  continued  low  temperature  of  winter  are  not  contra-indications  to 
this  open-air  treatment;  nor  are  cough,  hemoptysis,  fever,  emaciation,  etc. 
Excellent  results  have  been  achieved  by  the  tuberculosis  classes  inau- 
gurated by  J.  H.  Pratt.  It  is  not  necessary,  as  a  rule,  for  the  patient  to 
go  long  distances  from  home  to  secure  the  benefits  of  fresh  air;  indeeel, 
this  is  positively  contra-indicated  in  advanced  cases ;  in  those  with  strong 
home  ties,  in  whom  absence  from  home  often  causes  marked  mental 
depression;  and  in  those  to  whom  such  distant  travelling  occasions 
financial  hardships — which  are  not  commensurate  with  the  hoped-for 
advantages.  Climate  'per  se  is  not  the  major  factor  in  the  cure,  that 
region  being  satisfactory  that  combines  a  pure  atmosphere,  considerable 
sunshine,  anfl  equable  temperature  (absence  of  sudden  variations); 
other  desirable  features  comprise  dryness  of  the  atmosphere  (at  least  not 
excessive  humidity),  moderate  altitude,  and  the  facilities  for  good  food, 


128  BACTERIAL  INFECTIONS 

good  housing,  and  some  amusement.  Most,  especially  early,  cases, 
with  localized  lesions,  moderate  fever,  and  little  emaciation,  and  without 
excavations,  do  best  at  moderate  altitudes  (2000  to  2500  feet),  such  as 
the  Adirondacks,  Asheville,  Aiken,  etc.  These  afford  the  advantage  that, 
as  a  rule,  after  the  disease  has  been  arrested  the  patient  may  return  to 
the  sea  level  without  the  likelihood  of  reactivation  of  the  lesions.  Some 
patients  seem  to  do  better  at  higher  altitudes  (5000  feet  or  more),  such 
as  Colorado,  New  Mexico,  Arizona,  Davos  and  other  places  in  Switzer- 
land, etc.  Chronic  and  advanced  cases,  with  excavation,  fibrosis, 
emphysema,  repeated  hemoptysis,  emaciation,  etc.,  as  a  rule,  do  better 
at  the  sea  level  and  in  a  moist  climate,  such  as  Florida,  Bermuda,  etc. 
Subjects  with  slowly  progressing  lesions  are  often  much  benefited  by 
the  dryer  climate  of  Southern  California,  the  Riviera,  Egypt,  Algiers, 
etc.  The  sanatoriums  in  these  and  other  regions  combine  the  advan- 
tages of  strict  disciplinary  supervision  of  out-door  life,  rest,  exercise,  food, 
bathing,  clothing,  medicinal  and  other  treatment;  they  are  especially 
serviceable  in  early  cases;  and  since  they  also  exercise  an  educational 
influence  not  only  upon  the  patients,  but  also  among  the  people  of  their 
vicinity,  their  further  establishment  should  be  encouraged. 

If  the  patient  has  fever,  that  is,  if  the  highest  daily  temperature  is 
above  99.5°  to  100°  F.,  he  should  be  at  rest  in  bed,  or  at  least  in  a  reclining 
(steamer)  chair.  In  the  absence  of  fever,  properly  regulated,  supervised, 
and  graduated  exercise  should  form  a  part  of  the  general  management. 
This  may  consist  of  walking,  graduated  ascents  (as  is  used  in  German 
sanatoriums),  or  various  sorts  of  light  out-door  work,  the  results  of 
which,  that  is,  the  reaction  of  the  patient  to  which  (temperature, 
pulse-rate,  weight,  etc.),  must  be  carefully  noted.  These  exercises,  as 
a  rule,  are  most  advantageously  prescribed  in  the  morning  hours. 

Since  the  cure  of  tuberculosis  depends  upon  the  maintenance  and  improve- 
ment of  nutrition,  the  greatest  attention  must  be  paid  to  the  diet  and  the 
digestion.  The  food  must  be  readily  digestible,  nutritious,  varied,  and 
appetizing,  and  it  should  be  partaken  of  in  stated  amounts  at  stated 
intervals.  An  amount  in  excess  of  that  which  would  be  taken  in  health 
is  necessary,  but  the  excessive  hyperalimentation  in  vogue  several  years 
ago  seems  undesirable.  The  diet  should  consist  largely  of  milk,  cream, 
butter,  eggs,  fish,  bread,  meats  (especially  beaf,  mutton,  chicken,  and 
bacon),  olive  oil  and  other  fats,  etc.  In  addition  to  what  might  be  con- 
sidered a  goodly  amount  of  a  varied  diet,  the  patient  should  take  daily 
from  one  and  one-half  to  two  quarts  of  milk  and  from  four  to  six  eggs. 
Many  patients  do  best  by  taking  for  breakfast  some  fruit,  a  cereal,  bacon, 
two  eggs,  and  milk  (hot,  if  desired,  and  flavored  with  coffee,  tea,  or  cocoa); 
a  full  meal,  for  dinner,  in  the  middle  of  the  day,  consisting,  for  instance, 
of  soup,  fish,  meat,  two  or  three  vegetables,  a  salad,  and  fruit,  a  simple 
pudding  or  other  dessert,  or  cheese;  and  for  supper,  in  the  evening,  some 
cold  meat,  or  fish,  or  two  eggs,  and  toasted  bread,  boiled  rice,  or  stewed 
fruit,  and  milk  as  at  breakfast.  The  additional  milk  and  eggs  may  be 
given  between  breakfast  and  dinner,  between  dinner  and  supper,  and 


TREATMENT  OF   TUBERCULOSIS  129 

just  before  retiring  for  the  night;  with  the  milk  it  is  advisable  to  take 
several  crackers  or  a  small  amount  of  toasted  bread  to  assist  in  com- 
minuting the  curds.  If  the  milk  and  eggs  prove  nauseating  to  the  patient, 
they  may  be  flavored,  as  already  suggested,  with  coffee,  tea,  cocoa,  or 
with  chocolate,  sodium  chloride  or  bicarbonate,  or  a  small  amount  of 
brandy,  whiskey,  port  wine,  sherry  wine,  etc.;  and  from  time  to  time 
they  may  be  discontinued  for  a  day  or  two.  Peptonization  of  the  milk 
is  sometimes  serviceable  for  a  time;  or  one  may  give  kefir,  koumiss,  etc. 
Rarely  it  may  be  necessary  to  resort  to  Debove's  method  of  forced  feeding, 
Avhich  consists  of  preliminary  washing  of  the  stomach,  followed  by  the 
introduction  through  the  stomach  tube  of  a  quart  of  milk,  one  or  two  eggs, 
and  three  ounces  of  finely  minced  meat;  this  is  done  three  times  a  day. 
A  raw-meat  dietary  (zomotherapy),  consisting  of  the  use  of  one  to  two 
pounds  or  more  of  meat  daily,  either  minced  and  raw,  or  made  into  a 
soup,  has  been  readvocated  lately.  Anorexia  and  nausea  are  sometimes 
deterrents  to  proper  feeding;  but  several  days  of  life  in  the  open  air,  or 
a  change  of  scene,  or  an  ocean  voyage  usually  act  as  an  efficient  tonic  to 
a-  jaded  appetite.  Sometimes,  however,  it  may  be  necessary  to  admin- 
ister tonics;  but  care  must  be  exercised  that  medicines  employed  for 
other  purposes  do  not  derange  the  stomach.  Alcohol,  as  a  rule,  is  not 
indicated:  indeed,  most  patients  do  better  without  it  altogether;  but  there 
can  be  no  serious  objection  to  a  small  amount  of  brandy  or  wine  to  flavor 
the  milk  and  eggs  from  time  to  time.  In  advanced  cases  with  fever, 
emaciation,  rapid  pulse,  night  sweats,  poor  digestion,  etc.,  alcohol 
seems  to  do  good;  at  least  it  aids  digestion,  especially  the  digestion  and 
assimilation  of  fats,  stimulates  the  heart  and  the  nervous  system,  pro- 
motes a  feeling  of  well  being,  relieves  the  night  sweats,  induces  sleep,  and 
if  it  does  not  lead  to  fibrosis,  as  has  been  claimed,  it  does  not  accelerate 
the  progress  of  the  lesions. 

Specific  Remedies. — Tuberculin  is  a  valuable  adjuvant  to  other 
forms  of  treatment  in  selected  cases.  The  preferable  preparations  are: 
Koch's  new  tuberculin,  tuberculin  residue  (T.  R.),  consisting  of  the 
toxins  and  endotoxins  of  crushed  tubercle  bacilli  unchanged  by  heat  or 
chemicals;  bacillen  emulsion  (B.  E.),  which  consists  of  one  part  of  finely 
pulverized  virulent  tubercle  bacilli  and  one  hundred  parts  each  of  dis- 
tilled water  and  glycerin;  and  Deny's  bouillon  filtre  (B.  F.),  which  con- 
sists of  a  filtrate  from  a  bouillon  culture  and  contains  all  the  soluble  toxic 
and  other  products  of  the  tubercle  bacillus.  The  cases  suitable  for 
tuberculin  treatment  are  the  early  cases  with  circumscribed  lesions,  in 
which  there  is  little  if  any  fever  or  emaciation,  and  no  excavation,  and 
chronic  cases  with  good  nutrition  and  no  serious  complications;  distinct 
contra-indications  comprise  rapidly  advancing  lesions,  hectic  fever, 
rapid  heart  action,  and  progressive  emaciation.  Ti'udeau  advises:  to 
begin  with  small  doses,  such  as  y-^,7|^,y  milligram  (li(|ui(l  measure)  of  the 
bouillon  filtre  (B.  F.);  to  avoid  provoking  local  or  general  reactions;  to 
increase  the  dose  gradually,  at  intervals  of  three  or  four  days,  or  longer 
when  large  doses  are  given,  until  a  maximum  dose  of  1  c.c.  of  the  tuber- 
9 


130  BACTERIAL  INFECTIONS 

culin  is  reached;  in  case  a  reaction  occurs,  especially  if  this  be  associated 
with  fever  and  constitutional  disturbances,  to  reduce  the  next  dose  to 
about  half  of  that  which  induced  the  reaction;  and  to  continue  the  treat- 
ment for  months,  but  not  indefinitely  for  fear  of  exhausting  the  patient's 
power  to  respond,  by  the  formation  of  antibodies,  to  the  stimulus  of  the 
injection:  it  being  better  to  discontinue  the  treatment  for  from  three  to 
six  months  and  resume  it  again  if  anything  in  the  patient's  symptoms  or 
condition  seems  to  make  this  necessary. 

Medicinal  Agents. — The  medicinal  treatment  of  tuberculosis  is 
largely  symptomatic;  but  certain  remedies  are  given  with  the  view  to 
improve  nutrition  and  increase  the  powers  of  resistance  of  the  individual. 
Of  these,  the  most  valuable  are  arsenic,  especially  in  the  form  of  Fowler's 
solution,  5  minims  (0.30  gram)  three  times  daily;  mercuric  bichloride  or 
succinimide,  ^  to  -^^  grain  (0.005  to  0.0018  gram)  three  times  daily; 
strychnine,  cod-liver  oil,  iron,  the  hypophosphites,  etc.  Inunctions  of 
europhen  (5  per  cent,  in  olive  oil)  and  other  iodine  preparations  also 
have  been  commended. 

While  the  symptoms  of  tuberculosis  are  commonly  improved  by  fresh 
air,  nutritious  food,  regulated  rest  and  exercise,  they  sometimes  demand 
special  attention.  Cough,  unless  excessive,  need  not  be  restrained 
medicinally;  often  it  can  be  repressed  mentally;  since,  however,  it  serves 
to  remove  secretion,  it  is  to  some  extent  a  necessary  evil.  In  general, 
if  requiring  treatment,  it  should  be  met  with  the  measures  mentioned 
under  bronchitis.  Creosote  is  a  very  valuable  remedy,  and  may  be  given 
in  doses  beginning  with  3  minims  (0.18  gram)  and  gradually  increasing, 
three  times  daily,  in  milk,  hot  water,  brandy,  or  a  bitter  tincture.  Guaia- 
col  carbonate  is  sometimes  better  borne.  The  distressing  nocturnal 
cough  may  be  controlled  by  the  following: 

I^ — Codeine 3  grains  0(20 

Dilute  hydrocyanic  acid 24  minims  1  50 

Glycerin 1  ounce  30  00 

Cherry  laurel  water,  sufficient  to  make 3  ounces  100 1 00 — M. 

S. — Two  teaspopnfuls  (10  c.c.)  at  6  and  9  p.m.,  and  during  the  night  if  necessary. 

Comfort  is  sometimes  promoted  by  diffusible  stimulants,  such  as 
Hoffman's  anodyne,  spirit  of  chloroform,  etc.,  or  by  hot  whiskey  on 
retiring;  in  other  cases  morphine  may  be  required,  but  it  should  be  given 
cautiously  in  the  event  of  cavity  formation,  since  the  cavities  must  be 
emptied.  Inhalations  are  often  of  marked  benefit.  Beverley  Robinson 
extols  the  virtues  of  equal  parts  of  creosote  and  alcohol,  or,  when  there  is 
much  irritative  cough,  equal  parts  of  creosote,  alcohol,  and  spirit  of 
chloroform  (on  an  inhaler).  Lees  advocates  the  use  of  six  to  eight  drops 
of  the  following  on  an  inhaler,  every  hour  during  the  day,  and  two  or 
three  times  during  the  night,  if  the  patient  is  awake : 


I^ — Carbolic  acid 2  drams  8 

Creosote 2  drams  8 

Tincture  of  iodine 1  dram  4 

Spirit  of  ether 1  dram  4 

Spirit  of  chloroform 2  drams  8 


0 
0 
0 
0 
0— M. 


DIPHTHERIA  131 

The  treatment  of  hemoptysis  is  discussed  on  page  540.  Pleural 
pains  may  be  relieved  by  counterirritation  with  tincture  of  iodine  to 
which  a  small  amount  of  croton  oil  may  be  added;  by  a  blister;  by  rubbing 
with  a  mixture  of  equal  parts  of  menthol,  camphor,  and  chloral;  or  by 
strapping  the  side.  The  night  sweats  may  be  controlled  by  an  abundance 
of  fresh  air  at  night,  and  the  avoiding  of  too  many  bed-clothes;  by  sponging 
the  body  with  alcohol  and  alum  water;  and  by  the  use  of  camphoric 
acid,  20  to  40  grains  (1.3  to  2.5  grams),  four  hours  before  the  time  of  the 
expected  sweat;  atropine,  y^-o"  to  y^^j  grain  (0.0004 to 0.0006  gram)  at  bed- 
time; picrotoxin,  y^-jj-  grain  (0.0006  gram),  aromatic  sulphuric  acid,  agara- 
cin,  etc.  In  the  event  of  fever,  the  patient  should  be  at  rest  in  bed.  Rest 
in  bed,  fresh  air,  and  nutritious  food  comprise  the  best  treatment  for  the 
fever  as  such;  but  should  the  fever  become  high,  attention  should  be 
paid  to  a  sufficiency,  but  not  an  excess  of  bed-clothes;  the  body  should 
be  sponged  repeatedly  with  cool  water  or  with  alcohol  and  alum  water. 
Quinine,  the  salicylates,  and  the  coal-tar  products  are  distinctly  contra- 
indicated;  of  course,  they  may  reduce  the  temperature,  but  at  the  expense 
of  the  bodily  resistance.  Painful  dysphagia  may  be  relieved  by  spraying 
the  throat  with  cocaine  (2  per  cent.)  or  by  swabbing  the  throat  with 
orthoform  (5  per  cent.)  in  olive  oil.  The  treatment  of  so-called  dys- 
pepsia and  diarrhoea  is  similar  to  that  mentioned  elsewhere  under  these 
headings. 

Special  Forms  of  Tuberculosis. — In  miliary  tuberculosis,  treat- 
ment is  of  very  little  avail.  Supportive  measures  are  indicated,  espe- 
cially strychnine,  whiskey,  camphor,  etc.,  and  in  the  event  of  restlessness, 
headache,  and  other  cerebral  symptoms,  the  bromides  and  opiates.  In 
the  event  of  meningitis  lumbar  puncture  by  relieving  pressure  may  lead 
to  amelioration  of  the  symptoms;  other  measures  mentioned  under 
meningitis  may  be  resorted  to.  The  treatment  of  acute  tuberculous 
pneumonia  is  that  of  pneumococcic  infection  of  the  lung,  together  with 
such  of  the  aforementioned  measures  as  may  seem  indicated  when  the 
tuberculous  nature  of  the  disease  has  been  recognized.  The  treatment 
of  many  forms  and  localizations  of  tuberculosis  is  distinctly  surgical :  for 
instance,  tuberculosis  of  the  lymph  nodes,  of  the  serous  membranes,  of 
the  skin,  of  the  bones  and  joints,  etc.  Recourse  has  also  been  had  to 
surgical  intervention  in  certain  cases  of  localized  tuberculosis  of  the  lung 
and  with  some  encouraging  results,  details  of  all  of  which  may  be  found 
in  books  of  surgical  practice. 

DIPHTHERIA. 

Diphtheria  is  an  acute,  specific,  infectious,  and  highly  contagious 
disease  caused  by  Bacillus  diphtherial  (Klebs-Loffler),  and  characterized 
by  fibrinous  (croupous,  or  diphtheritic)  inflammation  of  a  mucous 
membrane,  fever,  and  divers  manifestations  of  toxemia. 

Etiology. — Diphtheria  is  peculiarly  a  disease  of  childhood,  occurring 
most  frequently  between  the  second  and  the  fifth  year,  and  attacking 


132  BACTERIAL  INFECTIONS 

the  sexes  equally  (under  similar  circumstances).  It  is  relatively  infre- 
quent after  the  tenth  year,  but  adolescents  and  adults  (nurses,  physicians, 
attendants,  etc.)  are  rather  commonly  affected  and  often  succumb.  The 
disease  occurs  in  almost  all  parts  of  the  world,  but  is  especially  prevalent 
in  the  temperate  zone.  It  is  endemic  in  most  large  cities,  and  frequently 
prevails  epidemically,  especially  during  the  colder  months  of  the  year — 
the  late  fall,  the  winter,  and  the  early  spring;  but  the  epidemics  vary 
considerably  in  severity.  In  some  sections  the  disease  is  relatively  more 
common  in  the  country  districts  than  in  the  cities.  General  insanitary 
conditions  are  of  etiological  significance  only  in  so  far  as  they  reduce 
the  vitality  of  the  individual  and  favor  the  harboring  and  multiplying 
of  the  bacilli.  Overcrowding,  such  as  obtains  in  schools,  asylums, 
tenements,  etc.,  is  of  significance  in  permitting  the  ready  dissemina- 
tion of  the  bacilli  among  large  numbers  of  susceptible  persons.  One 
attack  confers  an  incomplete  and  temporary  immunity.  Recurrences 
are  not  infrequent. 

The  exciting  cause  of  the  disease  is  Bacillus  diphtherise,  which  may 
be  isolated  from  the  local  fibrinous  inflammations,  the  secretions  and 
discharges  from  the  throat  and  nose,  sometimes  from  the  blood  and  the 
internal  organs,  especially  the  lung  (in  the  event  of  bronchitis  and 
bronchopneumonia),  but  also  the  liver,  spleen,  kidney,  etc.  The  disease 
is  highly  contagious  and  spreads  with  considerable  rapidity.  Infection 
may  be  transmitted  by  direct  inoculation;  by  contact  or  proximity; 
by  a  third  person  (physicians,  nurses,  in  whose  hair  the  bacilli  have  been 
found,  etc.);  by  fomites,  especially  room  furnishings,  room  dust,  bed- 
linen,  personal  linen,  dishes,  toys,  etc.,  to  which  the  bacilli  often  cling 
for  a  long  time;  by  infected  food  and  drink,  especially  milk  (answerable 
for  a  number  of  epidemics),  cheese,  etc.;  by  domestic  animals,  etc. 
Infection  is  usually  acquired  by  inhalation  or  swallowing,  but  it  may  also 
be  acquired  through  a  wound  or  abrasion.  Individual  susceptibility 
is  of  much  etiological  significance :  many  persons  exposed  to  the  infection 
do  not  acquire  it,  and  others  harbor  the  bacilli  in  their  throats,  and  them- 
selves escaping  infection,  often  disseminate  it.  In  the  throats  of  con- 
valescents, for  instance,  the  bacilli  may  remain  virulent  for  a  long  time 
(weeks  and  months) — so-called  "chronic  carriers,"  responsible  for  many 
outbreaks.  Chronic  nasopharyngeal  catarrh,  enlarged  tonsils,  carious 
teeth,  etc.,  also  favor  infection. 

Pathology. — The  characteristic  lesion  is  the  so-called  false  membrane, 
the  relative  frequency  of  the  situation  of  which  is  well  exemplified  l^y  the 
results  of  the  investigations  of  Councilman,  Mallory,  and  Pearce,  who, 
among  127  of  220  fatal  cases,  found  it  situated  as  follows:  In  the  larynx, 
75;  trachea,  66;  tonsils,  65;  epiglottis,  60;  pharynx,  51 ;  nasal  mucous  mem- 
brane, 43;  bronchi,  42;  soft  palate,  including  uvula,  13;  oesophagus,  12; 
tongue,  9;  stomach,  5;  vagina,  2;  duodenum,  1 ;  vulva,  1;  skin  of  the  ear, 
1;  conjunctiva,  1.  Thus,  in  fatal  cases  the  larynx  is  most  frecjuently  in- 
volved; but  this  is  not  true  of  all,  especially  non-fatal  cases,  in  the  majority 
of  which  the  tonsil  is  first  and  most  frequently  attacked,     This  false 


DIPHTHERIA  133 

membrane  may  be  circumscribed  in  extent  or  widespread.  Sometimes  it 
is  limited  to  a  small  region  of  the  tonsil  or  soft  palate;  in  other  cases  it 
covers  the  tonsils,  soft  palate,  pharynx,  larynx,  and  trachea;  it  may 
extend  to  the  nose  (which  may  become  completely  obstructed),  to  the 
conjunctiva  (through  the  tear  duct),  and  to  the  accessory  sinuses  (which, 
as  pointed  out  by  Councilman,  Mallory,  and  Pearce,  are  very  frequently 
involved,  and  the  unhealed  lesions  of  which  are  often  answerable  for 
the  persistence  of  diphtheria  bacilli  in  the  nose  and  throat).  It  may 
travel  through  the  Eustachian  tube  to  the  middle  ear,  over  the  tongue, 
and  involve  the  oral  mucous  membrane,  through  the  bronchi  to  their 
finest  ramifications,  through  the  oesophagus  to  the  stomach,  intestine, 
etc.;  and  by  transference  it  may  implicate  other  mucous  membranes, 
such  as  the  vulva,  vagina,  etc.  In  character,  the  membrane  varies  con- 
siderably: it  may  appear  as  a  thin,  whitish,  more  commonly  grayish  or 
fawn-colored,  pellicle,  easily  removable  without  loss  of  substance  or 
l)leeding;  or  it  may  present  all  gradations  of  severity  from  this  to  a  dense, 
tough,  grayish,  brownish,  or  blackish  membrane,  firmly  attached  in  the 
early  stages  and  separable  only  with  difficulty  and  leaving  a  bleeding- 
surface,  but  later  softer  and  more  shaggy;  or  the  lesions  may  be  markedly 
necrotic  or  really  gangrenous.  The  membrane  is  more  easily  removed 
from  the  .trachea  and  larynx  than  elsewhere,  being  sometimes  expelled 
by  coughing,  and  it  rarely  occasions  in  these  regions  a  loss  of  sub- 
stance extending  beyond  the  superficial  epithelium;  the  subepithelial 
layer,  however,  is  always  markedly  injected. 

Councilman,  Mallory,  and  Pearce,  who  have  studied  the  lesions  atten- 
tively, describe  them  as  follows:  The  earliest  lesions  are  due  to  the 
toxin,  produced  by  the  diphtheria  bacillus,  possibly  growing  in  the  fluids 
of  the  mouth  and  throat.  The  toxin  gives  rise  to  degeneration  and  necro- 
sis of  the  epithelium,  often  preceded  by  active  proliferation  of  the  nuclei 
of  the  cells  by  direct  division.  In  this  necrotic  tissue,  but  more  especially 
in  the  exudate  speedily  formed,  the  bacilli  become  implanted  and  there 
continue  their  deleterious  action;  but  the  bacilli  themselves  are  not 
found  growing  in  living  tissue.  "The  cells  may  either  break  up  into  a 
detritus,  with  fragmentation  of  the  nuclei,  or  they  may  become  changed 
into  refractive  hyaline  masses.  An  inflammatory  exudation  rich  in 
fibrin  factors  comes  from  the  tissue  below,  and  fibrin  is  formed  when  this 
comes  in  contact  with  the  necrotic  epithelium.  The  fibrin  in  part  is 
formed  into  a  reticulum  around  exudation  cells  and  degenerated  epi- 
thelium, in  part,  it  combines  with  the  hyaline  degenerated  cells  to  form 
a  hyaline  membrane.  It  is  probable  that  a  hyaline  membrane  may 
be  formed  without  the  exudation;  in  this  case  the  network  of  the  mem- 
l)rane  represents  the  edges  of  the  cells,  and  the  spaces  the  former 
nuclei.  The  hyaline  membrane  is  most  often  formed  on  those  surfaces 
which  are  covered  with  epitheliiuii  having  several  layers  of  cells.  It 
may  be  formed  by  a  hyaline  degeneration  of  exudation  cells;  in  this 
case  the  spaces  in  the  meshwork  are  smaller.  It  is  probable  that  the 
fibrinous  membrane  is  formed  both  on  the  surfaces  and  in  the  tissue. 


134  BACTERIAL  INFECTIONS 

The  fibrin  is  first  formed  around  cells  that  afterward  disappear.  In 
the  trachea  the  fibrinous  membrane  often  has  a  definite  structure. 
The  membrane  may  disintegrate  and  be  broken  up  into  a  mass  of 
detritus  (the  process  commences  on  the  surface),  or  it  may  be  cast 
off  as  a  whole  by  being  elevated  by  an  exudation  beneath.  Very 
thick  masses  of  membrane  may  be  formed  by  the  constant  addition  of 
fibrinous  exudation.  The  membrane  is  never  formed  primarily  on  an 
intact  epithelial  surface,  but  it  may  extend  over  it.  Nothing  is  to 
be  gained  by  making  an  anatomical  distinction  between  a  croupous 
and  a  diphtheritic  membrane.  .  .  .  The  membrane  formation 
is  accompanied  by  changes  in  the  tissue  beneath,  which  represent  a 
combination  of  degeneration  and  exudation.  The  connective  tissue 
and  bloodvessels  undergo  a  hyaline  fibrinoid  degeneration  very  similar 
to  the  degeneration  of  the  epithelium.  Necrosis  may  extend  deeply 
into  the  tissue,  but  there  is  little  tendency  to  deep  ulceration  or  abscess 
formation.  The  degeneration  in  the  mucous  glands  of  the  tissue  is 
so  pronounced  as  to  be  almost  specific.  Marked  degeneration  of  the 
epithelium  of  the  glands  may  be  found  without  any  change  in  the 
surrounding  tissue." 

The  organs  in  general  show  lesions  common  to  most  of  the  toxemias. 
In  the  kidneys  the  lesions  vary  from  cloudy  swelling  to  severe  nephritis. 
In  the  liver  the  degenerative  changes  are  not  so  marked,  nor  are  they 
specific.  The  spleen  is  sometimes  enlarged.  The  lymph  nodes, 
especially  those  nearest  the  primary  lesions,  show  changes — of  two 
kinds:  (1)  Congestion,  hemorrhage,  and  diffuse  and  circumscribed 
necrosis — found  in  many  conditions;  and  (2)  foci  of  proliferation, 
phagocytosis,  and  degeneration,  resembling  tubercles — distinctive  of 
diphtheria,  but  found  also  in  other  conditions.  Degeneration  of  the 
myocardium  is  common;  it  is  usually  fatty,  sometimes  hyaline.  Acute 
interstitial  myocarditis,  endocarditis,  and  pericarditis  also  occur. 
Bronchopneumonia  (acinous  pneumonia.  Councilman,  Mallory,  and 
Pearce)  is  found  in  more  than  half  of  the  fatal  cases.  Peripheral  neu- 
ritis (cranial  and  spinal)  is  common  and  answerable  for  many  of  the 
serious  sequels.  Poliomyelitis  and  hemorrhage  into  the  cord  and 
membranes  are  also  encountered. 

As  already  stated,  general  infection  with  the  diphtheria  bacillus 
(contrary  to  former  opinions)  is  not  uncommon,  especially  in  the  fatal 
cases;  but  in  these  cases  there  is  usually  also  associated  infection  with 
the  streptococcus  (the  most  important  and  most  common),  the  staphy- 
lococcus, the  pneumococcus,  etc.  These  organisms  are  also  frequently 
found  associated  with  the  diphtheria  bacillus  in  the  local  lesions  in  the 
throat  and  in  the  complications,  especially  the  bronchopneumonias 
and  the  suppurations.  These  cases  of  mixed  infection  are  often  unusu- 
ally severe  clinically,  and  not  infrequently  terminate  fatally — the  one 
bacterium  apparently  assisting  the  other  in  producing  the  severe  mani- 
festations of  the  infection. 


DIPHTHERIA  135 

Variations  in  Virulence  of  the  Diphtheria  Bacillus — Avirulent  Diphtheria 
Bacilli. — I  have  already  said  that  the  diphtheria  baciUi  may  be  found 
in  the  throats  of  healthy  persons,  and,  sometimes  for  a  long  time,  in 
the  throats  of  convalescents.  It  is  sometimes  found  also  in  throats 
in  which  the  lesions  are  only  a  mild  catarrhal  tonsillitis  or  faucitis  or 
a  lacunar  tonsillitis.  The  diphtheria  bacilli,  thus,  vary  considerably 
in  virulence:  some  are  slightly,  if  at  all,  virulent,  that  is,  they  produce 
little  if  any  toxin  (attenuated  bacilli);  others  are  more  virulent,  but 
the  resistance  of  the  individual  is  good  and  he  escapes  serious  infec- 
tion, though  he  may  transmit  serious  and  even  fatal  infection  to  others 
or  give  rise  to  a  more  or  less  widespread  epidemic.  In  other  cases 
bacilli  are  found  that  resemble  the  diphtheria  bacillus  more  or  less 
closely  morphologically,  but  differ  from  it  biologically — bacilli  often 
ill-advisedly  spoken  of  as  the  pseudodiphtheria  bacillus,  Bacillus 
xerosis  (found  in  the  healthy  and  diseased  conjunctiva),  and  bacilli 
found  also  in  many  other  places  and  conditions. 

Diphtheroid  Infections. — ^Vllereas  the  diphtheria  bacillus  is  the  most 
common  cause  of  pseudomembranous  inflammation,  it  is  absent  in 
some  cases,  the  causative  agent  being  usually  the  streptococcus,  occa- 
sionally the  pneumococcus,  the  staphylococcus,  and  sometimes  appar- 
ently other  organisms  ill  understood  and  cultivated  with  difficulty, 
if  at  all,  in  artificial  media  (such  as  Vincent's  bacillus,  etc.).  The 
preferable  designation  for  these  conditions  is  streptococcic,  pneumo- 
coccic,  or  staphylococcic  angina,  tonsillitis,  faucitis,  etc.  In  view,  how- 
ever, of  the  occurrence  of  necrosis  and  fibrinous  exudation  they  are 
not  infrequently  confounded  with  true  diphtheria,  and  are  sometimes 
spoken  of  as  pseudodiphtheria,  secondary  diphtheria,  diphtheroid, 
etc.  Diphtheroid  infection  is  the  least  objectionable  of  these,  but  it 
should  be  replaced  by  the  other  terms  suggested.  Thus,  there  is  not 
infrequently  a  discrepancy  between  the  clinical  and  the  bacteriological 
diagnosis,  some  cases  clinically  diphtheria  are  provoked  by  other  micro- 
organisms, and  certain  other  cases  clinically  very  mild,  with  little, 
if  any,  membrane,  are  examples  of  true  diphtheria.  The  many  note- 
worthy additions  to  our  knowledge  during  recent  years,  however,  have 
led  to  a  gradual  revision  of  our  conception  of  many  morbid  processes, 
and  to  the  establishment  of  certainty  and  exact  knowledge  where  formerly 
uncertainty  and  doubt  were  common ;  witness,  for  instance,  the  practical 
abandonment  of  the  idea  of  "croup"  as  a  distinct  and  separate  entity. 

These  diphtheroid  (streptococcic,  staphylococcic,  pneumococcic,  etc.) 
infections  or  inflammations  may  occur:  (1)  As  independent  disorders, 
varying  much  in  frequency,  but  sometimes,  according  to  Park  and 
Beebe,  constituting  as  much  as  40  per  cent,  of  the  then  existing  sore 
throats.  They  are  only  slightly  (if  at  all)  contagious;  the  symptoms, 
as  a  rule,  are  much  milder  than  those  of  true  diphtheria,  and  the 
mortality  is  much  less — not  more  than  2.5  per  cent.  (Park  and  Beel)e). 
(2)  As  secondary  infections  in  several  of  the  infectious  diseases,  especially 
scarlatina,  measles,  pertussis,  typhoid  fever,  etc.     The  symptoms  are 


136  BACTERIAL  INFECTIONS 

often  severe,  and  through  the  supervention  of  general  pyococcic  infection 
not  infrequently  lead  to  death.  Of  course,  true  diphtheria  also  may 
complicate  any  of  these  or  other  infectious  diseases. 

Symptoms. — ^The  period  of  incubation  in  true  diphtheria  varies  from 
two  to  seven  days,  but  in  severe  infections  it  may  be  scarcely  more  than 
twenty-four  hours.  As  a  rule,  prodromes  are  slight  or  absent — consist- 
ing, when  present,  of  general  indisposition  and  disinclination  to  play, 
and  possibly  headache.  The  onset  of  the  disease  is  usually  gradual, 
the  child  complaining  of  increasing  headache,  apathy,  general  neuro- 
muscular pains  and  aching,  slight  chilliness,  and  fever  which  soon 
reaches  102°  to  103°  F.  Occasionally  the  onset  is  abrupt — wdth  con- 
vulsions or  vomiting  and  fever  (103°  to  104°  F.).  The  subsequent 
local  and  general  manifestations  of  the  infection  vary  considerably, 
depending  upon  the  virulence  of  the  microorganisms,  the  localization 
of  the  process,  and  the  local  and  general  resistance  of  the  patient. 

In  pharyngeal  or  faucial  diphtheria  there  is  usually  more  or  less 
complaint  of  sore  throat  or  of  pain  on  swallowing;  but  in  many  cases 
the  absence  of  such  complaint  is  noteworthy.  On  inspecting  the 
throat  (a  procedure  that  should  never  be  neglected  in  sick  children) 
the  tonsils  are  found  swollen,  reddened,  often  peculiarly  cyanotic, 
and  a  small  patch  of  false  membrane — ^whitish,  grayish,  or  fawn-colored 
— may  be  visible.  This  forms,  as  a  rule,  first  on  one  or  the  other  tonsil, 
but  soon  involves  adjacent  structures.  In  some  cases  the  pseudo- 
membrane  remains  for  some  time  undetected,  having  formed  in  regions 
not  apparent  to  inspection,  such  as  the  posterior  surface  of  the  uvula, 
the  recesses  of  the  faucial  pillars,  etc.  In  these  cases  the  disease,  for 
the  time  being,  is  scarcely  to  be  distinguished  from  an  ordinary  ton- 
sillitis. 

In  mild  cases  the  membrane  remains  confined  to  the  tonsils,  the 
uvula,  and  the  soft  palate.  Frequently  it  may  be  removed  with  little 
loss  of  substance  (or  bleeding),  but  usually  attempts  to  remove  it  result 
in  exposing  a  raw-looking,  bleeding  surface — which  soon  becomes 
recovered.  The  fever  is  moderate  (102°  F.),  the  pulse  somewhat 
accelerated  (about  100  in  children  three  or  four  years  of  age);  the  sub- 
maxillary glands  are  slightly,  if  at  all,  swollen,  and  the  evidences  of  general 
intoxication  are  slight.  There  is  usually  a  moderate  leukocytosis  and  a 
trace  of  albumin  in  the  urine.  At  the  end  of  four  to  six  days  the  fever 
begins  to  subside,  and  the  membrane  to  shrivel,  to  curl  up  at  the  edge, 
and  gradually  to  separate.  By  the  eighth  or  ninth  day  it  is  usually 
gone,  but  the  surface  may  remain  red  and  inflamed  for  some  time. 

In  cases  of  moderate  severity,  the  false  membrane  is  more  widespread 
and  deeper,  inflammatory  oedema  and  congestion  are  more  marked, 
the  submaxillary  glands  are  considerably  swollen,  the  appetite  is  lost, 
the  fever  is  high  (103°  to  104°  F.),  the  pulse  is  rapid  (110  to  120),  the 
urine  is  lessened  in  amount  and  contains  albumin  and  casts,  prostration 
is  quite  marked,  and  the  child  is  more  or  less  restless  and  delirious. 


DIPHTHERIA  137 

These  cases  not  infrequently  eventuate  in  death,  but  recovery  may 
ensue  at  the  end  of  ten  days  or  two  weeks. 

In  severe  cases  (maHgnant  diphtheria)  the  child  is  usually  quite  ill  from 
the  beginning  (but  cases  beginning  mildly  may  become  severe) ;  vomiting, 
convulsions,  and  high  fever  may  usher  in  the  attack.  The  pharyngeal 
tissues  become  intensely  oedematous,  reddened,  and  swollen,  the  tonsils 
often  meeting  in  the  median  line ;  the  f aucial  tissues  become  covered  with, 
apparently  converted  into,  a  grayish,  brownish,  or  greenish-black,  ragged, 
malodorous  membrane  or  slough-like  mass;  a  fetid,  watery,  or  sanious 
discharge  issues  from  the  nostrils  and  the  mouth;  the  submaxillary  and 
other  regional  lymph  nodes  become  much  swollen  and  assist  in  quite 
fixing  the  jaw;  the  face,  later  the  neck  and  chest,  become  swollen  and 
oedematous,  and  in  some  cases  a  pallid  lividity  of  the  general  integument 
supervenes.  The  fever  may  be  quite  high  or  remarkably  low,  even  per- 
sistently subnormal  (bad  prognostically) ;  the  pulse  is  rapid,  irregular, 
and  weak,  the  respirations  embarrassed  and  noisy  (open  mouth  and 
obstructed  throat);  the  urine  is  much  diminished  in  amount  and  con- 
tains much  albumin  and  many  casts;  and  marked  prostration,  stupor, 
and  delirium  develop.  An  erythematous  or  purpuric  rash  is  not 
uncommon;  hemorrhages  may  issue  from  the  nose  or  mouth,  and  con- 
tribute to  a  speedy  fatal  issue ;  or  extensive  sloughing  and  gangrene 
of  the  neck  (Ludwig's  angina)  may  ensue.  Death  usually  results  in 
from  three  to  eight  days  from  toxemia,  cardiac  and  vasomotor  paralysis, 
or  certain  complications. 

Nasal  diphtheria  may  occur  as  a  primary  disorder  and  later  spread 
to  the  throat,  or  it  may  develop  secondarily  to  faucial  diphtheria.  It 
may  be  mild,  severe,  or  malignant  in  type.  There  may  be  little  if  any, 
membrane — only  a  profuse  serosanguineous  discharge,  which  quite 
naturally  excoriates  the  upper  lip  (formerly  believed  to  be  of  much  diag- 
nostic significance) ;  or  the  membrane  may  be  so  marked  as  completely 
to  occlude  the  nares.  Glandular  enlargement  is  usually  marked  (o wing- 
to  the  rich  lymphatic  supply  of  the  nose),  and  the  constitutional  dis- 
turbances (prostration,  albuminuria,  delirium,  etc.)  are  usually  severe. 
In  most  cases  of  pharyngeal  diphtheria  the  diphtheria  bacillus  may  be 
cultivated  from  the  nasal  secretions,  even  in  the  absence  of  noteworthy 
lesions  in  the  nose. 

Fibrinous  rhinitis  is  a  curious  disorder,  subacute  or  chronic  in  course, 
characterized  by  recurring  thick  fibrinous  exudation,  benign  in  nature, 
and  attended  by  slight  constitutional  disturbance — but  due  in  SO  per 
cent,  of  the  cases  (Ravenel's  collection  of  statistics)  to  the  diphtheria 
bacillus. 

Laryngeal  diphtheria  (formerly  so-called  membranous  croup)  develops 
usually  secondarily  to  pharyngeal  diphtheria,  but  it  may  occur  as  a 
primary  disorder,  and,  as  previously  mentioned,  laryngeal  lesions  are 
the  most  common  in  the  fatal  cases.  In  the  majority  of  cases,  the 
symptoms  in  the  beginning  are  not  unlike  those  of  pharyngeal  diphtheria 
— but  the  voice   soon   becomes   hoarse,  a  rough,  brassy,  or  "croupy" 


138  BACTERIAL  INFECTIONS 

cough,  develops,  and  the  respirations  become  embarrassed.  At  the 
end  of  twenty-four  or  forty-eight  hours,  commonly  at  night  at  first, 
evidences  of  laryngeal  or  bronchial  obstruction  (stenosis)  develop  sud- 
denly. At  first  these  are  often  paroxysmal  (spasm  of  the  glottis), 
but  later  they  become  continuous  (increasing  mechanical  obstruction). 
The  inspiratory  and  expiratory  efforts  are  attended  by  unusual  efforts ; 
they  become  loud  and  stridulous,  and  are  associated  with  retraction 
(on  inspiration)  of  the  intercostal  spaces  and  the  epigastrium;  the 
child  becomes  extremely  restless  and  makes  extraordinary  efforts  to  get 
air,  and  becomes  cyanotic  and  markedly  prostrated.  In  the  beginning 
these  attacks  sometimes  subside  spontaneously;  in  other  cases  they  are 
relieved  by  coughing  and  the  expelling  of  a  portion  of  false  membrane 
(sometimes  casts  of  the  larynx  or  a  bronchus);  in  most  cases,  how- 
ever, unless  relieved,  the  dyspnoea  and  cyanosis  become  aggravated  and 
continuous,  restlessness,  which  at  first  becomes  more  marked,  is  gradually 
replaced  by  stupor  and  coma,  prostration  increases,  and  the  child  dies 
of  asph^Tiiation.  In  some  cases,  in  which  the  false  membrane  extends 
to  the  bronchi,  death  from  suffocation  may  be  comparatively  slow. 
If  the  pharynx  is  not  much  involved,  the  evidences  of  toxemia  at  first 
are  slight  (on  account  of  the  poor  lymphatic  supply  of  the  larynx),  the 
fever  is  slight  or  moderate,  and  the  general  condition  of  the  child  is  good 
— until  the  onset  of  the  laryngeal  obstruction.  In  laryngeal  diphtheria, 
therefore,  there  is  usually  a  marked  disproportion  between  the  severity 
of  the  local  and  the  general  symptoms. 

Wound  diphtheria  occasionally  occurs — when  the  diphtheria  bacilli 
become  implanted  in  a  wound;  but  not  all  membranous  inflammations 
of  wounds  are  diphtheritic.  Diphtheria  occasionally  occurs  also  on 
other  mucous  membranes,  such  as  the  conjunctiva,  the  vulva,  vagina, 
anus,  etc.,  and  as  a  primary  or  a  secondary  infection. 

Complications  and  Sequels. — The  most  important  complications 
(due  usually  to  pyogenic  organisms  associated  or  not  with  the  diph- 
theria bacillus)  are:  Severe  and  even  fatal  hemorrhage  from  the  nose 
and  throat;  bronchitis,  bronchopneumonia  (acinar  pneumonia),  and 
pulmonary  atelectasis;  suppuration  of  the  lymph  nodes;  otitis 
media  and  disorder  of  the  accessory  sinuses  of  the  nose;  Ludwig's 
angina;  cutaneous  rashes  (erythema,  urticaria,  purpura,  gangrene); 
endocarditis;  arthritis  (simple  and  suppurative);  suppression  of  urine 
and  nephritis;  general  pj^emia  with  metastatic  abscess  formation 
(secondary  pyococcic  infection).  Diphtheria  may  also  complicate 
certain  of  the  infectious  diseases,  especially  scarlatina,  pertussis,  measles, 
typhoid  fever,  tuberculosis,  etc. 

The  most  important  sequels  are  the  paralyses — which  occur  in  about 
20  per  cent,  of  the  non-fatal  cases,  are  due  to  a  toxic  peripheral  neuritis, 
and  occur  usually  during  the  second  or  the  third  week  of  convalescence, 
though  they  may  come  on  as  early  as  the  seventh  or  eighth  day  of  the 
disease.  The  most  common  are:  Paralysis  of  the  palate  (return  of 
fluids  through  the  nose,  difficulty  in  swallowing,  a  nasal  quality  to  the 


DIPHTHERIA  139 

voice,  relaxation  and  impaired  sensation  of  the  palate) ;  of  the  internal 
muscles  of  the  eye  (paralysis  of  accommodation) ;  of  the  external  miLscles 
of  the  eye  (ptosis,  strabismus);  of  the  facial  muscles;  of  the  laryngeal 
muscles  (unilateral  or  bilateral);  of  the  extremities  or  trunk  (paresis, 
paresthesias,  incoordination,  loss  of  reflexes);  and  of  the  diaphragm. 
These  usually  subside  in  from  two  weeks  to  two  months.  The  most 
serious  paralysis  involves  the  heart  and  the  vasomotor  system.  This 
may  result  not  only  from  toxic  degeneration  of  the  nerves  supplying 
the  heart,  but  also  of  the  vasomotor  nerves,  and  from  toxic  myocarditis, 
heart  clot,  etc.  It  may  come  on  as  late  as  two  months  after  apparent 
convalescence,  and  may  follow  apparently  mild  attacks  of  diphtheria, 
though  it  is  more  common  after  severe  attacks.  Many  of  the  deaths 
occurring  during  the  course  of  diphtheria  are  due  to  this  cardiac  and 
vasomotor  paralysis.  The  pulse  is  often  slow  rather  than  rapid;  it 
becomes  weak,  the  temperature  sinks,  the  skin  becomes  pale,  and  the 
child  soon  dies.  During  convalescence  death  from  this  cause  may 
occur  suddenly,  and  entirely  unannounced;  it  not  infrequently  follows 
immediately  some  unusual  exertion.  It  is  sometimes  preceded  by 
a  warning  arrhythmia,  vertigo,  vomiting,  and  signs  of  cardiac  dilatation. 
Anemia  often  persists  for  a  long  time.  Nephritis,  laryngeal  stenosis, 
chorea,  etc.,  have  been  observed  as  sequels. 

Diagnosis. — In  many  cases  the  diagnosis  depends  upon  the  demon- 
stration of  the  diphtheria  bacillus — which  is  conclusive.  Provision 
for  the  ready  and  prompt  determination  of  the  bacteriological  factor 
in  cases  of  sore  throat  is  now  commonly  made  by  the  establishment  of 
municipal  and  State  laboratories ;  in  the  absence  of  these,  private  labora- 
tories are  usually  available.  But  what  is  still  better — the  physician 
should  train  himself  to  make  the  necessary  simple  examination.  A 
properly  prepared  cover-slip  preparation  will,  in  the  majority  of  cases, 
within  a  few  minutes  convert  doubt  into  certainty.  Cultures  also  should 
be  undertaken.  Such  examinations  should  be  made  in  all  cases  of  sore 
throat,  since,  as  already  mentioned,  many  cases  mild  clinically  are  truly 
diphtheritic  and  act  as  sources  of  infection.  In  the  event  of  doubt 
all  throat  disorders  in  children  should  be  regarded  as  diphtheritic, 
and  the  proper  prophylactic  and  curative  measures  should  be  instituted 
immediately.  Pending  the  detection  of  the  diphtheria  bacillus,  the 
presence  of  an  epidemic  (or  exposure  to  infection),  the  characteristic 
false  membrane,  a  sanious  discharge  from  the  nose  or  the  mouth,  swell- 
ing of  the  submaxillary  lymph  nodes,  and  albuminuria  are  of  much 
diagnostic  value. 

Streptococcic,  staphylococcic,  pneumococcic,  and  other  pseudo- 
membranous anginas  (such  as  Vincent's  angina,  etc.)  often  can  be 
excluded  only  by  bacteriological  examination;  but  in  these  the  onset  is 
usually  more  sudden  than  in  diphtheria,  the  fever  is  higher  and  of  shorter 
duration,  glandular  enlargement  is  less,  albuminuria  is  often  absent, 
there  is  less  tendency  for  the  lesions  to  spread  to  the  nose  and  the  larynx, 
and   there   is   no   history   of   exposure   to   diphtheritic   contagion.     In 


140  BACTERIAL  INFECTIONS 

scarlatina  the  throat  lesions  sometimes  become  "diphtheroid,"  and 
may  not  be  distinguishable  from  those  of  true  diphtheria  except  by 
bacteriological  examination.  Diagnostic  difficulties  are  sometimes 
enhanced  by  an  erythematous  rash  that  occasionally  occurs  in  diph- 
theria. However,  this  is  uncommon,  and  is  darker  and  of  shorter  dura- 
tion than  the  true  scarlatinous  rash,  and  it  is  usually  confined  to  the 
trunk.  The  two  diseases  not  infrequently  co-exist.  In  follicular  ton- 
sillitis the  exudate  is  yellowish  (rather  than  grayish  or  fawn-colored), 
patchy  (corresponding  to  the  follicles),  is  separated  by  intervening- 
areas  of  congested  red  tonsillar  tissue,  does  not  tend  to  spread  beyond 
the  tonsils,  may  be  removed  without  leaving  a  bleeding  surface,  and 
does  not  tend  to  reform  (as  in  diphtheria).  Spasmodic  laryngitis, 
"false  croup,"  "spasmodic  croup"  can  scarcely  be  confounded  with 
diphtheritic  laryngitis  ("true  croup"). 

Prognosis. — The  prognosis  varies  with  the  severity  of  the  infection, 
the  reaction  of  the  individual,  the  presence  or  absence  of  complications, 
and  especially  with  the  treatment  adopted.  In  some  epidemics  the 
death  rate  has  been  as  high  as  50  per  cent.  Since  the  introduction  of 
antitoxin  it  has  been  reduced  at  least  one-half;  and  in  some  large  series 
of  cases  the  prompt  use  of  antitoxin  has  reduced  the  mortality  to  between 
10  and  15  per  cent.  The  prognosis  is  poorer  in  very  young  children, 
in  the  event  of  laryngeal  and  nasal  involvement,  marked  toxemia,  heart 
weakness,  etc.  The  most  marked  discrepancies  sometimes  occur 
between  the  severity  of  the  local  lesions  and  the  degree  of  systemic 
toxemia:  minor  local  lesions  are  sometimes  attended  by  very  serious 
general  manifestations;  in  some  cases  the  patient  is  overwhelmed  with  the 
toxemia  and  dies  within  a  day  or  two — before  the  local  lesions  have  become 
noteworthy;  while  in  still  other  cases  well-marked  and  even  extensive 
local  lesions  run  their  course  without  evidence  of  serious  intoxication. 

Treatment.— Isolation  and  prophylactic  measures  of  the  strictest 
sort  should  be  carried  out  (page  29).  Special  attention  should  be 
directed  to  mild  cases,  ambulatory  cases,  convalescents  (in  whose  throats 
virulent  bacilli  may  remain  for  from  six  weeks  to  six  months  or  more 
after  the  attack),  and  to  attendants  upon  the  sick.  Catarrhal  disorders  of 
the  nasopharynx,  especially  in  children,  should  be  corrected.  Children 
exposed  to  infection  should  be  required  to  use  mild  antiseptic  nasal, 
oral,  and  pharyngeal  washes  (boric  acid,  potassium  permanganate 
0.5  to  1  per  cent.,  mercuric  bichloride  1  to  10,000),  and  should  be  given 
a  prophylactic  dose  of  antitoxin,  200  to  500  or  1000  units,  depending 
upon  its  age. 

The  general  hygienic  and  dietetic  management  of  the  developed 
disease  is  similar  to  that  appropriate  in  the  other  infectious  diseases 
in  children.  It  is  important,  however,  that  the  diet  throughout  should 
be  fluid,  concentrated,  and  readily  digested.  In  the  event  of  intubation 
or  tracheotomy  being  necessary,  rectal  alimentation  may  be  required. 

The  diagnosis  of  diphtheria  brings  with  it  the  imperative  indication 
for  the  use  of  the  specific  remedy — antitoxin.     Even  in  case  of  doubt 


DIPHTHERIA  141 

as  to  the  true  nature  of  a  throat  disorder  it  is  wise  to  administer  dipli- 
theria  antitoxin — since  in  the  event  of  the  disease  proving  to  be  diph- 
theria the  proper  remedy  has  been  administered  at  the  most  opportune 
moment,  an,d  in  the  event  of  its  proving  to  be  non-diphtheritic  in  nature, 
no  harm  has  been  done  (indeed,  possibly  some  good).  The  proper 
dose  of  antitoxin  is  that  sufficient  to  insure  the  desired  resuU;  it  is 
much  better  to  give  more  than  is  really  necessary  than  too  little.  In 
mild  cases  in  children  over  two  years  of  age,  3000  to  4000  units,  and 
in  severe  (including  laryngeal)  cases  4000  to  8000  units  should  con- 
stitute the  initial  dose.  This  should  be  repeated  in  from  six  to  eight 
hours  if  the  swelling  and  congestion  are  not  lessened,  and  the  membrane 
seems  to  maintain  its  tenacious  hold,  and  in  from  four  to  six  hours, 
if  the  local  lesions  seem  to  be  progressive  and  the  membrane  to  be 
spreading.  In  some  cases  a  third  dose  may  be  required  at  the  end 
of  four  to  eight  hours,  or  after  the  lapse  of  twenty-four  or  thirty-six 
hours;  and  in  a  few  cases,  even  a  larger  number  of  doses.  Dr. 
McCollom,  of  Boston,  has  obtained  the  most  gratifying  results,  in 
apparently  hopeless  cases,  by  using  as  much  as  70,000  units.  Large 
doses  given  early  usually  obviate  the  necessity  of  using  antitoxin  at  the 
end  of  a  week  or  thereabout  after  the  first  dose,  and  thus  remove  all 
possibility  of  producing  anaphylaxia.  The  use  of  globulin  preparations 
(from  which  some  of  the  non-antitoxic  serum  substances  have  been 
removed)  tends  to  lessen  the  likelihood  of  disagreeable  rashes  developing. 
The  antitoxin  should  be  injected  into  the  trunk  or  the  thigh,  and 
as  early  as  possible  (even  pending  the  bacteriological  report) ;  but  it  is 
important  to  administer  it  no  matter  when  nor  how  late  the  child  comes 
under  observation.  The  following  statistics  collected  by  Cohn  illustrate 
the  results  of  antitoxin  treatment  as  influenced  by  the  day  on  which  it 
is  commenced: 

Per  cent. 

Patients.  mortality. 

First  day 78  13 

Second  day 361  11.1 

Third  day 284  10.5 

Fourth  day 101  24.7 

Later  and  unknown 186  22.7 

Striking  results  often  follow  the  use  of  the  antitoxin.  When  admin- 
istered early,  at  the  end  of  ten  or  twelve  hours,  the  fever  often  abates, 
the  local  inflammatory  oedema  and  congestion  lessen,  the  pseudo- 
membrane  begins  to  curl  up  at  the  edge  and  soon  loosens,  and  the  evi- 
dences of  toxemia  diminish.  In  some  cases,  aside  from  anemia  and 
weakness,  the  patient  is  cjuite  convalescent  in  two  or  three  days.  The 
local  lesions,  however,  are  of  more  significance  as  suggesting  the  renewed 
use  of  antitoxin  than  the  general  manifestations,  ^^^len  the  antitoxin 
is  administered  late,  the  results  are  not  so  striking,  but  the  severity  of 
the  local  lesions  and  the  general  infection  are  midoubtedly  mitigated; 
many  patients  who  otherwise  would  require  it  are  spared  intubation 
3,nd   tracheotomy;  many   in   whom   otherwise    tracheotomy   would    be 


142  BACTERIAL  INFECTIONS 

required  recover  with,  intubation;  the  intubation  tube  may  be  removed 
much  earlier  than  in  pre-antitoxin  days;  and  the  mortality  of  intuba- 
tion and  tracheotomy  cases  is  reduced  one-half.  The  antitoxin,  being 
a  specific  remedy,  does  not  influence  the  lesions  due  to  associated  organ- 
isms (streptococci,  staphylococci,  pneumococci,  etc.),  nor  does  it  pre- 
vent complications  and  sequels,  except  in  so  far  as  it  influences  and 
mitigates  the  severity  of  the  primary  diphtheritic  infection. 

Local  treatment  is  advisable  in  most  all  cases,  but  it  must  be  employed 
with  discretion.  The  best  treatment  for  the  local  lesions  is  the  antitoxin 
internally;  with  no  other  remedy  at  our  command  are  we  so  well  able  to 
destroy  the  diphtheria  bacilli  in  the  mouth,  nose,  and  throat.  Cleanli- 
ness, therefore,  is  the  main  object  of  local  treatment.  The  best  local 
treatment  consists  of  irrigation  through  the  nose  or  mouth,  with  a  foun- 
tain syringe  or  a  hand  syringe,  using  physiological  saline  solution  (than 
which  nothing  is  better),  or  mild  antiseptic  solutions,  such  as  boric  acid; 
potassium  permanganate,  1  per  cent.;  hydrogen  dioxide,  10  to  20  per 
cent.;  carbolic  acid,  0.3  to  0.5  percent.;  mercuric  bichloride,  1  to  10,000; 
formalin,  0.5  to  1  per  cent.,  etc.  These  may  be  used  every  hour  or  two, 
depending  upon  the  severity  of  the  local  lesions  and  the  resistance  of 
the  child,  remembering  that  the  possible  good  that  may  be  thus  achieved 
may  be  more  than  counterbalanced  by  enfeebling  results  of  the  child's 
struggling.  Sprays  are  likely  to  frighten  the  child,  and  are  thus  some- 
times objectionable.  Many  physicians  are  partial  to  applications 
applied  directly  to  the  lesions  on  a  swab;  these  often  render  good  ser- 
vice, but  should  never  be  entrusted  to  other  than  trained  hands — 
the  physician  or  a  trained  nurse.  The  best  preparation  is  Loffler's 
solution:  Menthol,  10;  toluol,  36;  solution  of  iron  chloride,  4;  and 
absolute  alcohol,  60.  The  more  old-fashioned  preparation,  consisting 
of  tincture  of  iron  chloride,  3;  carbolic  acid,  0.5;  glycerin,  15;  and  water, 
15,  is  also  excellent.  Digestants  such  as  papain  and  trypsin,  etc., 
have  been  recommended,  but  I  have  not  much  faith  in  their  efficacy. 
Gargles  are  of  little  use,  since  usually  they  do  not  reach  the  place 
where  their  action  is  desired. 

In  the  event  of  laryngeal  diphtheria,  much  good  results  from  the 
inhalation  (by  means  of  a  steam  tent  or  croup  tent)  of  steam,  medicated 
with  salt,  lime,  or  compound  tincture  of  benzoin,  or  the  inhalation 
of  the  fumes  of  subliming  calomel.  External  applications  to  the  throat, 
hot  and  cold,  are  sometimes  grateful,  but  they  as  frequently  annoy 
and  embarrass  the  patient  as  they  help  him.  If  symptoms  of  laryngeal 
obstruction  develop,  and  the  child  is  not  too  weak,  the  effects  of  vomiting 
at  dislodging  the  false  membrane  may  be  tried:  syrup  of  ipecac,  ^  to 
1  ounce  (15  to  30  c.c);  tartar  emetic,  ^  grain  (0.03  gram),  hot  mustard 
water,  etc.  If  no  relief  follows,  intubation  should  not  be  delayed, 
and  it  should  always  be  undertaken  if  dyspnoea,  cyanosis,  and  restless- 
ness are  increasing,  and  if  retraction  of  the  interspaces  and  of  the  epigas- 
trium shows  the  difficulty  the  child  experiences  in  breathing.  If  intuba- 
tion does  not  afford  relief,  tracheotomy  must  be  performed. 


INFLUENZA  143 

Alcohol  seems  to  be  a  very  serviceable  remedy,  especially  when  the 
infection  is  severe,  the  prostration  marked,  and  the  first  sound  of  the 
heart  has  become  weak.  It  may  be  given  in  doses  varying  from  one 
to  six  ounces  in  the  twenty-four  hours.  Strychnine  also  is  valuable  in 
some  cases.  The  common  heart  tonics  are  not  of  much  value,  though 
apparently  indicated  on  superficial  observation;  but  in  the  event  of 
collapse  of  the  circulation  they  may  be  tried,  especially  the  more  diffu- 
sible stimulants.  Previous  to  antitoxin  days,  tincture  of  iron  chloride, 
calomel  and  other  preparations  of  mercury,  quinine,  etc.,  enjoyed  con- 
siderable reputation;  they  are  sometimes  valuable  adjuncts,  and  are 
especially  serviceable  during  convalescence  (particularly  the  iron). 

The  complications  are  to  be  treated  on  general  principles.  Prolonged 
rest  in  bed  (three  to  six  weeks)  during  convalescence  is  essential. 


INFLUENZA. 

(La  Grippe;  Grip;  Epidemic  Catarrhal  Fever.) 

Influenza  is  an  acute  specific,  infectious,  and  moderately  contagious 
disease  caused  by  Bacillus  influenzae  (Pfeiffer),  and  characterized  by 
fever,  catarrh  of  the  respiratory  and  the  gastro-intestinal  mucous  mem- 
brane, severe  neuromuscular  pains,  and  marked  prostration. 

Etiology. — Although  influenza  is  prone  to  attack  adults,  no  age  is 
exempt,  and  the  sexes  are  affected  about  equally.  While  the  most 
robust  persons  are  frecjuently  attacked,  the  disease  finds  its  readiest 
victims  among  those  debilitated  by  any  cause,  as  well  as  among  the 
aged,  in  whom  it  is  frequently  fatal.  It  usually  prevails  epidemically, 
especially  during  the  late  fall  and  the  winter,  and  has  been  practically 
pandemic  since  1889-90.  The  local  epidemic  visitation  of  the  disease 
continues  about  six  or  eight  weeks,  during  which  time  an  extremely 
large  proportion  of  the  population  may  be  affected.  One  attack  does 
not  confer  immunity,  since  relapses  are  common.  Some  persons  seem 
to  be  more  or  less  immune  naturally. 

The  exciting  cause  of  the  disease  is  Bacillus  influenzae,  which  may 
be  found  in  the  mucous  discharges,  and  in  the  lungs  and  other  organs 
in  the  event  of  complications.  The  disease  is  moderately  contagious, 
infection  being  transmitted  by  direct  contact,  possibly  by  a  third  person, 
and  by  fomites;  but  the  unusually  large  number  of  persons  affected 
almost  simultaneously  is  attributable  to  widespread  aerial  dissemination 
of  the  bacillus.  In  some  epidemics  the  infection  appears  to  have  been 
spread  by  the  ordinary  channels  of  commercial  intercourse.  Infection  is 
acquired  by  inhalation. 

Pathology. — Influenza  is  devoid  of  characteristic  lesions,  the  lesions 
found  consisting  of  catarrhal  inflammation  of  the  respiratory  antl  the 
gastro-intestinal  tract,  and  rarely  of  enlargement  of  the  lymph  follicles 
of  the  intestine  and  of  the  spleen.  The  complicating  lesions  exhibit 
nothing  specific. 


144  BACTERIAL  INFECTIONS 

Symptoms. — The  period  of  incubation  is  usually  two  to  four  days. 
The  onset  is  sudden,  with  severe  chill  or  chilliness,  high  fever  (often 
104°  to  105°  F.),  violent  headache,  especially  about  the  eyes  and  the 
root  of  the  nose,  severe  neuromuscular  pains  and  tenderness,  especially 
in  the  back  and  legs,  catarrh  of  the  respiratory  mucous  membrane, 
marked  prostration,  and  depression  of  spirits.  Depending  upon  the 
predominance  of  certain  symptoms  different  types  of  the  disease  are 
described,  but  all  gradations  between  the  different  t}"pes  occur:  (1) 
The  respiratory  type.  In  this,  symptoms  referable  to  catarrh  of  the 
respiratory  tract  are  marked — coryza,  conjunctivitis  with  excessive 
lacrymation,  sore  throat,  hoarseness,  harsh,  dry  cough.  Sometimes  the 
catarrh  is  more  marked  in,  or  confined  to,  the  upper  part  of  the  respira- 
tory tract,  sometimes  to  the  lower.  Occasionally  hemoptysis  is  obsen'ed. 
As  a  rule,  after  a  couple  of  days  there  is  a  little  mucous  expectoration, 
and  the  usual  evidences  of  bronchitis.  As  convalescence  sets  in  the 
sputum  becomes  mucopurulent  in  character,  but  a  harsh  dry  cough 
often  persists  for  a  long  time.  (2)  Gastro-intestinal  type.  In  addition 
to  the  general  manifestations,  nausea  and  vomiting  sometimes  occur 
as  initial  symptoms;  later,  abdominal  pain  and  diarrhoea  are  common, 
and  sometimes  lead  to  collapse.  Jaundice  has  been  observed,  and  the 
spleen  may  be  enlarged.  (3)  Nervous  type.  In  this  the  catarrhal  symp- 
toms are  relatively  slight,  but  the  neuromuscular  pains,  cutaneous 
hyperesthesia,  sweating,  and  prostration  are  marked.  Delirium  and 
stupor  sometimes  supervene,  and  with  continuation  of  the  fever  a  typhoid 
state  (typhoid  type)  develops.  (4)  A  cardiac  type,  with  feeble,  rapid, 
and  irregular  pulse,  sometimes  progressing  to  serious  cardiac  embarrass- 
ment has  been  described.  (5)  A  muscular  or  so-called  rheumatoid  type, 
with  severe  pains  and  tenderness  in  the  back,  extremities,  and  joints 
may  occur.  (6)  A  hyperpyretic  type,  and  (7)  an  apyretic  t^-pe  also  have 
been  described. 

In  most  cases  the  initial  high  fever  remits  at  the  end  of  twentv-four 
hours,  and  subsequently  pursues  an  extremely  irregular  course,  varying 
much  in  different  cases.  As  a  rule,  it  falls  by  lysis  and  reaches  the  nor- 
mal in  from  three  or  four  to  eight  days,  but  recurrence  of  the  fever  on 
slight  provocation  is  quite  common.  With  the  decline  of  the  fever, 
the  severe  neuromuscular  pains,  the  headache,  and  the  catarrhal  symp- 
toms abate  and  the  patient  gradually  convalesces,  though  marked 
prostration  and  occasional  sweatings  may  continue  for  a  long  time, 
and  relapses  are  quite  common.  A  second  attack  may  occur  during 
the  same  epidemic. 

Complications. — Secondary  infections  are  common.  Although  there 
is  a  true  influenzal  pneumonia,  the  frequent  lobar  pneumonia  and 
bronchopneumonia  are  often  due  to  mixed  infection  with  the  pneu- 
mococcus  and  the  streptococcus.  Abscess  and  gangrene  of  the  lung  and 
pleuritis  have  been  observed.  Myocardial  weakness  and  irregularity 
of  the  heart  action  is  common,  and  may  last  for  a  long  time.  Brady- 
cardia also  occurs,     Endocarditis,   pericarditis,   and  thrombophlebitis 


BACILLARY  DYSENTERY  145 

are  less  common.  Divers  nervous  complications,  such  as  neuritis, 
meningitis,  encephalitis,  etc.,  as  well  as  nephritis,  otitis  media,  kera- 
titis, herpes  labialis  and  other  cutaneous  manifestations,  etc.,  have 
been  reported. 

Treatment. — Rest  in  bed  is  the  most  important'  feature  of  the  treat- 
ment, and  should  be  insisted  upon  even  in  the  mildest  cases  in  the 
event  of  fever,  since  convalescence  is  much  hastened  by  a  few  days' 
rest  in  bed,  and  the  likelihood  of  complications  and  of  sequels  is  much 
lessened.  The  patient  should  be  isolated,  if  possible,  and  the  mucous 
discharges  should  be  disinfected.  The  diet  should  be  light  and  easily 
assimilable.  Aside  from  these  measures  the  treatment  is  largely  symp- 
tomatic, but  should  be  always  supportive.  A  warm  bath  or  a  hot 
mustard  foot-bath,  with  an  initial  dose  of  Dover's  powder  (10  grains, 
0.6  gram)  and  a  hot  drink  at  night,  often  serve  to  relieve  the  distress. 
Additional  relief  may  be  afforded  by  any  of  the  following  every  two  or 
three  hours  for  the  first  day  or  two:  aspirin,  5  to  10  grains  (0.3  to 
0.6  gram);  quinine,  2  grains  (0.13  gram),  and  salicin,  5  grains  (0.6 
gram);  salol,  5  grains  (0.3  gram),  and  acetphenetidin,  2  grains  (0.13 
gram),  to  which  one  may  add  small  doses  of  Dover's  powder,  ^  to  ^ 
grain  (0.015  to  0.03  gram),  or  camphor  monobromate,  1  grain  (0.06 
gram).  Intense  headache  may  be  relieved  by  an  ice-bag,  caffeine,  or 
the  bromides.  Rarely,  especially  in  the  event  of  very  severe  headache 
and  of  severe  neuromuscular  pains,  it  seems  almost  necessary  to  resort 
to  the  coal-tar  products,  but  aside  from  the  small  doses  of  acetphenetidin 
already  mentioned,  their  use  must  be  attended  by  caution,  since  although 
they  may  relieve  the  subjective  complaints,  they  only  add  to  the  already 
existing  prostration.  In  many  cases,  stimulants  are  called  for,  of  which 
the  most  valuable  are  whiskey,  brandy,  and  especially  strychnine,  and 
the  aromatic  spirit  of  ammonium.  The  treatment  of  the  catarrhal 
symptoms  is  similar  to  that  suggested  in  acute  coryza  and  bronchitis. 
The  emunctories  always  recjuire  attention:  mild  diaphoretic  remedies 
are  valuable;  the  bowels  should  be  opened  freely;  and  the  urine  should 
be  rendered  copious  by  the  generous  use  of  water  and  mild  alkaline 
diuretics.  Especial  care  must  be  exercised  in  the  cases  of  elderly  sub- 
jects to  prevent  the  development  of  complications,  especially  of  broncho- 
pneumonia, the  cause  of  many  fatalities  in  the  aged.  During  convalescence 
strychnine  is  often  required  for  a  long  time,  and  the  persistent  irritating 
cough  without  expectoration  may  require  codeine  or  heroin. 


BACILLARY  DYSENTERY. 

Bacillary  dysentery  is  a  specific  infectious  disease,  caused  by  Bacillus 
dysenteriae  (Shiga),  and    characterized  by  abdominal    pain,   frequent 
intestinal  discharges  containing  mucus  and  blood,  and  a  specific  serum 
reaction. 
10 


146  BACTERIAL  INFECTIONS 

Etiology. — It  is  now  generally  believed  that  the  common,  especially 
acute,  dysentery  of  the  tropics  and  temperate  zones  is  due  to  Bacillus 
dysenterise,  an  organism  discovered  by  Shiga  and  later  studied  by  Flexner 
and  his  pupils.  Several  strains  of  the  bacillus  are  now  recognized, 
that  most  common  in  this  country  being  known  as  the  Flexner-Harris. 
The  especial  habitat  of  the  disease  is  the  tropics,  particularly  Japan,  the 
Philippines,  Porto  Rico,  etc.,  where  widespread  and  fatal  epidemics 
are  common;  but  sporadic  cases  occur  elsewhere  in  the  tropics  and  in 
practically  the  entire  temperate  zone,  and  epidemics  are  by  no  means 
infrequent,  especially  in  the  summer  and  fall.  General  insanitary 
conditions,  such  as  may  prevail  in  barracks,  jails,  asylums,  etc.,  materially 
favor  the  spread  of  the  infection,  which  also  is  one  of  the  notable  scourges 
of  camp  life  and  frequently  numbers  more  victims  than  the  military 
prowess  of  the  enemy  (our  own  Civil  War,  the  South  African  War,  etc.). 
How  the  infection  is  transmitted  is  not  definitely  known;  the  factors  are 
believed  to  be  similar  to  those  of  typhoid  fever.  The  bacillus  may  be 
cultivated  from  the  intestinal  discharges  and  the  blood,  and  from  the 
intestinal  contents  and  wall  after  death.  In  many  cases  they  persist  in 
the  intestinal  tract  for  a  long  time  after  apparent  recovery,  and  may  be 
cultivated  from  the  intestinal  discharges,  either  periodically  or  at  all 
times:  these  cases  constitute  the  so-called  "chronic  carriers,"  who  are 
responsible  for  many  epidemics.  Amoeba  coli  may  be  found  associated 
with  Bacillus  dysenterise  in  some  cases. 

Dysentery  is  rather  common  also  as  a  terminal  event  in  certain  wasting 
and  debilitating  disorders,  and  similar  symptoms  are  observed  sometimes 
to  follow  the  ingestion  of  unwholesome  food,  especially  unripe  or  over- 
ripe fruit,  certain  preformed  poisons,  etc.  The  summer  diarrhoeas  of 
children  also  are  often  due  to  Bacillus  dysenterise  infection. 

Pathology. — ^Two  types  of  the  disease  may  be  recognized,  the  acute 
and  the  chronic.  In  acute  cases  ending  fatally  within  a  week,  the  mucous 
membrane  of  the  large  intestine  is  markedly  swollen,  oedematous,  and 
hyperemic,  and  covered  with  blood-stained  mucus,  the  solitary  follicles 
are  enlarged,  foci  of  hemorrhage  are  present  in  the  mucosa  and  sub- 
mucosa,  and  the  superficial  layer  of  the  mucosa  (in  folds,  irregular 
patches,  or  larger  areas)  is  necrotic  and  may  be  readily  removed.  In 
more  severe  infections  the  entire  wall  of  the  large  intestine  is  very  much 
thickened  and  stiffened  (oedema,  congestion,  and  cellular  infiltration), 
and  the  mucosa  is  grayish  black  in  color — necrotic  or  gangrenous. 
Even  the  serous  coat  may  be  involved,  and  sometimes  the  ileum  shows 
more  or  less  well-advanced  lesions.  The  changes  in  the  mucosa  consist 
of  coagulation  necrosis  with  the  exudation  of  fibrin  and  polynuclear  leuko- 
cytes (pseudomembrane).  The  submucosa  shows  hemorrhages,  fibrin 
formation,  and  irregular  cellular  accumulations  (chiefly  plasma  cells); 
these  are  believed  to  be  toxic  in  nature,  since  they  may  be  present  with 
an  intact  mucosa,  and  bacteria,  as  a  rule,  are  not  encountered  amidst 
them.  Ulceration  does  not  occur,  any  loss  of  tissue  resulting  being  due  to 
exfoliation  of  necrotic  mucosa  and  attached  pseudomembrane.     Should 


BACILLARY  DYSENTERY  147 

the  patient  not  die,  the  acute  lesions  may  subside  or  they  may  become 
chronic.  Of  the  chronic  infection,  follicular,  diphtheritic,  and  gangren- 
ous forms  are  sometimes  described — which,  however,  are  merely  stages 
of  the  one  disorder.  In  the  milder  follicular  type  there  is  necrosis  and 
ulceration  of  the  solitary  follicles,  with  the  gradual  extension  of  the  proc- 
esses to  the  mucosa  and  submucosa  and  sometimes  the  muscular  coat — 
Avhence  superficial  and  often  deep  ulceration  results  (doubtless,  in  part 
at  least,  attributable  to  secondary,  especially  pyococcic,  infection).  A 
croupous  or  so-called  diphtheritic  membrane  is  present  in  many  cases;  it 
is  usually  irregularly  distributed,  and  associated  with  more  or  less  ex- 
tensive sloughing,  so  that  a  characteristic  shaggy  appearance  is  produced. 
In  other  cases,  more  or  less  widespread  gangrene  occurs.  Healing  may 
ensue,  but  it  is  usually  extremely  slow,  being  much  retarded  by  the 
secondary  pyococcic  invaders;  as  it  occurs,  irregular  cicatrices  develop 
which  not  only  replace  the  mucous  membrane,  but,  contracting,  give 
rise  to  considerable  distortion  and  even  obstruction  of  the  intestines. 
Pol>^oid  outgrowths  also  are  a  feature  of  many  chronic  cases.  The 
specific  microorganism  may  be  isolated  from  the  lesions,  especially  during 
acute  exacerbations — which  are  quite  prone  to  occur. 

Symptoms. — The  period  of  incubation  is  believed  to  be,  as  a  rule, 
less  than  forty-eight  hours,  and  the  onset  of  the  disease  rather  sudden — 
with  abdominal  distress,  frequent  bowel  movements,  and  fever  (101°  to 
102°  F.).  In  other  cases  the  onset  seems  less  sudden,  the  dysenteric 
symptoms  developing  out  of  what  appears  to  be  an  ordinary  diarrhoea. 
In  whatever  way  developing,  the  bowel  is  soon  rid  of  fecal  matter,  and 
although  small  amounts  may  still  be  passed  from  time  to  time,  the  stools 
consist  largely,  if  not  exclusively,  of  mucus  admixed  with  blood  and 
sometimes  with  pus,  and  in  aggravated  cases  shreds  of  necrotic  mucous 
membrane  or  even  larger  sloughs  of  the  bowel.  The  stools  are  small 
in  amount  and  very  malodorous;  they  vary  in  number  from  ten  to  thirty, 
forty,  or  more  in  the  twenty-four  hours;  they  are  usually  accompanied 
and  followed  by  extremely  painful  and  distressing  tormina  and  tenesmus. 
The  abdomen  is  distended  and  often  tender  along  the  course  of  the  colon. 
The  constant  straining  may  result  at  first  in  spasm  and  later  paralysis  of 
the  sphincter,  and  even  prolapse  of  the  rectum.  Evidences  of  general  in- 
fection are  seen  in  the  fever,  which  may  increase  to  103°  to  104°  F.  in 
the  first  few  days,  headache,  occasional  vomiting,  loss  of  appetite,  coated 
tongue,  thirst,  scanty  albuminous  urine,  and  rather  rapid  emaciation. 
In  very  severe  infections,  the  rectal  tenesmus  and  efforts  at  stool  may  be 
almost  constant,  the  bloody  mucous  stools  may  be  replaced  by  more 
serous  discharges,  al^dominal  distress  and  colonic  tenderness  may  become 
extreme,  delirium  and  the  typhoid  state  (toxemia)  may  supervene,  and 
in  collapse  the  patient  may  die  within  three  or  four  days.  In  the  majority 
of  cases,  however,  the  stools  lessen  in  ninnber  in  from  four  to  six  days, 
the  tenesmus  subsides,  the  fever  disappears,  and  the  patient  begins 
to  improve  generally,  though  some  blood  and  mucus  may  persist  for 
several  weeks.     In  some  cases  improvement  is  arrested  after  ten  days 


148  BACTERIAL  INFECTIONS 

or  two  weeks,  and  the  general  nutrition  of  the  patient  begins  again 
to  fail;  he  becomes  anemic  and  emaciated,  his  pulse  becomes  weak 
and  small,  his  temperature  perhaps  subnormal,  and  he  passes  into 
chronic  dysentery.  He  may  have  three  or  four  stools  in  the  twenty-four 
hours — ^partly  fecal,  partly  mucous,  and  sometimes  admixed  with 
blood,  and  acute  exacerbations  may  occur  from  time  to  time ;  or  consti- 
pation may  alternate  with  diarrhoea.  Recovery  may  finally  ensue,  or 
death  may  eventuate  from  exhaustion  or  some  intercurrent  infection. 

Complications  and  Sequels. — Peritonitis  sometimes  occurs,  but  it  is 
due  rather  to  extension  through  the  wall  of  the  intestine  than  to  per- 
foration; perityphilitis  or  periproctitis  is  the  most  common.  Inflam- 
mation of  the  other  serous  membranes,  arthritis,  pylephlebitis,  etc., 
have  been  observed.  Anemic  oedema,  amyloid  disease,  neuritis  (with 
paraplegia  and  other  paralyses),  chronic  nephritis,  pyemia,  intestinal 
obstruction,  etc.,  may  follow  chronic  dysentery. 

Diagnosis. — The  diagnosis  is  usually  quite  apparent  from  attention 
to  the  stools.  The  nature  of  the  infection  may  be  ascertained  by  re- 
course to  the  serum  agglutination  test  with  the  dysentery  bacillus  (the 
Shiga  organism,  but  especially  the  Flexner-Harris  t}'pe  in  this  country); 
bv  cultivating  the  organism  from  the  stools;  and  by  the  deviation-  or 
fixation-of-the-complement  test. 

Prognosis. — The  prognosis  depends,  as  a  rule,  upon  the  severity  of 
the  infection.  The  acute  forms,  especially  when  occurring  in  epidemics, 
are  very  fatal.  In  milder  cases  the  persistence  of  blood  and  mucus 
is  unfavorable.  As  a  secondary  infection  in  debilitated  subjects,  dysen- 
tery often  determines  the  fatal  outcome. 

Treatment. — The  prophylactic  measures  advised  in  connection  with 
the  infectious  diseases  (page  29),  especially  t^^hoid  fever,  should  be 
carried  out,  since  there  is  reason  to  believe  that  the  factors  in  infection 
are  similar  to  those  of  tA-phoid  fever.  In  particular,  the  stools  should 
be  rigorously  disinfected. 

Rest  in  bed  during  the  acute  stage  is  essential.  The  diet  must  be 
the  blandest — milk  (peptonized,  or  diluted  with  barley  water,  lime  water, 
or  Vichy  water),  albumen  water,  raw  eggs,  beef  juice,  broths,  custard, 
milk  toast,  etc.  In  subsiding  or  chronic  infections  the  greatest  atten- 
tion also  must  be  paid  to  the  diet,  since  recurrences  are  not  infrequently 
provoked  by  dietetic  indiscretions.  It  is  wise  at  the  beginning  of  the 
attack,  if  there  has  been  little  diarrhoea,  to  clear  out  the  bowel  with  blue 
mass,  calomel,  or  castor-oil  to  which  20  minims  (1.25  c.c.)  of  tincture 
of  opium  may  be  added.  Following  this,  one  should  prescribe  so-called 
intestinal  antiseptics  and  astringents,  such  as : 

I^— Bismuth  subnitrate  (or  subgallate) 3  drams  12j0 

Salol 1  dram  4  0 

Deodorized  tincture  of  opium 2  drams  8  0 

Chalk  mixture,  sufficient  to  make 3  ounces  100  0.— M. 

S. — Two  teaspoonfuls  (10  c.c.)  every  two  or  three  hours,  as  required. 


TETANUS  149 

Bismuth  salicylate,  beta-naphthol,  resorcin,  creasote,  zinc  sulpho- 
carbolate,  and  similar  drugs  are  also  useful;  or  one  may  give  mercuric 
bichloride,  y^^-  grain  (0.0006  gram),  every  two  hours.  In  other  cases, 
the  following  often  leads  to  marked  amelioration  of  the  symptoms  : 

PJ — Lead  acetate 20  grains      113 

Powdered  opium 5  grains      03 

Camphor 10  grains      0|65 

Mix  and  make  ten  capsules. 

S. — One  capsule  every  two  or  three  hours,  as  required. 

In  some  sevefe  cases  of  undetermined  or  supposed  amoebic  nature, 
recourse  may  be  had  to  the  ipecac  treatment  mentioned  under  amoebiasis 
(page  177).  Irrigation  of  the  bowel  is  of  very  great  advantage  in  many 
cases,  but  the  pain  and  tenesmus  are  often  almost  insurmountable 
obstacles  to  its  use  in  acute  cases;  but  sometimes  these  may  be  at  least 
partially  overcome  by  a  preliminary  enema  of  laudanum  (J  to  1  dram, 
2  to  4  c.c.)  and  thin  starch  water  (2  to  4  ounces,  60  to  120  c.c),  or  a 
cocaine  or  iodoform  suppository.  The  irrigation  should  be  done  by 
means  of  a  fountain  syringe  and  the  tube  should  be  inserted  high  up  in 
the  sigmoid;  a  double  catheter  may  be  employed,  so  as  to  facilitate  the 
exit  of  the  fluid;  and  the  fluid  should  be  quite  cold  or  quite  hot  (110°  F.). 
From  two  to  four  pints  (1  to  2  liters)  of  any  of  the  following  solutions 
may  be  employed:  Silver  nitrate,  0.1  to  0.5  per  cent.;  zinc  sulphocar- 
bolate,  0.1  to  0.3  per  cent. ;  lead  acetate,  0.1  to  0.3  per  cent. ;  and  salicylic 
acid,  0.2  to  0.5  per  cent.  In  chronic  cases,  in  addition  to  attention  to  the 
diet,  large  doses  of  bismuth,  intestinal  antiseptics,  a  lead  and  opium 
pill,  and  irrigations,  especially  with  silver  nitrate  (1  to  5  per  cent.,  fol- 
lowed by  injection  of  sodium  chloride  solutions),  should  be  tried.  In 
some  chronic  cases  rebellious  to  medical  treatment,  appendicostomy 
with  subsequent  irrigation  of  the  colon  has  been  followed  by  much 
benefit.     A  satisfactory  antidysenteric  serum  has  not  yet  been  produced. 


TETANUS. 

(Lockjaw.) 

Tetanus  is  an  acute,  specific,  infectious  disease  caused  by  Bacillus 
tetani  (Nicolaier),  and  characterized  by  increased  reflexes  and  tonic 
spasms  of  the  voluntary  muscles. 

Etiology. — The  tetanus  bacillus  is  widely  distributed  in  nature,  being- 
found  in  the  intestine  of  herbivorous  animals,  in  manure,  in  the  soil, 
in  dust,  in  rust,  in  gun-powder,  etc.  An  essential  factor  in  the  etiology 
of  the  disease  is  a  wound — whence  infection  occurs;  since,  although 
two  varieties  of  tetanus  are  described,  the  so-called  idiopathic  and  the 
traumatic,  careful  observation  is  reducing  materially  the  supposed 
idiopathic  cases.  These  are  said  to  develop  after  exy)()sure  to  the 
inclemencies  of  the  weather,  especially  after  sleeping  on  damp  ground, 
but   small    abrasions    caimot    be   excluded    in    these    cases.     In    other 


150  BACTERIAL  INFECTIONS 

cases,  doubtless,  insignificant  wounds  of  the  nose  or  the  mouth  ali'ord 
ready  entrance  for  the  tetanus  bacilhis.  The  obviously  traumatic 
cases  follow  wounds,  especially  contused  and  punctured  wounds  of  the 
hands  and  feet,  but  also  gun-shot  wounds  of  any  part  of  the  body;  they 
are  not  (or  were  not)  infrequent  in  the  newborn  (tetanus  or  trismus 
neonatorum),  infection  occasioned  by  filthy  dressings  occurring  by  way 
of  the  umbilicus;  and  they  sometimes  occur  in  puerperal  women,  infec- 
tion occurring  by  way  of  the  genital  tract.  The  disease  is  said  to  be  more 
common  in  the  negro  than  in  the  white  race,  and  in  the  tropics  than  in 
the  temperate  zone — doubtless,  however,  merely  in  "consequence  of 
accidental  factors. 

The  tetanus  bacillus,  having  gained  access  to  a  wound,  develops  and, 
especially  when  associated  with  pyogenic  cocci,  produces  a  toxin  of 
extreme  activity  (a  fractional  part  of  a  milligram  having  been  estimated 
to  be  a  fatal  dose).  This  is  taken  up  by  the  lymphatics  of  the  nerves 
and  conveyed  to  the  central  nervous  system,  where  it  enters  into  such 
firm  combination  with  the  nerve  cells  that  it  frequently  cannot  be  dis- 
sociated nor  its  effects  overcome — although  a  potent  antitoxin  can  be 
produced  in  the  lower  animals.  The  tetanus  bacillus  may  be  isolated 
from  the  wound,  and  recently  has  been  found  also  in  the  lymph  nodes 
adjacent  to  the  infected  wound. 

Pathology. — ^Irregular  congestions  of  the  central  nervous  system, 
degeneration  of  nerve  cells,  and  swelling  and  oedema  of  the  peripheral 
nerves  are  encountered,  but  the  lesions  are  in  no  way  characteristic. 

Symptoms. — ^The  period  of  incubation  is  from  five  to  fifteen  days, 
as  a  rule.  The  shorter  the  period  the  more  severe  the  symptoms  and 
the  more  likely  death.  Generally  there  are  no  noteworthy  prodromes. 
Preceded  sometimes  by  general  malaise,  headache,  occasionally  chilli- 
ness, the  disease  begins  with  gradually  increasing  stiffness  and  tension  of 
the  muscles  of  the  jaw  and  the  neck,  and  difficulty  in  mastication.  In 
a  few  cases  the  first  manifestations  are  in  the  muscles  near  the  site  of 
infection.  Gradually  the  tonic  spasm  involves  almost  all  the  voluntary 
muscles  of  the  body:  the  jaws  become  locked,  immobile;  the  forehead 
becomes  wrinkled,  the  eyelids  partly  closed  and  the  eyes  staring,  and 
the  angles  of  the  mouth  drawn  down  and  out  (risus  sardonicus);  the 
head  becomes  retracted;  spasm  of  the  spinal  muscles  causes  arching  of  the 
vertebrae  (opisthotonos).  The  abdominal  muscles  become  rigidly  con- 
tracted; sometimes  such  is  the  contraction  that  the  body  may  be  arched 
forward  (emprosthotonos)  or  rupture  of  the  muscle  may  occur.  The  body 
is  rarely  arched  to  the  side  (pleurosthotonos).  The  legs  and  the  trunk 
are  sometimes  extremely  rigid  (orthotonos),  the  patient  being,  as  it  were, 
held  in  a  vice.  The  arms,  as  a  rule,  are  relatively  unaffected.  Occa- 
sionally strabismus  develops.  The  persistent  tonicity  of  the  muscles  is 
made  worse  by  paroxysmal  exacerbations,  which,  induced  by  the  slightest 
jar  or  noise,  recur  at  irregular  intervals,  last  from  ten  to  thirty  seconds, 
are  accompanied  by  profuse  perspiration,  and  occasion  the  greatest 
agony.     The  distress  is  frequently  augmented  by  spasmodic  dy.sphagia, 


TETANUS  151 

and  by  spasm  of  the  muscles  of  respiration,  of  the  diaphragm,  and  of 
the  glottis,  causing  asphyxia  which  may  prove  fatal. 

The  mind  is  usually  clear,  the  superficial  and  the  deep  reflexes  are 
greatly  exaggerated,  and  the  patient  is  often  wakeful  (but  the  spasms 
often  lessen  during  sleep).  The  pulse  is  rapid  (100  to  140).  The 
temperature  may  be  normal,  but  it  is  usually  somewhat  elevated;  hyper- 
pyrexia is  common  in  fatal  cases  (108°,  110°,  112°  F.),  and  may  even 
increase  after  death.  The  urine  may  be  suppressed,  or  difficulty  in 
voiding  urine  secreted  may  be  experienced.  Occasionally  slight  albu- 
minuria or  glycosuria  is  found. 

Acute  and  chronic,  severe  and  slight,  cases  may  be  distinguished. 
In  the  acute  cases  the  phenomena  develop  rapidly  and  soon  become 
intense,  paroxysm  following  paroxysm  with  rapidity;  death  usually 
follows  within  three  or  four  days  from  exhaustion,  asphyxia,  or  heart 
failure.  In  more  favorable  cases  the  paroxysms  become  less  frequent 
and  less  severe,  and  the  patient  may  recover  after  the  lapse  of  several 
weeks,  though  exhaustion  may  last  for  a  long  time  and  eventually  prove 
fatal. 

A  special  form  is  the  cephalic  tetanus  of  Rose,  which  follows  injuries 
to  the  cranial  nerves  (especially  the  face),  and  is  characterized  by 
paralysis  of  the  muscles  supplied  by  the  facial  nerve  on  the  side  of  the 
injury,  and  spasm  of  the  masseters  and  of  the  muscles  of  deglutition 
(tetanus  hydrophobicus),  and  sometimes  of  the  muscles  of  the  neck 
and  the  trunk. 

Diagnosis. — The  disease  is  usually  unmistakable.  In  strychnine 
poisoning,  as  contrasted  with  tetanus,  there  is  often  a  history  of  the 
ingestion  of  a  supposed  poison ;  the  spasms  are  violent  from  the  beginning, 
but  do  not  begin  with  trismus,  and  are  marked  in  the  extremities  (relative 
freedom  of  the  arms  in  tetanus);  there  are  intervals  of  complete  relaxa- 
tion (as  contrasted  with  the  persistent  tonicity  of  tetanus) ;  and  strychnine 
may  be  found  in  the  gastric  contents.  Tetany  is  often  associated  with 
rickets  or  gastric  dilatation;  the  spasms  involve  the  extremities,  especially 
the  hands  and  the  feet  and  the  larynx;  and  Erb's,  Chvostek's,  and  Trous- 
seau's signs  may  be  elicited.  In  hydrophobia  there  is  a  history  of  the  bite 
of  a  supposedly  rabid  animal ;  the  spasms  involve  especially  the  muscles 
of  deglutition  and  of  respiration;  there  are  marked  psychic  symptoms; 
and  there  is  no  lockjaw,  no  persistent  tetanic  spasm,  and  no  opisthotonos. 
Hysteria  occurs  especially  in  neurotic  women;  the  spasms  may  begin 
suddenly  and  last  for  hours  or  days;  laughing  and  crying  spells  are  com- 
mon, especially  upon  the  relaxation  of  the  spasm;  and  other  phenomena 
of  hysteria  may  be  elicited. 

Prognosis. — The  mortality  of  acute  traumatic  tetanus,  of  puerperal 
tetanus,  and  of  tetanus  in  the  newborn  is  over  90  per  cent.  In  the  sub- 
acute or  chronic  cases  the  mortality  is  not  more  than  50  per  cent.  Favor- 
able symptoms  are  late  onset  of  the  .symptoms  (two  weeks  or  more  after 
the  injury),  more  or  less  restriction  of  the  spasms  to  the  jaw  and  neck, 
lessening  of  the  paroxysmal  exacerbations,  and  the  absence  of  fever. 


152  BACTERIAL  INFECTIONS 

Treatment. — ^The  patient  should  be  kept  absolutely  quiet  in  a  darkened 
and  secluded  room,  free  from  all  irritating  noises  and  solicitous  friends. 
The  diet  must  be  light  and  nutritious,  and  administered  in  small  amounts 
at  frequent  intervals.  Should  the  patient  be  unable  to  swallow,  a  stomach 
tube  may  be  passed  through  the  nose  or  mouth  (space  left  by  absent 
teeth)  and  the  patient  thus  fed,  or  recourse  may  be  had  to  rectal  alimen- 
tation. Inasmuch  as  the  toxin  is  manufactured  in  the  local  wound, 
wisdom  suggests  its  removal;  should  this  be  impossible  the  wound  must 
be  thoroughly  cleansed  and  antisepticized. 

The  tetanus  antitoxin  has  not  sustained  the  early  claims  made  for  it, 
not  so  much,  however,  because  it  is  impotent  as  because  by  the  time  it 
is  generally  used  the  tetanus  toxin  has  already  effected  such  a  firm  com- 
bination with  the  nerve  cells  as  to  prohibit  all  efforts  at  its  dissociation. 
It  is  imperative,  therefore,  that  the  antitoxin  be  administered  at  the 
earliest  possible  moment,  and  in  large  amounts  (2000  to  7000  units) .  It 
should  be  injected  into  and  subcutaneously  about  the  wound,  and  it 
may  also  be  injected  into  the  nerve  trunks  leading  from  the  infected 
area,  where  perhaps  it  may  meet  and  neutralize  the  toxin,  being  thus 
conveyed  to  the  central  nervous  system.  The  antitoxin  has  been 
administered  to  a  fairly  large  number  of  persons  (mostly  children) 
injured  with  toy  pistols  (Fourth-of-July  celebrations)  with  a  marked 
reduction  of  the  morbidity  incidence  and  the  mortality.  In  view  of  the 
uncertain  results  attending  the  subcutaneous  and  intravenous  injection 
of  the  antitoxin,  its  injection  beneath  the  cerebral  membranes  or  directly 
into  the  brain  tissue  has  been  practised — with  improved  results.  This 
seems  to  me  a  rather  unnecessary  and  hazardous  proceeding,  especially 
in  view  of  the  fact  that  the  same  object  can  be  achieved  by  injecting  it 
into  the  subarachnoid  space  by  means  of  lumbar  puncture.  One  should 
first  assure  himself  that  he  has  penetrated  the  arachnoid  membrane, 
by  withdrawing  a  considerable  amount  of  the  cerebrospinal  fluid,  and 
should  then  inject  the  antitoxin  (30  c.c.)  and  subsequently  more  or  less 
invert  the  body  so  as  to  insure  the  thorough  mixing  of  the  antitoxin  with 
the  remaining  cerebrospinal  fluid.  The  procedure  should  be  repeated 
in  accordance  with  the  exigencies  of  the  case.  Meltzer,  Miller,  and 
others  recently  have  obtained  good  results  from  the  subarachnoid  injec- 
tion of  a  25  per  cent,  solution  of  magnesium  sulphate,  of  which  from 
1  to  2.5  c.c,  may  be  used  daily  or  every  second  day,  depending  upon 
the  indications.  Baccelli  speaks  highly  of  the  hypodermic  use  of 
carbolic  acid — in  2  per  cent,  solution,  from  3  to  5  grains  daily.  I 
have  thought  that  I  have  seen  it  do  good.  The  spasms  are  best  con- 
trolled by  the  use  of  chloroform  and  morphine,  either  or  both  of  which 
should  be  given  in  sufficient  dose.  Chloral  and  the  bromides  are  useful 
adjuvants.  Stimulants  (alcohol,  digitalis,  caffeine,  etc.)  are  often  called 
for  to  combat  exhaustion  and  to  maintain  the  failing  heart.  Cannabis 
indica,  calabar  bean,  belladonna,  curare,  amyl  nitrate,  etc.,  have  also  been 
recommended. 


CHOLERA  153 

CHOLERA. 

{Asiatic  Cholera.) 

Cholera  is  an  acute,  specific,  infectious,  and  moderately  contagious 
disease  caused  by  Microspira  comma  (Koch),  and  characterized  by 
vomiting,  profuse  "rice-water"  intestinal  discharges,  suppression  of 
urine,  collapse,  and  frequently  death. 

Etiology. — Cholera  is  endemic  in  India  and  has  occasionally  pre- 
vailed epidemically  in  Europe  and  this  country.  It  always  follows 
the  channels  of  commercial  intercourse  (immigrants,  pilgrims,  shipping, 
etc.),  and  is  in  consequence  more  common  in  sea-ports  than  in  inland 
towns.  Age,  sex,  and  race  are  of  no  etiological  importance.  Persons 
debilitated  from  any  cause,  the  impoverished,  alcoholics,  subjects  of 
chronic  gastro-intestinal  catarrh,  mental  depression,  etc.,  seem  especially 
susceptible.  Some  persons  (50  per  cent,  of  the  population,  Koch) 
are  apparently  naturally  immune.  One  attack  <;onfers  a  temporary 
immunity. 

Infection  is  spread  especially  by  water — that  used  for  drinking  pur- 
poses, that  used  in  preparing  foods,  such  as  milk,  lettuce,  and  other 
foods  eaten  uncooked,  and  that  used  in  domestic  washings,  etc.  Infec- 
tion, thus,  is  acquired  by  ingestion.  Flies  seem  to  be  active  agents 
in  disseminating  the  infection.  The  disease  is  only  slightly  contagious. 
Infection  is  not  transmitted  by  the  air  (the  comma  bacilli  die  soon  when 
dried),  but  some  persons  have  become  infected  from  handling  infected  bed- 
linen,  dishes,  etc.,  and  several  cases  of  laboratory  infection  have  been 
observed. 

Pathology. — In  consequence  of  the  great  loss  of  fluids  through  vomit- 
ing and  diarrhoea,  the  body  after  death  is  shrunken  and  withered.  Post- 
mortem rigidity  comes  on  soon,  is  extreme  (occasioning  distortion  of 
the  body),  and  persists  for  a  long  time.  Postmortem  twitchings  of  the 
muscles  (causing  movements  of  the  dead  body)  and  even  elevation 
of  the  temperature  have  been  observed.  The  blood  is  thick  and  dark- 
colored,  and  the  organs,  as  a  rule,  are  unusually  free  of  blood  and  dry. 
The  important  lesions  are  in  the  intestinal  tract.  The  peritoneum 
is  dry,  though  sometimes  curiously  sticky,  and  the  coils  of  intestine 
are  shrunken  and  thin.  The  intestinal  contents  resemble  the  "rice- 
water"  discharges.  The  mucous  membrane  at  first  is  swollen  and  con- 
gested and  covered  with  an  excessive  secretion  of  mucus;  later  the 
lymphoid  follicles  become  swollen,  and  may  reveal  irregular  foci  of 
congestion,  occasionally  of  hemorrhage;  the  epithelium  desquamates 
and  may  even  be  shed  in  rather  large  masses,  leaving  the  submucosa 
denuded.  Occasionally  extensive  necrosis  and  ulceration,  rarely 
perforation,  may  be  observed.  The  mesenteric  lymph  nodes  are  often 
swollen;  the  spleen  is  not  enlarged.  The  other  organs  manifest  the  lesions 
common  to  most  toxemias,  modified,  however,  by  the  unusual  loss  of 
fluids.     The  comma  bacilli  may  be  found  in  the  contents  of  the  intestine 


154  BACTERIAL  INFECTIONS 

and  in  the  mucous  membrane;  in  protracted  cases  they  may  be  found 
in  the  wall  of  the  intestine  and  even  in  the  mesenteric  lymph  nodes. 

Symptoms. — ^The  period  of  incubation  is  from  one  to  three  days. 
In  some  cases  a  premonitory  stage  may  be  distinguished — in  which 
there  may  be  some  epigastric  distress,  diarrhoea,  and  weakness.  Often, 
however,  the  onset  of  the  disease  is  abrupt,  coming  on  apparently  in 
the  midst  of  perfect  health,  with  chilliness,  profuse  diarrhoea,  and  extreme 
prostration  or  collapse  (stage  of  collapse).  The  stools  are  at  first  fecal 
in  character,  but  they  soon  become  grayish,  alkaline,  watery,  odorless, 
and  contain  flakes  of  mucus,  epithelial  cells,  and  granular  debris  ("rice- 
water"  stools),  occasionally  blood,  and  they  usually  reveal  the  comma 
bacillus  in  pure  culture.  There  may  be  thirty  or  more  stools  within  the 
first  twenty-four  hours.  Usually  they  are  passed  painlessly,  but  occasion- 
ally there  is  complaint  of  abdominal  pain  and  tenesmus.  Vomiting  soon 
comes  on  and  becomes  persistent,  thirst  is  extreme  and  very  distressing, 
painful  cramps  develop  in  the  muscles  of  the  abdomen  and  legs,  prostra- 
tion and  collapse  become  more  marked,  and  the  toxemia  and  concen- 
tration of  the  blood  increasing,  the  patient  passes  into  the  algid  stage. 
The  cutaneous  temperature  is  much  below  normal  and  the  skin  feels 
cold  and  clammy,  though  the  internal  (rectal)  temperature  may  be  103° 
to  105°  F. ;  the  extremities  are  cyanotic,  the  face  grayish,  ashen,  or 
exhibits  a  slight  cyanotic  tint;  the  features  are  pinched,  the  eyes 
and  cheeks  sunken,  and  the  skin  in  general  withered  and  wrinkled. 
The  pulse  becomes  weak,  the  heart  sounds  indistinct,  the  blood  pressure 
low,  the  voice  hoarse  and  weak,  the  breathing  labored  and  superficial 
(asphyxic  stage),  and  the  urine  much  reduced  in  amount,  and  contains 
albumin,  casts,  and  erythrocytes;  not  infrequently  it  is  totally  sup- 
pressed. Consciousness  is  often  maintained  throughout,  but  the  patient 
may  pass  into  coma,  with  or  without  delirium,  and  die — sometimes 
within  the  first  twenty-four  or  forty-eight  hours. 

In  some  cases,  however,  the  patient  improves  and  the  stage  of  reaction 
(tepid  stage)  sets  in.  The  vomiting  ceases,  the  intestinal  discharges 
lessen  and  become  more  fecal  in  character,  the  pulse  becomes  stronger, 
the  respirations  easier,  slower,  and  deeper,  and  the  surface  temperature 
normal;  not  infrequently  the  skin  is  covered  with  sweat,  and  the  func- 
tions of  the  kidneys  are  gradually  restored,  though  albuminuria  per- 
sists for  some  time.  In  favorable  cases  the  patient  continues  to  improve, 
and  convalescence  is  established  at  the  end  of  ten  days  or  two  weeks. 
Not  infrequently,  however,  diarrhoea  recurs  at  the  end  of  two  or  three 
days,  the  patient  passes  rapidly  again  into  the  algid  stage,  and  soon 
dies.  In  other  cases  so-called  typhoid  cholera  develops;  the  patient 
becomes  delirious  and  often  feverish,  and  the  pulse  rapid  and  weak; 
the  urine  is  again  suppressed,  coma  and  perhaps  convulsions  super- 
vene, and  death  usually  ensues,  though  recovery  has  been  observed. 

Varieties. — Some  attacks  are  so  mild  that  the  patient  is  slightly, 
if  at  all,  indisposed,  complaining  only  of  a  little  diarrhoea;  indeed, 
during  epidemics  the  cholera  bacillus  has  been  found    in  the  stools 


CHOLERA  155 

of  presumably  healthy  persons.  The  term  cholerine  has  been  applied 
to  cases,  resembling,  if  not  identical  with,  cholera  nostras  (due  to  bacteria 
other  than  Microspira  comma),  in  which  there  is  profuse  diarrhoea, 
possibly  vomiting,  but  only  moderate  collapse,  and  rather  cjuick  recovery. 
In  other  cases  the  patient  is  overwhelmed  with  the  intoxication  and 
dies  within  a  few  hours,  in  coma,  even  before  the  onset  of  diarrhoea 
{cholera  sicca).  As  a  rule,  the  symptoms  are  directly  proportional  to 
the  loss  of  fluid  and  the  salts  of  the  blood. 

Complications  and  Sequels. — The  most  common  are:  protracted  con- 
valescence and  anemia,  nephritis,  uremia,  cutaneous  rashes  (roseola, 
erythema,  urticaria),  pneumonia,  arthritis,  parotitis,  chronic  enteritis 
and  colitis,  gangrene,  especially  of  the  toes,  etc. 

Diagnosis. — In  the  presence  of  an  epidemic  it  may  be  difficult  or 
impossible  to  distinguish  between  cholera  asiatica  and  cholera  nostras, 
except  by  a  bacteriological  examination  of  the  intestinal  discharges. 
The  "rice-water"  discharges  of  the  earlv  davs  of  true  cholera  usually 
reveal  the  cholera  bacillus  in  pure  culture;  later  certain  contaminating 
bacteria  are  usually  encountered;  while  still  later  the  cholera  bacillus 
may  be  detected  only  with  difficulty.  The  agglutination  test  njay  prove 
of  service.  Certain  forms  of  food-poisoning,  of  fungus-poisoning,  and 
of  metallic  poisonings  (arsenic,  antimony,  and  corrosive  sublimate)  may 
simulate  cholera,  but  the  associated  phenomena  usually  preclude  diag- 
nostic error. 

Prognosis. — The  mortality  varies  from  50  to  80  per  cent,  in  different 
epidemics,  and  is  in  direct  ratio  to  the  severity  of  the  infection.  ]\Iost 
deaths  occur  during  the  algid  stage. 

Treatment. — Prophylactic  measures  are  of  the  greatest  importance,  and 
the  strictest  sanitary  measures  must  be  enforced  (page  29).  As  in  the 
past,  rigid  quarantine  will  prevent  the  introduction  of  the  disease  into 
this  country.  Haffkine's  preventive  inoculations  have  proved  of  some 
service,  and  seem  to  merit  continued  trial.  During  the  prevalence  of  an 
epidemic  all  drinking  water  and  milk  should  be  boiled,  and  no  uncooked 
food  should  be  eaten.  Dilute  sulphuric  acid,  20  minims  (1.25  c.c),  in  a 
pint  (500  c.c.)  of  water,  three  times  daily,  is  believed  to  be  a  serviceable 
prophylactic,  since  dilute  acids  kill  the  vibrios.  All  diarrhoeic  attacks  of 
whatsoever  nature  must  be  promptly  treated — by  preliminary  cleansing 
of  the  bowel  (castor  oil),  and  by  astringents,  such  as  bismuth,  lead  acetate, 
aromatic  sulphuric  acid,  and  opium. 

When  the  disease  has  developed  the  patient  must  be  kept  at  rest  in 
bed  in  a  warm  room  (to  help  maintain  the  bodily  heat),  and  upon  the 
development  of  the  algid  stage,  he  should  be  surrounded  by  hot  bottles, 
etc.  Morphine  or  Dover's  powder  is  useful  in  the  early  stage  in  allaying 
the  pain;  hot  applications  to  the  abdomen  (mustard  plaster,  spice 
poultice,  turpentine  stupe,  etc.)  are  grateful.  In  the  event  of  vomiting, 
small  doses  of  calomel  should  be  administered;  most  other  remedies, 
such  as  cocaine,  are  useless.  Efforts  may  be  made  to  restrain  the  diar- 
rhoea (aromatic  sulphuric  acid  and  astringents),  but  unfortunately  oiu- 


156  BACTERIAL  INFECTIONS 

best  directed  efforts  are  usually  in  vain.  Enteroclysis  with  hot  physiologi- 
cal saline  solution,  to  which  tannic  acid  (1  per  cent.)  and  tincture  of  opium 
have  been  added,  may  be  tried.  Intestinal  antiseptics  seem  to  be  indi- 
cated on  theoretical  grounds,  and  good  results  have  been  claimed  for 
salol;  naphthalene,  resorcin,  etc.,  may  also  be  tried.  The  most  etfi- 
cacious  treatment  appears  to  be  that  recommended  by  Rogers  and 
others — the  intravenous  injection  of  hypertonic  (1.35  per  cent.)  sodium 
chloride  solution:  four  drams  (16  grams)  to  a  quart  (liter)  of  water. 
Of  this  two  liters  should  be  injected  at  a  time,  and  repeated  as  occasion 
may  warrant.  Rogers  adds  to  the  first  and  second  injection  fluid,  cal- 
cium chloride,  6  grains  (0.4  gram)  to  the  quart  (liter),  to  overcome  the 
low  coagulability  of  the  blood.  The  fluid  may  also  be  injected  into  the 
peritoneal  cavity;  and  this  may  be  augmented  by  hypodermoclysis  and 
hot  enteroclysis  (107°  to  110°  F.).  If  the  patient  is  not  vomiting,. fluid 
should  also  be  given  by  the  mouth.  Strychnine,  whiskey,  brandy,  cam- 
phor, hot  coffee  or  tea,  and  more  diffusible  and  rapidly  acting  stimu- 
lants, such  as  aromatic  spirit  of  ammonium,  and  compound  spirit  of 
ether,  etc.,  are  also  indicated  in  most  cases.  The  uremic  manifestations, 
which  are  likely  to  develop  during  the  reaction  stage,  are  associated 
with  low  blood  pressure  (80  to  90  mm.  Hg.),  and  are  to  be  combated 
by  the  hypodermic  or  intravenous  administration  of  adrenalin  and  digi- 
talis. Should  the  patient  survive  the  algid  stage,  he  must  be  fed  care- 
fully with  bland  liquid  foods,  small  amounts  at  stated  intervals,  and 
every  precaution  must  be  observed  not  to  provoke  diarrhoea. 


PLAGUE. 

(Bubonic  Plague;  Bubonic  Pest;  Oriental  Plague.) 

Plague  is  an  acute,  specific,  infectious,  and  slightly  contagious  dis- 
ease caused  by  Bacillus  pestis  (Kitasato),  and  characterized  by  fever, 
inflammation  of  the  lymph  nodes  (buboes),  of  the  lungs,  and  of  the 
cellulo-cutaneous  tissues,  and  a  general  bacteremia. 

Etiology. — The  plague  has  prevailed  epidemically  since  the  early 
days  of  the  Christian  era,  and  has  been  answerable  for  great  loss  of  life 
— notably  during  the  fourteenth  century,  when  a  fourth  of  the  population 
is  said  to  have  succumbed,  and  in  1665,  when  70,000  persons  died  in 
London.  Following  a  period  of  comparative  quiescence,  the  plague 
recently  has  appeared  in  different  parts  of  the  world — having  been  dis- 
seminated from  India,  where  it  has  been  endemic.  It  has  been  carried 
to  many  ports  of  Europe,  Africa,  Australia,  and  this  country,  and  small, 
local  epidemics  in  and  about  the  seaports  have  developed;  but  proper 
sanitary  measures  have  served  to  prevent  serious  outbreaks.  Age, 
sex,  race  are  without  etiological  significance.  The  disease  is  especially 
common  among  the  poor  and  those  living  under  unhygienic  conditions. 
It  prevails  especially  during  the  warm  seasons,  but  also  during  the  colder. 
One  attack  confers  partial  immunity. 


PLAGUE  157 

The  exciting  cause  of  the  disease  is  Bacillus  pestis,  which  may  be  found 
in  the  blood,  lymph  nodes,  secretions,  and  viscera  of  patients  and  of 
subjects  dead  of  the  disease.  The  disease  is  only  slightly  contagious — 
contagion  being  a  factor  in  less  than  3  per  cent,  of  the  cases  (Plague 
Commission).  The  infection  is  spread  largely  through  the  medium  of 
rats;  an  epidemic  among  rats  commonly  precedes  infection  in  man  in 
new  localities.  The  infection  is  transmitted  from  rat  to  rat,  and  from 
rat  to  man,  by  means  of  rat  fleas — which  may  be  carried  from  place  to 
place  by  human  subjects  on  their  person  or  in  their  baggage,  etc.  Re- 
cently in  California  the  ground  squirrel  has  been  found  to  be  infected, 
and  doubtless  propagates  the  disease.  Infection  is  acquired  in  the  great 
majority  of  cases  by  means  of  the  bites  of  infected  rat  fleas,  but  it 
may  also  be  acquired  by  direct  inoculation  into  a  wound  or  abrasion 
(handling  of  infected  material,  laboratory  investigations,  etc.),  by  inhala- 
tion (pneumonic  type),  and  perhaps  by  ingestion  (contaminated  food 
and  drink — probably  rare). 

Pathology. — The  lesions  vary  somewhat  with  the  type  of  the  infection, 
but  in  all  there  is  a  general  plague  bacillemia;  the  lymph  nodes  are 
swollen,  hj'peremic,  later  hemorrhagic,  purulent,  and  more  or  less  difflu- 
ent; the  lymphatic  vessels  are  inflamed,  and  about  both  there  is  more  or 
less  oedema.  Hemorrhagic  foci  are  present  in  the  skin,  the  serous  mem- 
branes (pleura,  pericardium,  peritoneum),  and  in  the  mucous  membrane 
of  the  gastro-intestinal  tract.  The  liver  and  kidneys  show  cloudy  swell- 
ing and  often  hemorrhages,  and  the  spleen  is  much  enlarged  and  softened. 
In  the  pneumonic  type  there  is  swelling  and  congestion  of  the  bronchial 
mucous  membrane,  and  foci  of  bronchopneumonia. 

Symptoms. — ^The  period  of  incubation  is  usually  two  or  three  days, 
although  it  may  be  as  long  as  five  or  seven.  Several  varieties  of  the  dis- 
ease may  be  distinguished :  bubonic  plague,  pneumonic  plague,  cellulo- 
cutaneous  plague,  septicemia  plague,  and  pestis  minor. 

Bubonic  or  glandular  plague  is  the  most  common  (80  per  cent,  of 
the  cases).  In  most  cases,  following  several  days  of  irregular  prodromes, 
such  as  malaise,  chilliness,  and  headache,  the  disease  develops  suddenly 
with  fever  (103°  to  104°  F.),  increased  headache,  anxiety,  resdessness, 
and  general  neuromuscular  pains  or  aching.  The  pulse  becomes  rapid 
(a  valuable  diagnostic  sign),  the  respirations  increased  in  frequency, 
the  face  and  the  conjunctiva  injected,  the  tongue  coated,  the  bowels 
constipated  (though  diarrhoea  may  supervene),  and  the  patient  becomes 
greatly  depressed.  Usually  there  is  a  polynuclear  leukocytosis.  In 
severe  cases  the  patient  may  become  collapsed,  the  urine  scanty, 
almost  suppressed,  delirium  may  supervene,  and  in  uremic  coma 
or  convulsions  the  patient  may  die,  even  within  the  first  twenty-four 
hours  (pestis  siderans).  In  three-fourths  of  the  cases,  however,  at 
the  end  of  twenty-four  or  forty-eight  hours  (rarely  later),  the  charac- 
teristic lymph-node  swellings  (buboes)  develop,  usually  on  one  side,  some- 
times on  both,  and  most  frequently  in  the  groin,  less  commonly  in 
the  axilla,  the  neck,  or  internally.     The  swellings  vary  much  in  size, 


158  BACTERIAL  IXFECTIOXS 

up  to  that  of  an  orange,  and  they  are  tender  and  painful.  Soon  peri- 
glandular swelling  and  oedema  develop  to  such  a  degree  as  to  obscure 
or  obliterate  the  outlines  of  swollen  lymph  nodes.  By  the  second  or  third 
day  the  fever  has  reached  its  maximum;  it  often  drops  somewhat  on  the 
third  or  fourth  day,  then  rises  (sometimes  to  108°  F.),  and  in  favorable 
cases  by  the  seventh  or  the  eighth  day  begins  to  fall  by  lysis  and  gradually 
reaches  the  normal.  The  glandular  swellings  may  undergo  resolution 
or  suppuration  (commonly  a  good  sign);  in  some  cases,  however,  more 
or  less  extensive  sphacelation  and  generalized  furunculosis  occur.  In 
other  cases  concurrent  with  the  development  of  the  buboes  hemorrhages 
into  the  skin  occur  (plague  spots,  "fatal  tokens" — whence  the  designa- 
tion "  black  death").  Hemorrhages  from  the  mucous  membranes  are  also 
encountered.  In  the  event  of  suppuration,  the  purulent  discharge  may 
rapidly  abate,  or  the  sinuses  may  become  indolent  and  the  patient  event- 
ually die  of  exliaustion,  amyloid  disease,  or  secondary  infections.  The 
mortality  is  about  75  per  cent. 

Pneumonic  plague  is  characterized  by  the  development  of  patches  of 
bronchopneumonia.  The  disease  begins  with  the  ordinary  manifesta- 
tions of  pneumococcic  infection  of  the  lung  (pneumonia),  for  which  it 
is  frequently  mistaken.  The  fever  is  high  and  may  become  intermittent; 
the  patient  becomes  delirious,  prostrated,  and  much  sicker  than  the  physi- 
cal signs  in  the  lung  indicate.  The  sputum  is  thin,  serosanguineous  (not 
rusty),  and  contains  plague  bacilli  in  abundance.  Death  occurs  usually 
before  the  fifth  day.     The  mortality  is  very  high — 96  to  100  per  cent. 

Cellulocutaneous  plague  is  characterized  by  inflammation  and  necrosis 
of  the  skin  and  subcutaneous  tissues,  and  is  often  associated  with  in- 
volvement of  the  lymph  nodes.  The  local  lesions  usually  spread  from 
day  to  day  until  a  very  large  area  may  become  involved,  whereupon  in 
favorable  cases  the  process  may  become  circumscribed  by  a  well  devel- 
oped line  of  demarcation,  and  in  the  course  of  time  a  spachelus  may  be 
discharged.  The  general  manifestations  are  those  mentioned  under 
bubonic  plague. 

Septicemic  plague  is  a  severe  plague  bacteremia — the  general  lym- 
phatic system  and  the  blood  being  overrun  with  plague  bacilli.  The  fever 
is  usually  moderate  only  (100°  to  102°  F.),  the  depression  extreme,  and 
hemorrhages  common.  The  patient  usually  dies  before  the  lymph  nodes 
become  palpably  enlarged.     The  mortality  is  over  95  per  cent. 

Pestis  minor,  pestis  amhulans,  is  a  mild  form  of  the  disease,  character- 
ized by  mild  fever  of  several  days'  duration,  swelling  and  possibly 
suppuration  of  the  lymph  nodes,  but  usually  with  general  symptoms 
so  slight  as  not  to  necessitate  the  patient's  taking  to  bed.  The  patients, 
however,  are  infectious,  and  may  give  rise  to  widespread  dispersion  of 
the  disease. 

Complications  and  Sequels. — Complications  and  sequels  are  rather 
common.  Suppurative  disorders  of  the  eye  and  of  the  ear  (leading  to 
loss  of  sight  and  of  hearing),  irritability  and  rapid  action  of  the  heart, 


GLANDERS  159 

divers  nervous  disorders  and  paralyses,  and  general  asthenia  are  among 
the  more  common. 

Diagnosis. — During  an  epidemic  the  disease  is  readily  recognized. 
In  case  of  doubt,  fluid  obtained  from  a  bubo  (by  a  sterile  h;y'podermic 
needle),  the  blood,  or  the  sputum  should  be  examined  for  the  plague 
bacillus;  and  recourse  may  be  had  to  the  agglutination  test.  Cultures 
and  animal  inoculations  should  be  undertaken  in  the  suspicious  cases  in 
the  absence  of  an  epidemic. 

Prognosis. — The  prognosis  is  bad;  the  mortality  varies  with  the  type 
of  the  infection  from  50  to  100  per  cent. 

Treatment. — Prophylactic  measures  of  the  strictest  sort  should  be 
rigidly  carried  out.  The  patient  should  be  isolated,  all  utensils  and 
the  body  linen  should  be  disinfected  or  destroyed,  rats  and  similar 
animals  should  be  killed  and  their  carcasses  burned  (as  well  as  dead 
bodies);  attendants  should  observe  all  sanitary  precautions  (page  29), 
and  should  wear  close-fitting  undergarments  so  as  to  prevent  as  far  as 
possible  bites  of  fleas.  Haft'kine's  prophylactic  injections,  or  "vaccine," 
consisting  of  gradually  increasing  doses  of  heat-killed  bacilli,  seem  to 
confer  more  or  less  immunity  for  from  six  to  eighteen  months,  especially 
if  a  second  injection  is  made  about  a  month  after  the  first.  This  is 
true  also  of  Lustig's  preventive  inoculations.  At  all  events,  the  measure 
merits  continued  trial. 

The  treatment  of  the  developed  disease  is  purely  symptomatic :  hydro- 
therapy for  the  headache,  delirium,  and  other  nervous  symptoms;  mor- 
phine for  the  neuromuscular  pains  and  general  restlessness ;  and  stimulants 
(strychnine,  camphor,  ether,  whiskey,  hypodermoclysis,  adrenalin  chlo- 
ride, etc.)  for  the  depression  and  collapse.  An  ice-bag,  or  belladonna  oint- 
ment, or  glycerin  and  belladona,  or  evaporating  lotions  will  diminish  the 
pain  of  the  buboes — which,  when  suppuration  has  occurred,  should  be 
incised.  Cantlie  recommends  early  purgation  with  calomel  and  salines, 
and  free  stimulation.  The  evidence  for  or  against  Yersin's  and  Roux's 
antitoxic  serum  is  not  yet  conclusive,  although  some  good  results  have 
been  reported. 

GLANDERS. 

(Farcy;  Malleus  Humidus.) 

Glanders  is  a  specific  infectious  and  highly  contagious  disease  of  horses 
caused  by  Bacillus  mallei  (Loeffler-Schutz),  and  communicable  to  man;  it 
characterized  by  the  development  of  a  granuloma  that  ultimately  under- 
goes softening,  and  by  general  septicemia. 

Etiology. — Glanders  is  preeminently  a  disease  of  horses,  but  occurs 
sometimes  in  asses  and  mules,  and  is  rarely  transmitted  to  men.  Infec- 
tion is  transmitted  directly  to  men,  and  is  acquired  through  the  medium 
of  a  wound  or  al^rasion  of  the  skin  or  the  oral  or  nasal  mucous  mem- 
brane; but  the  ingestion  of  infected  meat  may  also  transmit  tlie  disease. 

Pathology. — Glanders  is  one  of  the  infectious  granulomas,  and  consists 
of  foci  of  epitheloid  cells,  giant  cells,  small  round  cells,  and  the  specific 


160  BACTERIAL  INFECTIONS 

bacillus ;  these  foci  tend  to  undergo  softening  and  form  ulcers  or  abscesses. 
Two  forms  are  recognized:  (1)  Glanders,  in  which  the  lesions  develop 
in  the  respiratory  mucous  membrane,  especially  the  nose,  and  where 
by  breaking  down  they  result  in  the  formation  of  ulcers;  and  (2)  farcy, 
in  which  the  lesions  develop  in  the  subcutaneous  tissues,  especially  the 
lymphatic  vessels  and  nodes,  and  where  by  breaking  down  they  result 
in  the  formation  of  abscesses  which  may  discharge  through  sinuses. 
Both  forms  are  commonly  associated;  either  may  antedate  the  other. 
Furthermore,  a  bacteremia  may  ensue,  and  lesions  may  be  found  in  any 
of  the  internal  organs — the  lungs  (bronchopneumonia),  the  liver,  the 
spleen,  the  kidneys,  the  brain,  the  muscles,  etc. ;  abscesses  are  then  com- 
mon, as  well  as  hemorrhages  into  the  serous  and  the  mucous  membranes. 

Symptoms. — The  period  of  incubation  is  from  three  to  seven  days, 
rarely  as  long  as  three  weeks.  Acute  and  chronic  forms  may  be  dis- 
tinguished. 

In  acute  glanders  the  onset  is  abrupt,  and  is  characterized  by  fever, 
chilliness,  headache,  neuromuscular  pains  in  the  limbs  and  joints,  and 
the  local  lesions — swelling  and  congestion  of  the  nose,  which  is  painful 
and  tender  and  discharges  a  sanious  purulent  lluid.  Examination  re- 
veals considerable  nodular  swelling  of  the  nasal  mucous  membrane,  and 
in  the  course  of  several  days  more  or  less  extensive  ulceration,  which 
may  progress  to  necrosis  of  the  bone.  Lymphangitis  is  marked  and 
the  adjacent  lymph  nodes  are  swollen  and  tender.  An  eruption,  at 
first  papular,  but  soon  becoming  pustular,  and  often  leading  to  ulcera- 
tion, occurs  on  the  face,  about  the  joints,  and  sometimes  on  the  trunk; 
it  has  been  mistaken  for  smallpox.  Pneumonia,  arthritis,  and  other 
evidences  of  bacteremia  usually  develop,  and  the  patient  dies  within 
ten  days. 

Chronic  glanders  resembles  and  is  usually  mistaken  for  chronic  coryza. 
It  is  likely  to  escape  diagnosis  for  some  time,  unless  the  nodular  swelling 
and  ulceration  attract  the  attention  of  an  observing  physician.  It  may 
last  for  months,  and  the  patient  may  eventually  recover. 

Acute  farcy,  the  result  of  cutaneous  infection,  resembles  ordinary 
pyococcic  infections,  or  septicemia.  The  site  of  the  inoculation  often 
presents  phlegmonous  inflammation,  the  lymphatic  vessels  become 
inflamed  and  thickened,  and  along  their  course  nodular  swellings  (so- 
called  farcy  buds)  develop,  and  usually  go  on  to  suppuration.  Swelling 
and  suppuration  of  the  lymph  nodes,  septic  arthritis,  disseminated 
abscesses,  in  short  the  manifestations  of  pyemia,  ensue,  and  the  patient 
usually  dies  within  two  weeks.  The  nose  is  not  involved  and  the  cuta- 
neous rash  of  ordinary  glanders  is  not  present. 

Chronic  farcy  presents  the  local  lesions  of  acute  farcy  but  with 
little  reaction,  and  without  the  severe  general  manifestations.  The 
farcy  buds  often  soften  and  form  abscesses,  and  ultimately  deep,  more 
or  less  indolent  ulcers.  The  disease  may  go  on  for  years,  but  finally 
death  results  from  exhaustion  or  acute  pyemic  glanders. 


ANTHRAX  161 

Diagnosis. — Acute  glanders  and  farcy  are  usually  readily  recognized, 
but  the  chronic  forms  often  escape  detection;  in  both,  the  occupation 
of  the  patient  may  afford  the  first  clue.  In  suspected  cases  some  of  the 
discharge  should  be  examined  for  Bacillus  mallei.  Some  of  it  may  be 
injected  into  the  peritoneal  cavity  of  a  male  guinea-pig,  the  testicles  of 
which,  in  the  event  of  glanders,  at  the  end  of  two  days,  become  swollen 
and  soon  suppurate,  and  in  the  course  of  two  weeks  the  animal  dies 
of  generalized  nodular  glanders  (Strauss'  test).  The  mallein  reaction 
(similar  to  the  tuberculin  reaction)  is  also  of  diagnostic  value  in  suspected 
cases.  In  acute  cases  the  infecting  bacillus  may  be  cultivated  from  the 
blood. 

Prognosis. — The  prognosis  is  bad. 

Treatment. — Treatment  in  the  acute  cases  is  usually  unavailing,  but 
supportive  measures  should  be  employed.  In  the  more  chronic  cases  sur- 
gical measures  are  indicated.  Potassium  iodide  internally  and  mercury 
by  inunction  are  said  to  have  been  of  much  service  in  some  cases.  Mal- 
lein has  not  yet  proved  of  much  value  as  a  therapeutic  remedy.  Some 
encouraging  results  following  the  use  of  bacterial  vaccines  have  recently 
been  reported. 

ANTHRAX. 

(Malignant  Pustule;  Anthrax,  or  Mycosis  Intestinalis;  Anthrax,  or  Mycosis  Pulmo- 
nalis;  Splenic  Fever;  Wool-sorter's  Disease;  Rag-picker's  Disease;  Charbon.) 

Anthrax  is  an  acute,  specific,  infectious  disease  caused  by  Bacillus 
anthracis  (Pollender-Davaine) ,  and  characterized  by  local  oedema  and 
inflammation,  and  often  by  bacteremia. 

Etiology. — Anthrax  is  a  widespread  disease  of  the  lower  animals  — 
most  common  among  the  herbivora,  less  common  among  the  omnivora, 
and  least  common  among  the  carnivora.  It  frequently  leads  to  extreme 
devastation  of  herds  of  cattle  and  of  sheep,  especially  in  Russia,  Siberia, 
and  certain  parts  of  Europe — where  it  is  much  more  frequent  than  in 
this  country.  Infection  in  animals  is  acquired  by  direct  inoculation 
— through  the  bites  and  stings  of  infected  insects,  and  through  feed- 
ing upon  infected  grain  (infected  by  the  feces  of  diseased  animals,  for 
instance),  and  upon  the  carcasses  of  animals  dead  of  the  disease.  Infec- 
tion may  be  transmitted  to  man  directly  through  the  bites  and  stings 
of  infected  insects  (flies,  mosquitoes,  etc.),  through  the  secretions  of 
infected  animals,  through  handling  infected  hides,  hair,  or  wool,  or 
through  the  ingestion  of  infected  food  (milk,  butter,  meat,  sausage, 
etc.).  Infection  is  acquired  through  a  cutaneous  wound,  through  the 
respiratory  tract  (inhaling  infected  dust) ,  or  through  the  gastro-intestinal 
tract.  The  disease  is  most  common  among  stablemen,  butchers,  tanners, 
wool-sorters,  rag-pickers,  hair-cleaners,  brush-makers,  etc.  Most  of  the 
cases  in  this  country  result  from  handling  imported  hides,  hair,  and  wool. 
Either  the  bacilli  or  their  spores  may  transmit  the  infection.  One  attack 
of  the  disease  confers  a  partial  immunity. 
U 


162  BACTERIAL  INFECTIONS 

Pathology. — ^Tlie  lesions  in  man  vary,  depending  upon  the  mode  of 
infection;  cutaneous,  respiratory,  and  gastro-intestinal  forms  may  be 
recognized,  but  in  many  cases  the  lesions  are  widespread.  Cutaneous 
infection  occurs  most  frequently  on  exposed  surfaces  (the  hand,  arm, 
face,  neck),  and  is  characterized  by  the  development  of  the  so-called 
malignant  pustule  (which,  however,  is  a  misnomer,  since  the  lesion  is  in 
no  way  related  to  ordinary  pyococcic  pustules).  Preceded  usually  by 
itching,  a  papule  develops  at  the  site  of  inoculation;  this  soon  becomes 
a  vesicle,  filled  w^ith  a  clear,  more  commonly  a  sanious,  fluid,  and 
surrounded  by  a  wide  area  of  inflammatory  oedema  and  induration. 
By  the  end  of  thirty-six  hours  the  vesicle  has  dried  and  a  blackish 
eschar  has  formed;  about  this  there  may  be  a  series  of  vesicles.  The 
inflammatory  phenomena  spread  along  the  lymphatics  and  give  rise  to 
lymphangitis,  lymphadenitis  (and  sometimes  phlebitis),  and  to  the 
most  extreme  and  widespread  oedema.  I  have  seen  a  small  lesion  of 
the  chin  give  rise  to  extreme  oedema  of  the  face,  neck,  arm,  and  chest. 
Respiratory  infection  results  in  severe  bronchitis,  bronchopneumonia, 
pleuritis,  swelling  of  the  bronchial  lymph  nodes,  and  marked  oedema  of 
the  mediastinal  tissues  and  sometimes  of  the  neck.  Intestinal  infection 
results  in  the  development  in  the  mucosa  of  the  small  intestine,  the 
stomach,  rarely  the  large  intestine,  of  small  foci  of  inflammatory  oedema 
and  hemorrhage  progressing  to  central  necroses,  and  swelling  of  the 
mesenteric  lymph  nodes.  Secondary  intestinal  infection  is  common  in 
the  other  forms  of  the  disease.  In  most  cases  bacteremia  develops  at  the 
end  of  forty-eight  hours.  In  fatal  cases  the  spleen  is  enlarged,  softened, 
and  hemorrhagic,  and  the  ordinary  manifestations  of  toxemia  (paren- 
chymatous degeneration,  etc.),  as  well  as  small  hemorrhages,  are  en- 
countered in  the  dift'erent  organs. 

Symptoms. — The  period  of  incubation  in  cutaneous  infections  is  from 
three  to  six  days,  at  the  end  of  which  time,  attended  by  chill  or  chilliness, 
fever  (102°  to  103°  F.),  headache,  malaise,  the  above-described  "malignant 
pustule"  develops.  Despite  the  extensive  swelling,  pain  is  rarely  a  con- 
spicuous symptom.  The  fever  often  lasts  only  two  or  three  days,  after 
which  the  temperature  may  become  normal.  In  unfavorable  cases 
symptoms  of  intestinal  infection  (vomiting,  diarrhoea,  etc.),  and  cerebral 
symptoms,  such  as  delirium,  and  coma,  develop,  the  pulse  becomes 
rapid  and  weak,  profuse  sweats  ensue,  and  the  patient  may  die  in  less 
than  a  week.  In  more  favorable  cases  the  eschar  is  separated  and 
cicatrization  proceeds,  the  swelling  subsides,  and  the  patient  eventually 
recovers.     All  of  the  three  patients  that  I  have  seen  recovered. 

Malignant  anthrax  oedema  is  the  name  given  to  a  condition  differing 
from  the  foregoing  in  the  absence  of  a  local  lesion.  The  oedema  is 
secondary  to  the  general  infection,  involves  the  face,  head,  and  some- 
times the  arms,  and  is  often  so  extreme  that  gangrene  results,  and  the 
patient  usually  dies. 

In  ■pulmonary  anthrax  the  usual  manifestations  of  severe  bronchitis 
and  of  bronchopneumonia  develop — chill,  high  fever  (103°  F.),  cyanosis, 


ANTHRAX  1C3 

cough,  expectoration  (often  hemorrhagic  and  containing  the  anthrax 
baciUus),  prostration,  profuse  sweats,  and  collapse.  Crackling  rales  and 
harsh  bronchovesicular  breathing,  sometimes  scattered  foci  of  dulness 
(due  sometimes  to  patches  of  solidification  and  sometimes  to  enlarged 
lymph  nodes),  and  bronchial  breathing  may  be  detected.  So  severe  is  the 
infection  in  some  cases  that  the  patient  succumbs  within  twenty-four  to 
forty-eight  hours  under  manifestations  of  profound  intoxication. 

In  intestinal  anthrax  the  symptoms  usually  resemble  severe  poisonings 
— sudden  onset,  with  chill  or  chilliness,  fever,  nausea,  vomiting,  head- 
ache, pains  in  the  back  and  legs;  later  diarrhoea,  hematemesis,  and 
sometimes  blood  (and  the  anthrax  bacillus)  in  the  stools,  cutaneous 
and  mucous  membrane  petechise,  and  symptoms  of  toxemia,  such  as 
coma,  etc.,  may  ensue.  Death  usually  results  in  from  two  to  five  days. 
Intestinal  symptoms  are  common  in  all  forms  of  the  infection. 

Coma  and  delirium  are  not  infrecpient  in  all  forms  of  the  infection,  and 
are  attributable  in  most  cases  to  toxemia,  but  in  some  fatal  cases  an  un- 
usual infection  of  the  cerebral  vessels  with  the  anthrax  bacillus  has  been 
encountered.  On  the  other  hand,  in  quite  a  few  cases  the  mind  is  clear 
through  the  disease. 

Diagnosis. — The  cutaneous  lesions  are  quite  characteristic  and  scarcely 
to  be  mistaken  for  anything  else.  From  the  ordinary  carbuncle  they  may 
be  distinguished  by  the  absence  of  pus  and  of  the  slough  (so-called  core). 
The  diagnosis  may  be  confirmed  by  examining  some  of  the  fluid  for  the 
anthrax  bacillus,  or  injecting  it  into  a  guinea-pig  or  a  mouse,  which, 
in  the  event  of  anthrax,  succumbs  in  a  few  days  to  anthrax  bacteremia. 
The  occupation  of  the  patient  may  afford  the  first  clue  as  to  the  real 
nature  of  the  disease  in  internal  infections  (respiratory  and  intestinal). 

Prognosis. — The  prognosis  depends  upon  the  severity  of  the  infection. 
The  mortality  in  cutaneous  infections  about  the  face  is  about  25  per  cent. ; 
in  those  about  the  hand,  10  per  cent.;  in  internal  infections,  about  90 
per  cent. 

Treatment. — Preventive  inoculation  of  animals  (Pasteur)  with  an 
organism  of  reduced  virulence  has  been  practised  in  certain  parts  of  the 
world  with  asserted  good  results.  Serum  therapy  as  yet  affords  us  no 
specific  in  the  treatment  of  the  developed  disease,  although  some  good 
results  have  followed  the  use  of  Sclavo's  serum.  In  cutaneous  infec- 
tions the  local  lesion  should  be  destroyed  with  the  cautery  or  excised;  the 
wound  then  should  be  cauterized  with  carbolic  acid,  and  treated  with 
antiseptic  dressings  (carbolic  acid  and  mercuric  bichloride.)  Injections 
into  the  advancing  oedema  of  carbolic  acid  (2  per  cent.)  or  of  mercuric 
bichloride  (1  to  4000)  may  be  of  service.  Large  doses  of  quinine  in- 
ternally have  seemed  of  value  in  some  cases.  Stimulants  and  good  food 
are  required  in  all  cases. 


164  BACTERIAL  INFECTIONS 


MALTA  FEVER. 

{Mediterranean  Fever;  Gibraltar  Fever;  Rock  Fever;  Neapolitan  Fever; 
Undulant  Fever.) 

Malta  fever  is  a  subacute  or  chronic,  specific,  infectious,  and  non- 
contagious disease  caused  by  Micrococcus  melitensis  (Bruce),  and 
characterized  by  peculiar  undulatory  febrile  attacks,  profuse  sweats, 
swelling  of  the  joints,  enlargement  of  the  spleen,  and  a  specific  serum 
reaction. 

Etiology. — Malta  fever  is  endemic  in  the  Island  of  Malta,  and  in  the 
other  islands  and  along  the  shores  of  the  Mediterranean  Sea;  and  it 
has  been  observed  in  China,  India,  Porto  Rico,  the  Philippines,  and 
the  United  States  (imported  cases).  It  is  not  unlikely  that  certain  of 
the  ill-understood  fevers  of  the  tropics,  especially  of  Central  and  South 
America,  may  ultimately  be  determined  to  be  of  similar  nature.  The 
disease  occurs  at  all  periods  of  life,  but  is  especially  frequent  between 
the  sixth  and  the  thirtieth  year.  Sex  is  devoid  of  etiological  influence. 
The  development  of  the  disease  seems  to  be  favored  by  dry  weather, 
whence  it  is  most  common  during  June,  July,  and  August. 

The  specific  cause  of  the  disease  is  Micrococcus  melitensis.  In  Malta 
the  British  Army  surgeons  seem  definitely  to  have  proved  that  the  infec- 
tion is  derived  from  the  goat;  10  to  15  per  cent,  of  these  animals  have 
the  micrococcus  in  their  milk,  and  their  blood  serum  gives  a  positive 
agglutination  test.  With  this  infected  milk  the  disease  was  transmitted 
to  monkeys;  and  stopping  the  use  of  the  milk  remarkably  reduced  the 
disease  among  the  British  troops.  Whether  the  disease  may  be  other- 
wise spread,  for  instance,  by  other  food  or  drink,  by  the  air,  by  the  bites 
of  insects  (mosquitoes,  as  has  been  suggested),  by  fomites,  etc.,  and 
whether  it  may  be  acquired  by  inhalation  and  direct  inoculation  (or 
through  the  conjunctiva,  as  in  Strong's  case),  as  well  as  by  ingestion, 
have  not  yet  been  definitely  determined.  One  attack  of  the  disease 
confers  a  more  or  less  permanent  immunity. 

Pathology. — ^The  conspicuous  lesions  consist  of  enlargement  of  the 
spleen,  which  is  hyperemic,  soft,  and  almost,  if  not  quite,  diffluent, 
and  contains  an  excess  of  lymphoid  cells;  hyperemia  of  the  gastro- 
intestinal tract  (occasionally  progressing  to  inflammation  and  ulcera- 
tion), of  the  liver,  of  the  kidneys  (sometimes  progressing  to  glomerulo- 
nephritis), and  sometimes  of  the  meninges.  The  spleen  contains  large 
numbers  of  the  specific  micrococcus,  which  may  be  cultivated  without 
difficulty. 

Symptoms. — The  period  of  incubation  varies  from  three  to  twenty 
days.  The  onset  is  gradual  and  marked  by  lassitude,  malaise,  head- 
ache, neuromuscular  pains  in  the  limbs,  anorexia,  and  fever,  which 
increases  day  by  day,  in  a  more  or  less  well-marked  "step-ladder" 
fashion,  until  at  the  end  of  a  week  or  ten  days   it  reaches  103°  or 


MALTA   FEVER  165 

104°  F.,  in  the  evening.  The  morning  remissions  of  the  fever  are  often 
attended  by  profuse  perspiration.  As  the  disease  progresses  the  head- 
ache may  become  severe;  the  Hver  and  spleen  are  found  enlarged  and 
tender;  symptoms  of  bronchial  and  of  intestinal  catarrh  may  supervene 
(though  constipation  rather  than  diarrhoea  is  the  rule);  divers  joints 
may  become  swollen,  tender,  and  painful;  and  the  patient  usually 
emaciates.  At  the  end  of  three  weeks  (or  sooner)  the  fever  gradually 
subsides,  the  other  symptoms  abate,  and  the  patient  apparently  enters 
upon  a  convalescence.  At  the  end  of  two  or  three  days  of  apyrexia, 
however,  the  fever  and  the  other  manifestations  gradually  return,  and 
the  patient  is  in  a  relapse.  A  series  of  such  relapses,  with  pyrexial  periods 
varying  from  one  to  three  weeks  and  separated  by  periods  of  apyrexia 
of  from  one  to  three  days  duration,  may  prolong  the  disease  into  months 
— even  a  year  or  more.  The  long-continued  fever,  often  with  remis- 
sions so  great  as  to  simulate  malaria,  and  the  profuse  sweats,  lead 
usually  to  marked  loss  of  strength  and  flesh. 

As  a  rule,  in  from  seventy  to  ninety  days,  convalescence  ensues, 
but  it  may  be  unusually  slow  and  protracted  (six  to  twelve  months), 
and  is  not  infrequently  complicated  by  arthritis,  inflammation  of  fibrous 
structures,  neuralgias,  orchitis,  etc.  Death  may  occur,  in  scarcely 
more  than  2  per  cent,  of  the  cases,  from  exhaustion  or  an  intercurrent 
disorder. 

Several  types  of  the  disease  are  recognized.  The  term  undulatory 
is  usually  applied  to  the  common  form.  Occasionally  the  onset  is 
rather  sudden,  and  death  may  occur  within  ten  days — acute  or  malig- 
nant type.  In  other  cases  the  constitutional  symptoms  are  slight, 
consisting  only  of  slight  evening  fever,  malaise,  and  progressive  emacia- 
tion, though  more  severe  symptoms  may  develop  at  any  time — so-called 
intermittent  type. 

Diagnosis. — Malta  fever  must  be  distinguished  from  typhoid  fever 
and  from  malaria.  Malaria  is  readily  excluded  by  the  absence  of  the 
malarial  parasite  from  the  blood  and  the  non-response  to  quinine.  Most 
cases,  at  least  in  regions  remote  from  the  Mediterranean,  are  mistaken 
at  the  beginning  for  typhoid  fever,  but  the  absence  of  many  of  the 
characteristic  symptoms  of  typhoid  fever  should  be  deemed  significant. 
The  diagnosis  is  rendered  certain  by  the  absence  of  the  Gruber-Widal 
serum  reaction  with  Bacillus  typhosus  and  its  presence  with  Micro- 
coccus melitensis  (in  some  cases  as  early  as  the  fourth  day  of  the  fever). 
The  peculiar  character  of  the  fever  also  is  quite  characteristic,  even  in 
the  absence  of  the  specific  serum  reaction.  The  micrococcus  in  some 
cases  may  be  cultivated  from  the  blood. 

Prognosis. — The  duration  of  the  disease  is  long,  but  the  mortality 
is  low — not  more  than  2  per  cent. 

Treatment. — Treatment  is  purely  symptomatic,  since  an  efficient 
serum-  or  vaccine-therapy  has  not  yet  been  produced.  Hydrotherapy 
and   the  general   measures   suitable   in   typhoid    fever   are   indicated. 


166  BACTERIAL  INFECTIONS 

During  the  periods  of  pyrexia  it  is  wise  to  adhere  to  the  diet  recom- 
mended in  typhoid  fever.  Drugs,  so  far  as  known,  seem  to  have  no 
influence  on  the  course  of  the  disease.  Convalescence  is  promoted  by 
tonics,  change  of  climate,  or  a  sea  voyage. 


LEPROSY. 

Leprosy  is  a  chronic,  specific,  infectious  disease  caused  by  Bacillus 
leprae  (Hansen),  and  characterized  by  granulomas  involving  the 
skin,  the  mucous  membranes,  the  nerves,  the  lymphatics,  and  the 
viscera. 

Etiology. — Leprosy  is  known  to  have  prevailed  centuries  before  the 
Christian  era.  At  present  it  is  found  in  all  parts  of  the  world,  but  is 
endemic  in  India,  China,  Japan,  and  other  parts  of  Asia,  Africa,  Russia, 
Persia,  Norway,  Sweden,  Spain,  Portugal,  Central  and  South  America, 
the  West  Indies,  Mexico,  Iceland,  Canada,  Australia,  the  Sandwich 
Islands,  etc.,  and  in  our  own  United  States,  especially  Louisiana  and 
other  southwestern  States.  From  time  to  time  isolated  cases  have 
been  observed  in  many,  if  not  all,  the  States,  but  most  of  the  cases  have 
been  imported. 

The  exciting  cause  of  the  disease  is  Bacillus  leprae,  which  is  found 
in  leprous  lesions,  in  the  secretions  therefrom,  and  in  the  saliva,  and 
oral  and  nasal  discharges  in  the  event  of  lesions  about  the  nose  and 
mouth.  The  disease  is  not  markedly  contagious,  since  prolonged 
and  rather  intimate  personal  contact  seems  necessary  for  infection; 
but  that  the  disease  may  be  spread  by  fomites  cannot  be  denied.  It 
has  been  suggested  that  fleas,  lice,  bed-bugs,  and  the  itch  parasite 
are  the  active  agents  in  transmitting  the  infection.  Hutchinson  be- 
lieves that  infection  is  spread  largely  by  uncooked  fish,  in  confirma- 
tion of  which  opinion  he  points  to  the  prevalence  of  the  disease  in 
fish-eating  communities.  How  infection  is  acquired  is  not  definitely 
known:  should  we  believe  Hutchinson,  it  may  be  acquired  by  inges- 
tion; it  may  be  acquired  by  inhalation — witness  the  lesions  in  the 
nose,  believed  by  some  observers  to  be  an  initial  lesion;  and  the 
frequency  of  leprosy  of  the  hands  and  the  feet  (often  uncovered),  to- 
gether with  the  presence  of  lepra  bacilli  in  the  earth,  suggests  that  infec- 
tion may  be  acquired  by  direct  inoculation  through  wounds.  Heredity 
is  of  little,  if  any,  etiological  influence;  the  youngest  subjects  are  rarely 
less  than  three  to  six  years  of  age ;  beyond  this  no  age  is  exempt. 

Pathology. — Leprosy  is  one  of  the  so-called  granulomas.  The 
lesions  consist  of  nodular  masses  or  diffuse  infiltrations  made  up  of 
small  rounded  and  fusiform  cells,  larger  endothelial  often  vacuolated 
cells,  and  giant  cells,  in  and  between  which  the  lepra  bacilli  are  found 
in  profusion.  These  lesions  are  found  usually  in  the  skin,  the  mucous 
membranes,  and  the  viscera.  On  the  surface  the  lesions  not  infre- 
quently progress  to  softening  and  ulceration  attended  by  marked  loss 


LEPROSY  167 

of  tissue  and  noteworthy  mutilation.  In  the  nerves  nodular  and  diffuse 
infiltrations  are  observed,  with  overgrowth  of  the  connective  tissue  and 
atrophy  of  the  axons.  Changes  analogous  to  tabetic  arthropathy  are 
sometimes  observed  in  the  bones.  The  lymph  nodes  are  often  palpably 
enlarged. 

Symptoms. — ^^Fhe  period  of  incubation  is  from  three  to  five  years 
(Hansen),  but  a  case  of  presumed  direct  inoculation  has  been  observed 
in  which  the  period  of  incubation  was  four  weeks.  Some  observers 
believe  in  the  existence,  of  a  primary  sore  (the  existence  of  which  is  not 
altogether  unlikely),  and  have  located  it  commonly  in  the  nose  (where 
they  have  observed  ulceration),  but  the  evidence  is  not  yet  conclusive. 
During  the  period  of  incubation  the  patient  suffers  from  irregular  attacks 
of  fever,  malaise,  headache,  and  pains  in  the  joints.  In  many  cases 
the  initial  manifestations  consist  of  dusky  red  erythematous  and  hyper- 
esthetic  patches  on  the  skin,  especially  of  the  face,  extensor  surfaces 
of  the  hands  and  forearms  (macular  leprosy);  these  soon  become  pig- 
mented, later  anesthetic,  and  gradually  lose  their  pigment  and  become 
white  (lepra  alba).  Soon  the  disease  takes  on  the  characters  of  one  of 
the  two  well-recognized  types,  the  nodular  (tubercular)  or  anesthetic; 
but  commonly  the  disease  is  of  mixed  type. 

The  nodular  type  is  characterized  by  the  development  of  nodules, 
varying  in  size  from  that  of  a  pea  to  that  of  a  cherry,  and  of  diffuse 
fibrous  infiltration  of  the  skin  and  the  mucous  membranes.  Beginning 
usually  in  the  skin  of  the  face  (nose,  lips,  or  chin)  or  the  ears,  they 
produce  painless,  irregular  thickenings,  nodosities,  and  folds,  leading 
to  much  distortion  and  ultimately  to  the  condition  known  as  facies 
leontina.  Gradually  nodules  and  thickenings  develop  elsewhere, 
especially  on  the  hands,  forearms,  feet,  legs,  buttocks,  knees,  etc.,  until 
much  of  the  cutaneous  surface  is  involved.  Occasionally  some  of  the 
nodules  lessen  in  size,  and  even  disappear,  but  usually  they  soften  and 
ulcerate,  and  thus  add  to  the  already  existing  deformity.  Involvement 
of  the  mucous  membrane  of  the  nose,  mouth,  throat,  and  larynx  is 
evident  in  the  nasal  discharge,  hoarseness,  aphonia,  dyspnoea,  etc., 
and  is  quite  manifest  upon  local  examination — irregular  nodular  and 
diffuse  thickenings  and  ulcerations.  Inhalation  pneumonia  not  infre- 
quently results;  and  from  involvement  of  the  conjunctiva  and  cornea 
blindness  may  ensue.  The  disease  runs  a  course  of  years  (five  to  ten 
or  more),  and  ultimately  leads  to  death  from  exhaustion  or  from  pul- 
monary or  other  complications. 

The  anesthetic  type  manifests  itself,  in  addition  to  the  macules  already 
mentioned,  by  early  pain  in  the  limbs  and  areas  of  hyperesthesia  and 
paresthesia,  followed  by  anesthesia  (often  only  analgesia)  and  trophic 
lesions  (bullae)  of  the  skin  of  the  extremities.  Anesthetic  areas,  how- 
ever, may  develop  without  preceding  macules,  and  not  infrequently 
become  extensive.  The  bullae  often  break  down  and  lead  to  the  forma- 
tion of  extensive  perforating  ulcers  and  widespread  destruction  of  tissues. 
The  nerve  trunks  are  often  palpably  thickene<^l;  the  muscles  waste; 


168  NON-BACTERIAL  FUNGUS  INFECTIONS 

the  fingers  become  clubbed  and  contracted  (claw-like) ;  wasting,  necrosis, 
and  gangrene  ensue;  and  the  fingers  and  toes  may  drop  ofl^  (leprosy 
mutilans);  or  arthropathies  (resembling  those  of  tabes)  may  develop. 
The  lesions  pursue  an  extremely  chronic  course  (ten  to  thirty  years), 
and  ultimately  lead  to  death  through  exhaustion  or  an  intercurrent 
infection. 

Diagnosis. — In  advanced  cases  the  diagnosis  is  unmistakable.  In 
the  early  stages  the  dusky  red  areas  of  erythema,  at  first  hyperesthetic, 
later  anesthetic,  and  devoid  of  pigment;  the  nodular  neuritis;  and  the 
detection  of  lepra  bacilli  in  the  nasal  secretion  or  in  an  excised  nodule, 
suffice  for  diagnosis.  Serum  diagnosis — the  agglutination  of  the  lepra 
bacilli  by  the  blood  serum  of  a  leprous  patient — may  prove  of  some 
service. 

Prognosis. — The  patients  frequently  live  from  ten  to  thirty  years, 
unless  carried  off  by  an  intercurrent  infection.  In  some  cases  the 
disease  seems  to  have  been  entirely  arrested. 

Treatment. — Segregation  is  advisable  in  all  cases.  Special  attention 
should  be  paid  to  general  hygienic  measures,  and  the  patient  should 
have  an  abundance  of  good  nutritious  food,  of  sunshine,  and  of  fresh 
air.  Recently  almost  specific  properties  have  been  claimed  for  chaul- 
moogra  oil,  10  minims,  gradually  increased  to  2  drams,  three  times  daily. 
Dyer  reports  several  cures  from  its  use.  Dyer  has  also  had  good  results 
from  Calmette's  antivenene.  Gurjun  oil,  ichthyol  (Unna),  mercuric 
bichloride,  salicylic  acid,  and  many  other  remedies  have  been  recom- 
mended from  time  to  time.  A  supposed  antileprous  serum  also  has 
been  introduced  of  late.  Nastine,  a  bacterial  fat  recommended  by 
Deycke,  does  not  seem  to  be  of  much  value. 


NON-BACTERIAL  FUNGUS  INFECTIONS. 

The  non-bacterial  fungus  infections  comprise  a  group  of  diseases 
caused  by  microorganisms  that  are  sometimes  described  as  higher  bac- 
teria, sometimes  as  fungi,  but  which  probably  represent  low  forms  of 
life  intermediate  between  the  bacteria  and  the  more  highly  developed 
fungi.  They  have  been  incompletely  studied  and  classified,  but  Park 
suggests  the  following  attempt  at  differentiation:  (1)  Actinomyces, 
characterized  by  radiating  wreath-like  forms  which  it  alone  produces 
in  the  living  body.  (2)  Streptothrix,  characterized  by  an  abundant 
true  branching,  wavy  growth,  later  fragmentation,  and  the  formation 
of  conidise,  which  serve  as  organs  of  propagation,  and  in  this  sense  may 
be  considered  as  spores.  (3)  Cladothrix,  characterized  by  false  branch- 
ing, rapid  fragmentation,  and  then  bacillary  characteristics  in  old  cul- 
tures. (4)  Leptothrix,  characterized  by  lack  of  observed  branching, 
non-wavy  growth,  but,  on  the  contrary,  stiff,  almost  straight  threads,  in 
which  division  processes  are  seldom  or  never  observed. 


ACTINOMYCOSIS  169 


ACTINOMYCOSIS. 


Actinomycosis  is  a  chronic,  specific,  infectious  disease  caused  by  Strep- 
tothrix  actinomyces,  or  ray  fungus,  and  characterized  by  the  develop- 
ment of  a  chronic  granuloma  that  ultimately  softens  and  discharges 
characteristic  actinomycotic  granules. 

Etiology. — Actinomycosis  is  common  in  cattle,  in  whom  it  causes 
"big  jaw"  and  "wooden  tongue,"  in  horses,  and  in  pigs.  It  is  believed 
to  be  non-contagious,  since  direct  transference  from  the  sick  to  the  well 
is  not  observed.  Inasmuch  as  the  fungus  occurs  on  grain,  such  as 
oats,  barley,  rye,  etc.,  infection  is  probably  acquired  with  the  food — 
certainly  in  the  lower  animals.  In  man  infection  may  be  acquired  in  a 
similar  manner,  an  abrasion  of  the  mucous  membrane  or  a  carious 
tooth  (in  which  the  fungus  has  been  found)  being  probably  the  infectious 
atrium;  but  it  may  be  acquired  also  by  inhalation  (as  at  threshing,  for 
instance),  or  through  a  cutaneous  wound.  The  disease  is  three  times 
as  common  in  men  as  in  women. 

Pathology. — Actinomycosis  is  one  of  the  so-called  infectious  granulomas, 
and  consists  of  foci  of  epithelioid  cells,  giant  cells,  small  round  cells,  and 
the  fungus,  and  the  later  development  of  marked  hyperplasia  of  the  con- 
nective tissue — a  condition  not  altogether  unlike  tuberculosis;  but  so 
great  is  the  enlargement  that  it  is  sometimes  mistaken  for  sarcoma. 
Later  softening  and  suppuration  occur  and  many  sinuses  form,  from 
which  issues  a  thin,  sanious,  purulent  fluid  containing  characteristic, 
small,  sulphur-yellow,  actinomycotic  granules  which,  upon  microscopic 
examination,  reveal  the  ray  fungus. 

Symptoms. — Almost  any  organ  of  the  body  may  be  involved,  but  for 
obvious  reasons,  the  jaw  and  the  adjacent  tissues  are  most  frequently 
affected.  Usually  a  firm,  indurated  mass  develops;  this  gradually 
increasing  in  size,  ultimately  softens,  whereupon  its  contents  are  dis- 
charged through  several  sinuses.  In  consequence  of  involvement  of  the 
periosteum  and  the  bone,  necrosis  not  infrequently  ensues,  and  gradu- 
ally other  organs  become  implicated,  such  as  the  tongue,  the  tissues  of 
the  neck,  the  ear,  and  sometimes  even  the  meninges,  from  direct  exten- 
sion, and  more  distant  organs,  such  as  the  liver,  the  lung,  the  brain 
(symptoms  of  tumor),  by  metastasis.  The  region  of  the  cecum  and 
appendix  is  not  infrequently  the  seat  of  primary  involvement,  but  any 
part  of  the  large  or  the  small  intestine  may  be  involved,  and  the  actino- 
myces may  be  found  in  the  stools.  The  liver  is  rather  frequently  the 
seat  of  secondary  abscesses  (reticulated  or  honey-combed  abscesses). 
The  lungs  may  reveal  miliary  actinomycosis,  fetid  l^ronchitis,  chronic 
interstitial  pneumonia,  or  bronchopneumonia,  which  may  progress  to 
abscess  or  cavity  formation  or  gangrene;  the  actinomyces  may  be  found 
in  the  sputum.  The  pleura  may  be  markedly  thickened,  and  from 
this  by  contiguity  the  adjacent  soft  parts,  the  ribs,  or  the  vertebrae  may 


170  NON-BACTERIAL  FUNGUS  INFECTIONS 

become  involved.  Cutaneous  lesions  and  chronic  suppurative  and  ulcer- 
ative processes  have  occasionally  been  observed. 

Diagnosis. — The  disease  may  be  suspected  in  cases  of  long-standing 
suppuration  with  a  tendency  to  involvement  of  the  bones,  but  it  is  con- 
firmed only  by  finding  the  specific  cause,  the  actinomyces. 

Prognosis. — ^The  prognosis  depends  largely  upon  the  extent  of  the 
lesions  and  whether  or  not  they  are  amenable  to  surgical  interv^ention. 

Treatment. — The  treatment  is  primarily  surgical.  But  recently  in  view 
of  the  success  that  has  attended  its  administration  potassium  iodide, 
upward  of  one  dram  (4  grams)  daily,  has  come  to  be  looked  upon  as 
almost  a  specific.  Good  results  have  also  attended  the  use  of  the 
a:-rays. 

MYCETOMA. 

(Madura  Foot.) 

Mycetoma  is  a  chronic,  specific,  infectious  disease  caused  by  Strep- 
tothrix  madurse  or  Streptothrix  mycetomse,  and  characterized  by  nodular 
enlargement  and  deformity  proceeding  to  oily  degeneration  and  sinus 
formation. 

Etiology.- — Mycetoma  has  been  observed,  usually  sporadically,  in 
Asia,  Europe,  South  America,  and  the  United  States.  It  is  most  common 
between  the  twentieth  and  the  forty-fifth  year,  and  occurs  more  frequently 
in  men  (especially  those  who  go  bare-footed)  than  in  women.  How 
infection  occurs  is  not  definitely  known,  though  it  is  not  unlikely  through 
a  wound  or  abrasion,  or,  as  some  believe,  through  the  sweat  glands. 

Symptoms. — Two  varieties  of  mycetoma  are  recognized,  the  melanoid, 
or  mycetoma  with  black  granules,  and  the  ochroid,  or  mycetoma  with 
yellowish  or  white  granules — due  respectively  to  Streptothrix  madurse 
and  Streptothrix  mycetomee.  The  disease  begins  with  the  development 
of  a  hard,  firm,  painless  nodule  on  the  sole  of  one  foot,  usually  the  right, 
though  other  parts  may  be  affected,  such  as  a  toe,  the  hand,  or  a  finger. 
The  nodule  soon  softens  and  at  the  end  of  about  a  month  ruptures  and 
discharges  a  peculiar,  viscid,  oily,  slightly  purulent,  and  sometimes  blood- 
streaked  fluid  in  which  the  blackish  or  yellowish  granules  are  suspended. 
Similar  lesions  develop  elsewhere  in  the  foot,  which  ultimately  becomes 
much  enlarged.  The  lesions  gradually  attack  the  muscles,  ligaments, 
and  bones  and  convert  them  into  a  thick,  greasy,  yellowish  mass  into 
which  a  probe  may  be  inserted  in  any  direction  to  a  considerable  depth 
without  provoking  pain  or  hemorrhage.  The  lesions  show  little  or  no 
tendency  to  heal,  the  sinuses  being,  as  a  rule,  permanent.  As  the  foot 
enlarges  and  can  no  longer  be  used,  the  leg  atrophies  from  disuse.  In 
some  cases  the  lesions  tend  to  spread  along  the  lymphatics  and  set  up 
new  foci  of  infection.  The  general  health  remains  unimpaired  for  a 
long  time;  the  patient  may  live  ten  or  twenty  years,  but  ultimately 
succumbs  to  exhaustion  or  an  intercurrent  infection. 

Diagnosis. — The  disease  is  only  likely  to  be  mistaken  for  actinomy- 
cosis to  which  the  disease  is  much  allied.    Doubtless  manv  of  the  ca.ses 


PULMONARY   ASPERGILLOSIS  171 

reported,  especally  in  this  country,  were  really  actinomycotic.  The 
differential  diagnosis  is  to  be  made  largely  by  a  microscopic  examination 
of  the  discharge.  In  some  cases  the  lesions  may  simulate  those  of 
syphilis  or  sarcoma. 

Treatment. — The  treatment  consists  of  resection  if  a  small  area  only 
is  involved,  and  of  amputation  if  the  disease  is  more  widespread.  The 
amputation  must  be  done  well  above  the  infected  area.  Potassium 
iodide  is  useless. 

NOCARDIOSIS. 

(Streptothricosis ;  Cladothricosis;  Pseudotuberculosis;  Atypical  Actinomycosis.) 

Nocardiosis  is  a  generic  term,  suggested  by  Wright,  to  describe  a  group 
of  diseases  caused  by  nocardia,  microorganisms  to  which  the  terms 
streptothrix,  cladothrix,  pseudotubercle  bacillus,  and  atypical  actin- 
omycosis have  also  been  applied. 

Etiology. — ^These  nocardia  are  widely  distributed  in  nature.  Infection 
is  usually  acquired  through  inhalation,  rarely  by  means  of  cutaneous  or 
mucous  membrane  wounds;  and  it  is  predisposed  to  by  general  malnutri- 
tion.    The  infection  is  rare  in  man. 

Pathology. — The  lesions  consist  of  inflammation,  necrosis,  suppuration, 
abscess  formation,  and  granulation  tissue.  In  some  cases  the  lesions 
resemble  tuberculosis,  that  is,  there  are  tubercles,  fibrocaseous  nodules, 
and  calcification.  The  lesions  are  most  common  in  the  lungs;  metastases 
have  been  observed  in  the  brain,  kidney,  myocardium,  lymph  nodes,  etc. 

Symptoms. — ^The  process  may  be  acute  or  chronic.  The  symptoms 
vary,  depending  upon  the  seat  of  the  lesions,  but  in  general  they  are  those 
of  inflammation  and  suppuration.  When  occurring,  as  is  common,  in 
the  lung,  the  symptoms  are  those  of  pneumonia,  abscess,  tuberculosis,  or 
empyema.  In  the  brain,  the  symptoms  are  those  of  abscess,  tumor,  or 
meningitis.  Multiple  abscesses  may  occur  in  the  skin  and  subcutaneous 
tissues. 

Diagnosis. — Occasionally  the  symptoms  have  been  somewhat  atypical 
of  the  disease  suspected,  but,  as  a  rule,  the  diagnosis  depends  solely  upon 
detecting  the  causative  microorganism  in  the  sputum  or  other  discharge 
or  fluid  of  the  body. 

Prognosis. — The  outlook  is  bad,  since  the  great  majority  of  the  sub- 
jects finally  succumb. 

Treatment. — ^There  is  no  specific  treatment.  In  general,  the  treatment 
is  that  of  the  disease  suspected — pneumonia,  tuberculosis,  abscess  of  the 
lung,  etc.     Abscesses  should  be  treated  surgically. 


PULMONARY  ASPERGILLOSIS. 

Pulmonary  aspergillosis  is  a  chronic  disease  caused  by  Aspergillus 
fumigatus  and  characterized  by  inflammation  and  necrosis  of  the  lung. 


172  NON-BACTERIAL  FUNGUS  INFECTIONS 

Etiology. — Aspergillus  fumigatus  is  widely  distributed  in  nature,  and 
is  often  found  as  a  harmless  parasite  on  different  surfaces  and  in  certain 
cavities  of  the  body.  Most  of  the  cases  of  infection  occurring  in  man  are 
secondary  or  terminal,  developing  especially  in  tuberculosis;  but  appar- 
ently primary  cases  have  been  observed.  The  infection  is  believed  to 
be  acquired  from  infected  birds  or  infected  seed  fed  to  birds  (occurring 
thus  in  pigeon  feeders),  or  from  the  dust  of  rye  flour  used  to  remove 
grease  from  hair  (whence  the  infection  occurs  in  hair-sorters). 

Pathology. — The  lesions  consist  of  inflammatory  processes  akin  to  those 
of  bronchopneumonia,  in  the  midst  of  which  the  fungus  may  be  en- 
countered. From  coalescence  of  adjacent  foci  more  or  less  widespread 
solidification  may  occur.  Ultimately  necrosis  and  softening  may  ensue, 
cavity  formation  develop,  and  gangrene  may  supervene. 

Symptoms. — ^The  symptoms  are  those  of  chronic  tuberculosis,  chronic 
interstitial  pneumonia,  bronchiectasis,  etc.,  and  aside  from  the  presence 
of  the  fungus  in  the  expectoration  may  not  present  special  characteristics. 

Diagnosis. — ^The  diagnosis  depends  upon  detecting  the  fungus  in  the 
sputum.  In  most  cases,  cases  of  secondary  or  terminal  infection,  the 
infection  may  be  of  minor  importance;  the  tubercle  bacillus  may  be 
found  associated  with  the  fungus. 

Prognosis. — ^The  outlook  is  bad,  largely  because  of  the  associated 
conditions. 

Treatment .^The  treatment  is  that  of  the  underlying  disease,  such  as 
tuberculosis,  etc.  Arsenic  and  potassium  iodide  have  also  been  recom- 
mended. Prophylactic  measures,  looking  to  the  avoiding  of  inhaling 
infected,  dust-laden  atmosphere,  should  be  undertaken  with  a  view  to 
prevent  the  primary  cases. 


OIDIOMYCOSIS. 

{Blastomycosis;  Saccharomycosis ;  Blastomycetic  Dermatitis;  Protozoic  Derviatitis; 
Dermatitis  Coccidio'ides;  Coccidioidal  Granuloma;  Psorospermiasis.) 

Oidiomycosis  is  a  chronic  infectious  disease  of  the  skin  and  internal 
organs  caused  by  fungi  of  the  genus  Oidium,  and  characterized  by  granu- 
lomatous inflammation  proceeding  to  suppuration. 

Etiology. — The  organism  is  widely  distributed  in  nature,  but  the  factors 
leading  to  infection  in  man  are  not  well  understood. 

Pathology. — ^The  lesions  may  be  limited  to  the  skin  or  the  lungs,  or 
they  may  involve  also  other  organs,  such  as  the  liver,  spleen,  kidneys, 
adrenals,  lymph  nodes,  meninges,  etc.  In  general  they  consist  of  granu- 
lomatous formations  tending  to  softening  and  abscess  formation.  In 
some  cases  the  slow  progression  of  the  lesions  and  the  absence  of  soften- 
ing suggest  tuberculosis.  In  the  skin  the  lesions  may  simulate  those  of 
tuberculosis  or  squamous  epithelioma. 

Symptoms. — In  the  skin  the  symptoms  consist  of  the  development  of  a 
papular  or  pustular  area,  which  gradually  increases  in  size  to  form  a 


PROTOZOAN  INFECTIONS  173 

rough,  scaly,  elevated  fungus-like  surface,  variously  the  seat  of  minute 
abscesses  and  of  scars  in  different  stages  of  cicatrization.  In  the  lungs 
and  other  viscera  the  symptoms  are  analogous  to  those  of  tuberculosis. 

Diagnosis. — The  diagnosis  depends  upon  the  detection  of  the  causative 
microorganism. 

Prognosis. — The  disease  is  chronic,  lasting  many  years.  When  limited 
to  the  skin  the  process  may  be  brought  to  a  standstill  or  cured;  but  when 
the  viscera  become  involved  death  usually  eventually  ensues. 

Treatment. — Potassium  iodide  in  large  doses  (150  grains,  10  grams, 
daily)  has  been  followed  by  good  results  in  some  cases.  The  x-rays  are 
also  of  service  in  some  cutaneous  lesions;  or  these  lesions  may  be  curetted, 
excised,  or  treated  with  antiseptics. 


ZOOPARASITIC  INFECTIONS. 


PROTOZOAN  INFECTIONS. 

The  protozoa  are  unicellular  animal  organisms  that  reproduce  by 
division  or  sporulation.  There  are  four  important  phyla  (tribes)  or 
primary  divisions : 

1.  Sarcodina,  protozoa  that  throw  out  changeable  protoplasmic 
processes,  called  pseudopodia,  which  serve  the  double  purpose  of  nutri- 
tion and  locomotion.  To  these  belong  the  class  Rhizopoda  (those  with 
lobose  or  reticulose  pseudopodia).  These  include :  Entamoeba  dysenteriae 
(or  histolytica),  the  cause  of  one  form  of  dysentery;  Entamoeba  coli, 
believed  to  be  a  harmless  intestinal  parasite;  and  Leydenia  gemmipara, 
which  has  been  found  in  ascitic  fluid  in  cases  of  carcinomatosis,  but  is 
perhaps  of  no  pathogenic  significance. 

2.  Mastigophora,  protozoa  provided  with  undulating  membranes 
or  flagella  that  serve  as  means  of  locomotion  and  obtaining  food.  To 
these  belong  the  class  Flagellata  (small  forms  with  one  or  several  flagella). 
These  include:  (a)  Spirochsetse  (spiral  in  shape  and  provided  with  an 
undulating  membrane,  but  no  flagella),  of  which  Spirochfeta  recurrentis 
(or  obermeieri)  is  the  cause  of  relapsing  fever  of  Europe,  and  is  perhaps 
related  to  Spirochseta  carteri  (relapsing  fever  of  India),  Spirocha^ta  novyi 
(relapsing  fever  of  America),  and  Spirochfeta  duttoni  (relapsing  fever 
of  Africa) ;  Spirochfeta  vincenti  is  found,  associated  with  a  fusiform 
bacillus,  in  some  cases  of  inflammation  of  the  throat,  called  Vincent's 
angina;  and  Spirochfeta  refringens  is  found  in  ulcerations  of  the  genitalia, 
and  is  often  associated  with  Treponema  })alli(hnn  in  syphilitic  lesions. 
(/;)  Treponemfe,  those  with  a  flagellum  at  botii  ends,  but  witliout  an 
undulating  membrane.  Of  these,  Treponema  pallidum  is  the  cause  of 
syphilis;  and  Treponema  pertenuis  is  believed  to  be  the  cause  of  yaws 


174  PROTOZOAN  INFECTIONS 

(framboesia).  (c)  Trypanosomse,  those  with  a  more  or  less  spiral-shaped 
body,  along  one  side  of  which  there  is  an  undulating  membrane  from 
which  a  flagellum  projects.  Of  these,  Trypanosoma  gambiense  is^the 
cause  of  human  trypanosomiasis,  or  sleeping  sickness.  The  following 
trypanosomes  also  are  found  in  mammals:  Trypanosoma  lewisi,  which 
infects  rats,  but  seems  usually  not  to  occasion  noteworthy  symptoms; 
Trypanosoma  evansi,  the  cause  of  surra  in  horses  and  mules,  especially 
in  India  and  the  Philippines;  Trypanosoma  brucei,  the  cause  of  nagana 
in  horses,  and  found  also  in  many  game  animals  in  Africa;  Trypanosoma 
equiperdum,  transmitted  by  coitus,  the  cause  of  dourine  (maladie  du 
coit)  in  horses  and  donkeys;  Trypanosoma  equinum,  the  cause  of 
vial  de  caderas  in  horses  in  South  America;  Trypanosoma  theileri,  the 
cause  of  galziekte  (gall  sickness)  in  cattle;  and  Trypanosoma  dimorphon, 
the  cause  of  Gambian  horse  disease,  (d)  Leishmania  (oval  intracellular 
parasites),  of  which  Leishmania  donovani  is  the  cause  of  kala-azar,  and 
Leishmania  tropica  is  the  cause  of  oriental  sore,  (e)  Trichomonas, 
a  parasite  with  a  fusiform  body,  an  undulating  membrane  and  three 
flagella  arising  from  its  anterior  end.  These  include:  Trichomonas 
vaginalis,  which  is  common  in  acid  vaginal  mucus;  and  Trichomonas 
(or  Cercomonas)  hominis,  which  is  found  in  the  intestine,  where  appar- 
ently it  may  set  up  an  acute  enteritis ;  and  it  may  invade  or  be  introduced 
into  the  bladder  and  set  up  cystitis.  (/)  Lamblia  intestinalis  (a  pear- 
shaped,  flagellated  organism),  which  is  common  in  the  intestine,  w^here 
it  may  perhaps  set  up  acute  or  chronic  diarrhoea ;  it  has  been  found  also 
in  the  expectoration  of  bronchiectasis  and  gangrene  of  the  lung,  in  pleural 
exudates,  etc. 

3.  Infusoria,  protozoa  with  cilia.  To  these  belong  the  ciliata  (those 
with  contractile  vacuoles  and  many  fine  cilia  which  are  shorter  than 
flagella  and  exhibit  a  sweeping  motion).  These  include  Balantidium  coli, 
a  parasite  that  is  common  in  hogs,  and  may  set  up  a  dysenteric  disorder 
in  man. 

4.  Sporozoa,  protozoa  without  motile  organs,  that  reproduce  by 
sporulation.  These  include:  (a)  Coccidiaria,  of  which  Eimeria  stiedse 
(Coccidium  cuniculi  or  oviforme)  is  most  frequently  found  in  the  epithe- 
lium of  the  bile  ducts  of  animals,  especially  rabbits,  and  the  oocyst  of 
which  may  be  found  in  the  feces.  The  disorder  is  known  as  coccidiosis; 
several  cases  have  been  reported  in  man.  Isospora  bigemina  (Coccidium 
bigeminum)  is  common  in  the  intestine  of  dogs  and  cats,  and  has  been 
observed  in  the  human  subject,  (h)  Hcemosporidia,  of  which  Plasmodium 
malarite  is  the  cause  of  malarial  fever.  Similar  organisms  have  been 
found  in  other  animals:  Plasmodium  kochi  in  monkeys;  Plasmodium 
prsecox  in  birds  (causing  proteosoma;  halteridium  in  crows  and  pigeons); 
and  other  hsemosporidia  in  other  animals. 


AMCEBIASIS  175 

AMCEBIASIS. 

(Amoebic  Dysentery;  Amoebic  Colitis.) 

The  common^manifestation  of  amoebiasis  is  an  acute  or  chronic  in- 
flammation and  ulceration  of  the  colon  caused  by  Entamoeba  dysenteriae 
(or  histolytica).  Schaudinn,  Craig,  and  others  distinguish  two  forms 
of  amoebae  that  may  be  found  in  the  intestine,  the  pathogenic  Entamoeba 
dysenterise,  and  Entamoeba  coli,  believed  to  be  a  harmless,  non-patho- 
genic form. 

Etiology. — ^Amoebic  dysentery  is  endemic  in  the  tropics,  where  it  is  a 
very  common,  if  not  the  commonest  form  of  dysentery  encountered. 
Sporadic  cases  occur  from  time  to  time  throughout  the  subtropical  and 
the  temperate  zones,  and  epidemics  are  by  no  means  unknown.  The 
disease  is  most  common  in  young  male  adults;  it  prevails  especially 
among  the  poor,  and  it  is  predisposed  to  by  general  malnutrition  and 
unhygienic  surroundings.  The  infection  is  usually  transmitted  by  the 
drinking  water. 

Pathology. — ^The  lesions  may  involve  the  entire  colon,  and  sometimes 
even  the  lower  part  of  the  ileum;  but  they  are  most  common  and,  as  a  rule, 
most  marked  in  the  cecum,  in  the  hepatic  and  sigmoid  flexures,  and  in  the 
rectum.  They  consist  of  inflammation,  oedema,  and  cellular  infiltra- 
tion of  the  submucosa,  which  are  soon  followed  by  necrosis  and  ulcera- 
tion. In  the  early  stages  there  are  localized  areas  of  thickening  and 
infiltration,  the  mucous  covering  of  which  soon  becomes  soft  and  necrotic, 
and  eventually  being  discharged,  leaves  a  roundish,  ovoid,  or  irregular 
ulcer.  The  base  of  the  ulcer  is  often  much  larger  than  the  point  of  dis- 
charge of  the  necrotic  tissue,  that  is,  the  edges  of  the  ulcer  are  undermined 
or  overhanging;  and  adjacent  ulcers  often  communicate  by  means  of 
sinuous  tracts,  the  mucosa  overlying  which  may  be  more  or  less  normal, 
although  it  is  usually  more  or  less  thickened  and  inflamed.  The  floor 
of  the  ulcer  may  be  made  up  of  the  submucosa,  the  muscularis,  or  the 
serosa;  or  it  may  be  adhesions  that  bind  the  colon  to  adjacent  organs 
or  tissues.  Perforation  may  occur  into  these  adhesions  or  into  the 
surrounding  connective  tissue  or  the  peritoneum.  In  advanced  cases, 
the  intestinal  wall  is  much  thickened  and  infiltrated,  and  the  seat  of 
numerous  and  extensive  ulcerations,  with  here  and  there  areas  of  more 
or  less  intact  mucosa;  or  there  may  be  widespread  sloughing,  pseudo- 
membrane  formation,  or  gangrene.  Healing  of  the  ulcerations  and 
cicatrization  occur  irregularly  and  to  a  varying  degree,  and  they  lead  to 
more  or  less  deformity  and  partial  obstruction  (stricture)  of  the  bowel. 
Microscopic  examination  reveals  the  ordinary  changes  of  inflammation 
and  ulceration,  with,  however,  only  moderate  polynuclear  leukocytic 
infiltration:  necrosis  rather  than  suppuration  being  conspicuous.  In 
chronic  cases  there  is  also  considerable  connective  tissue  proliferation. 
The  amoebae  may  be  found  in  the  base  of  the  ulcer,  in  the  adjacent 
lymph  spaces,  and   sometimes   in   the  bloodvessels — whence  they  are 


176  PROTOZOAX  IXFECTIOXS 

readily  conveyed  to  the  liver,  T\-here  they  give  rise  to  widespread  necrosis 
and  a  so-called  amoebic  abscess.  The  amoebae  may  be  cultivated,  with 
difficulty,  from  the  intestinal  discharges,  the  intestinal  wall,  and  the  liver 
abscesses.  In  the  intestinal  tract  they  may  be  associated  with  other 
protozoa,  such  as  trichomonas,  cercomonas,  etc.,  and  with  various 
metazoa,  such  as  Taenia  saginata,  Ascaris  lumbricoides,  Uncinaria 
duodenalis,  etc.  They  have  been  found  also  in  the  peritoneal  cavity, 
the  pleura,  lung,  bladder  and  urine,  abscess  of  the  mouth,  necrosis  of 
the  jaw,  etc. 

Symptoms. — Strong  divides  the  cases  into  three  classes,  which,  how- 
ever, are  not  sharply  demarcated  the  one  from  the  other:  (1)  Mild  cases 
and  those  of  moderate  severity;  (2)  cases  with  acute  onset;  and  (3) 
advanced  and  chronic  cases.  In  the  mild  cases  the  onset  is  insidious, 
the  patient  often  being  unable  to  state  when  the  disease  began.  The 
chief  symptoms  consist  of  more  or  less  abdominal  pain  and  diarrhoea; 
the  diarrhoea  may  be  periodic  and  may  alternate  with  constipation. 
The  stools  may  contain  mucus  and  the  amoebae;  often  little  if  any  blood. 
In  addition  there  may  be  such  general  symptoms  as  lassitude,  headache, 
loss  of  weight,  etc.  The  disorder  mav  last  for  months,  the  mildness 
of  the  s\Tnptoms  often  warranting  the  terms  latent  or  masked  infection; 
but  the  disorder  may  become  aggravated  and  pass  on  to  one  of  the  other 
t^■pes.  The  cases  with  acute  onset  may  represent  an  acute  infection  or 
an  acute  exacerbation  of  a  mild  or  latent  infection.  The  chief  s}TQp- 
toms  consist  of  abdominal  pain  (torminaj,  frequent  stools  containing 
mucus,  blood,  and  the  amoebae,  and  more  or  less  constant  and  distressing 
tenesmus.  Sloughs  of  the  bowel  also  may  be  passed.  Usually  there  is 
abdominal  tenderness,  especially  along  the  course  of  the  colon,  moderate 
fever,  and  the  patient  emaciates  rapidly.  The  pulse  may  become  rapid 
and  feeble,  and  death  may  ensue  within  a  week  or  ten  days  from  asthenia, 
toxemia,  syncope,  hemorrhage,  or  peritonitis  from  perforation.  In 
other  cases,  after  four  or  five  days,  the  acute  manifestations  subside  and 
may  eventually  disappear,  or  the  condition  may  become  chronic.  The 
advanced  and  chronic  cases  may  result  from  the  acute  cases  or  they 
may  be  subacute  or  chronic  from  the  beginning.  They  are  characterized 
by  alternating  periods  of  diarrhoea  and  constipation;  the  diarrhoeic 
attacks  are  characterized  by  abdominal  pain,  frequent  stools  containing 
mucus,  blood,  and  the  amoebae,  more  or  less  tenesmus,  and  slight  or 
moderate  fever.  There  may  be  more  or  less  emaciation  and  impair- 
ment of  the  general  health;  so-called  indigestion,  and  provoking  of  the 
attacks  apparently  by  dietetic  indiscretions.  The  tongue  is  likely  to  be 
red  and  raw-looking.  The  condition  may  last  for  six  months,  or  a  year 
or  more.  In  the  protracted  cases  emaciation  may  be  extreme,  and  death 
may  eventually  ensue. 

Complications  and  Sequels. — Liver  abscess  is  common;  it  may  involve 
the  lung  and  lead  to  a  so-called  hematopulmonary  abscess.  Intestinal 
perforation  and  peritonitis,  arthritis,  etc.,  also  occur. 


AMOEBIASIS  177 

Diagnosis. — The  diagnosis  is  readily  made  from  attention  to  the  bloody 
mucous  character  of  the  stools,  and  the  detection  therein  of  the  amoebae. 
The  liver  should  always  be  carefully  studied  for  signs  of  abscess  (en- 
largement, local  pain  or  discomfort,  chills,  fever,  sweats,  and  leukocytosis). 

Prognosis. — The  mild  cases  usually  yield  to  treatment,  but  relapses 
are  common.  In  chronic  cases  the  outlook  is  not  encouraging,  but  with 
care  and  attention  recovery  may  be  brought  about. 

Treatment. — The  prophylactic  measures  mentioned  on  page  29  should 
be  carried  out,  since  there  is  much  reason  to  believe  that  the  disease  is 
spread  and  acquired  as  is  typhoid  fever.  During  the  acute  stage  the 
patient  should  be  in  bed.  The  diet  should  be  the  blandest — milk 
(peptonized  or  diluted  with  barley  water,  lime  water,  or  Vichy  water), 
albumin  water,  raw  eggs,  beef  juice,  broths,  custard,  milk  toast,  etc. 
In  subsiding  or  chronic  infections  the  greatest  attention  also  must  be 
paid  to  the  diet,  since  recurrences  are  not  infrequently  provoked  by 
dietetic  indiscretions.  At  the  beginning  of  an  attack,  especially  if  there 
has  been  little  diarrhoea,  the  bowels  should  be  cleared  with  blue  mass, 
calomel,  or  castor  oil  to  which  20  minims  (1.25  c.c.)  of  tincture  of  opium 
may  be  added.  Ipecac  is  believed  by  men  of  large  experience  to  exert 
an  almost  specific  effect,  and  assuredly  should  be  tried.  Not  less  than 
three  hours  after  the  patient  has  had  food,  mild  counterirritation  (a 
mustard  plaster  or  tincture  of  iodine)  should  be  applied  to  the  abdomen, 
and  10  to  15  minims  (0.6  to  1  c.c.)  of  tincture  of  opium  given  by  the 
mouth,  or  \  grain  (0.015  gram)  of  morphine  administered  hypodermicly. 
After  the  lapse  of  ten  to  fifteen  minutes,  30  to  60  grains  (2  to  4  grams) 
of  freshly  powdered  ipecac  root  should  be  administered,  preferably  in 
salol-coated  pills  or  capsules.  The  patient  must  maintain  the  recumbent 
posture  for  several  hours:  this  as  well  as  the  salol-coated  pills  or  capsules 
tend  to  obviate  nausea  and  vomiting;  but  should  vomiting  occur,  the  dose 
of  ipecac  should  be  repeated  after  a  short  intei'val.  Decreasing  doses 
(5  to  10  grains,  0.3  to  0.6  gram,  less  than  the  initial  dose)  should  be  given 
on  succeeding  days.  The  use  of  purgative  doses  of  sodium  or  magnesium 
sulphate  has  also  been  much  conimended:  one  dram  (4  grams)  at  fre- 
quent intervals  (every  fifteen  to  thirty  minutes)  until  the  intestine  has 
been  thoroughly  cleansed,  whereupon  aromatic  sulphuric  acid  (believed 
to  be  detrimental  to  the  infecting  microorganisms)  may  be  given  in  rather 
large  doses.  Irrigation  of  the  bowel  is  of  great  advantage  in  many  cases, 
but  the  pain  and  tenesmus  are  often  obstacles  to  its  use  in  acute  cases; 
but  sometimes  these  may  be  lessened  by  a  preliminary  enema  of  tincture 
of  opium  (^  to  1  dram,  2  to  4  c.c.)  and  thin  starch  water  (2  to  4  ounces, 
60  to  120  c.c).  The  irrigation  should  be  done  by  means  of  a  fountain 
syringe,  and  the  tube  should  be  inserted  high  up;  the  best  solution  is 
quinine,  1  to  5000  gradually  increased  to  1  to  1000,  of  which  one  to  two 
quarts  should  be  injected  twice  daily  and  retained,  if  possible,  for  at  least 
fifteen  minutes.  Ice-water  enemas  also  may  prove  grateful.  The  rectal 
tenesmus  may  be  relieved  by  an  opium  and  belladonna  suppository. 
12 


178  PROTOZOAN  INFECTIONS 

In  chronic  cases  that  do  not  improve  on  medical  treatment,  resort  may 
be  had  to  colostomy  or  appendicostomy  and  drainage  and  irrigation  of 
the  colon  through  the  wound. 


RELAPSING  FEVER. 

{Recurring  Fever;  Seven  Day  Fever;  Famine  Fever;  African    Tick  Fever; 
Spirochetosis;  SpiriUosis . ) 

Relapsing  fever,  originally  believed  to  be  a  single,  acute,  specific, 
infectious  disease  characterized  by  alternating  periods  of  fever  and  of 
apyrexia  of  about  six  days  each,  is  now  known  to  include  at  least  four 
forms  of  such  fever,  each  more  or  less  distinctive,  more  or  less  limited 
in  geographical  distribution,  and  caused  by  four  species  of  spirochetes: 
Spirochseta  recurrentis  (Spirillum  obermeieri),  the  cause  of  the  relapsing 
fever  of  Europe,  especially  of  Russia,  the  Balkans,  etc.;  Spirochseta 
duttoni,  the  cause  of  the  relapsing  fever  of  Africa  (African  tick  fever); 
Spirochseta  carteri,  the  cause  of  the  relapsing  fever  of  India;  and  Spiro- 
chseta novyi,  the  cause  of  the  relapsing  fever  of  America. 

Etiology. — ^The  disease  prevails  especially  amidst  destitution,  squalor, 
and  general  unhygienic  surroundings.  Personal  factors,  such  as  age, 
sex,  and  race,  as  well  as  climate  and  season,  are  without  special  etiologi- 
cal significance,  although  the  disease  is  said  to  prevail  especially  among 
young  adults,  and  during  the  winter.  One  attack  confers  a  partial 
immunity. 

The  exciting  cause  of  the  disease  is  one  of  the  aforementioned  spiro- 
chetes. The  infection  is  believed  to  be  transmitted  by  insects  or  ticks. 
This  has  been  definitely  proved  in  the  case  of  Spirochseta  duttoni,  a 
tick,  Ornithodorus  moubata,  being  the  transmitting  agent.  The  bed-bug 
(Cimex  lectularius)  is  believed  to  be  the  transmitting  agent  of  Spirochseta 
recurrentis,  and  the  body-louse  (Pediculus  corporis)  that  of  Spirochseta 
carteri,  but  the  evidence  is  not  yet  conclusive.  Nothing  is  known  of  the 
mode  of  transmission  of  Spirochseta  novyi.  Nor  has  it  yet  been  definitely 
determined  whether  the  transmission  is  purely  mechanical  or  whether 
the  spirochetes  undergo  some  developmental  process  within  the  body 
of  the  transmitting  insects  or  ticks. 

Pathology. — There  are  no  characteristic  lesions.  The  spleen  is  en- 
larged and  soft;  the  liver,  kidneys,  heart,  etc.,  reveal  parenchymatous 
degeneration  and,  occasionally,  hemorrhagic  infarction;  and  the  bone 
marrow  has  been  found  hyperplastic. 

Symptoms. — The  period  of  incubation  is  from  five  to  eight  days. 
Usually  without  prodromal  symptoms,  the  disease  begins  suddenly, 
with  severe  chill,  high  fever,  rapid  pulse  (120  to  140  per  minute),  general 
neuromuscular  pains  and  sensitiveness,  extreme  prostration,  and  some- 
times delirium.  In  children  and  adolescents  there  may  be  nausea  and 
vomiting,  rarely  convulsions.  By  the  end  of  twenty-four  or  thirty-six 
hours,  the  temperature  has  attained  its  maximum  (105°  to  106°  F.), 


RELAPSING  FEVER  179 

and  it  continues  high  with  slight  morning  remissions.  During  the  period 
of  fever,  the  spleen  is  much  enlarged  and  palpable,  and  there  may  be 
jaundice,  nausea,  vomiting,  slight  bronchitis,  profuse  sweating,  sudamina, 
herpes  labialis,  slight  albuminuria,  stupor,  delirium,  and  a  slight  leuko- 
cytosis. After  the  lapse,  usually  of  six  (sometimes  five,  or  seven,  rarely 
ten)  days,  the  temperature  falls  rapidly  within  twelve  hours  or  less,  to  the 
normal  or  below,  the  patient  sweats  profusely,  or  has  a  critical  diarrhoea, 
and  by  the  following  day  feels  almost  entirely  well,  although  there  may 
be  a  slight  elevation  of  temperature  for  a  day  or  two.  Rarely  there  is  but 
a  single  paroxysm,  but  in  most  cases,  on  or  about  the  fourteenth  day,  that 
is,  after  a  period  of  apyrexia,  lasting  six  or  seven  days,  a  severe  chill 
occurs,  and  the  febrile  attack  is  repeated;  sometimes  there  is  a  third, 
fourth,  and  even  fifth  relapse.  Usually  the  succeeding  paroxysms  are 
of  decreasing  severity  and  duration.  In  unusual  (toxic)  cases,  a  typhoid 
condition  with  marked  delirium  and  coma,  sometimes  petechial  hemor- 
rhages, localized  necrosis  of  the  mucous  membranes,  and  bed  sores, 
develop,  and  death  occurs  from  toxemia  and  cardiac  collapse. 

The  African  tick  fever  resembles  the  other  types  of  relapsing  fever,  but 
it  may  differ  in  some  respects :  the  periods  of  fever  may  be  as  short  as 
three  days,  the  periods  of  apyrexia  may  be  irregular  (one  day  to  three 
weeks),  diarrhoea  and  dysentery  may  be  present,  etc. 

Complications. — Complications  are  rare.  The  most  common  are  pneu- 
monia, sepsis,  ititis,  choroiditis,  neuritis  (with  consequent  paralysis), 
rupture  of  the  spleen,  gastro-intestinal  catarrh,  and  hemorrhage  from  the 
kidneys,  nose,  gastro-intestinal  tract,  etc. 

Diagnosis. — In  the  early  stages  the  disease  may  be  mistaken  for  typhoid 
or  typhus,  and  even  yellow  fever,  but  the  subsequent  course  of  the  disease 
and  the  results  of  examining  the  blood  are  conclusive.  The  spiro- 
chetes may  be  found  in  the  peripheral  blood  during  the  period  of  fever; 
they  lessen  in  number  with  the  decline  of  the  fever,  and  they  are  absent 
after  the  crisis  and  during  the  periods  of  apyrexia,  although  the  blood 
remains  infectious  to  susceptible  animals.  The  recurrence  of  the  parox- 
ysms at  regular  intervals  indicates  the  protozoan  nature  of  the  parasite 
and  that  it  passes  through  a  definite  cycle  of  development.  A  form  of 
lymphatic  tuberculosis,  clinically  resembling  pseudoleukemia,  or  Hodg- 
kins'  disease,  much  simulates  relapsing  fever,  but  the  paroxysms  of  fever 
and  of  apyrexia  are  more  irregular  in  course,  development,  and  frequency; 
the  lymph  nodes  may  be  enlarged,  the  spirochete  is  absent  from  the  blood, 
and  the  patient  may  react  to  tuberculin  injections.  Irregular  forms  of 
malaria  may  be  distinguished  by  the  course  of  the  fever  and  the  results 
of  examining  the  blood. 

Prognosis. — The  prognosis  is  good  in  the  absence  of  extreme  severity 
of  infections  and  complications.  The  mortality  rate  is  low — 2  to  4 
per  cent. 

Treatment. — Efforts  should  be  made  to  prevent  the  infection  by  in- 
culcating and  practising  habits  of  personal  and  domestic  cleanliness, 
by  avoiding  vermin-infested  places,  and  the  use  of  beds  high  from  the 


180  PROTOZOAX  IXFECTIOXS 

ground  and  protected  by  mosquito  netting,  or  of  hammocks  suspended 
by  ropes.  The  treatment  of  the  developed  disease,which  must  be  based 
upon  general  principles,  consists  largely  of  good  hygienic  surroundings, 
good  nursing,  and  good  food.  The  s^Tuptoms  are  to  be  treated  symp- 
tomatically — the  high  fever  by  cold  sponging,  the  neuromuscular  pains 
bv  local  applications,  embrocations,  and  anodynes,  such  as  Dover's 
powder  internally  or  morphine  subcutaneously.  Toxemia  and  cardiac 
debility  are  to  be  treated  on  general  principles.  The  evidence  in  favor 
of  an  antispirochetic  serum  is  not  yet  conclusive;  Xovy  and  Knapp  have 
had  success  in  curing  the  infection  in  rats  with  an  immune  serum. 


SYPHILIS. 

i^Lues:  The  Pox.) 

Svphilis  is  a  chronic,  specific,  infectious,  congenital  or  acquired 
disease,  caused  by  Treponema  pallidum  (Schaudinn  and  Hoffmann); 
it  is  characterized,  when  acquired,  by  a  so-called  primary  lesion,  the 
chancre,  at  the  seat  of  inoculation;  certain  constitutional  disturbances, 
and  disorders  of  the  skin,  mucous  membranes,  and  lymph  nodes  (so-called 
secondaries);  specific  granulomatous  growths  in  the  viscera,  blood- 
vessels, bones,  muscles,  skin,  and  mucous  membranes  (so-called  ter- 
tiaries);  and  sometimes  by  certain  so-called  paras^-philitic  or  meta- 
svphilitic  diseases  of  the  neiwous  system,  especially  tabes  dorsalis  and 
general  paresis  (so-called  quartanaries).  Aside  from  the  primary  lesion, 
the  lesions  of  the  congenital  form  of  the  infection  do  not  differ  essentially 
from  those  of  the  acc|uired  form. 

Etiology. — S}-philis  prevails  in  all  parts  of  the  world;  it  is  peculiarly 
a  disease  of  mankind,  and  occurs  at  all  ages  and  in  both  sexes.  Until 
recently  the  lower  animals  were  believed  to  be  immune,  but  ]Metch- 
nikoff  and  Roux  have  shown  that  experimentally  the  infection  can  be 
transmitted  to  the  anthropoid  apes.  The  specific  infectious  agent  is 
Treponema  pallidum,  which  may  be  demonstrated  in  the  blood  and  in 
the  lesions. 

Acquired  syphilis  is  usually,  but  not  always,  transmitted  hy  sexual 
intercourse,  or  pers'ersions  thereof.  But  the  disorder  is  not  always  a 
lues  venera,  since  it  may  be  transmitted  by  way  of  the  lips  in  kissing, 
and  by  way  of  even  slight  abrasions  or  wounds  of  the  skin  or  mucous 
membranes,  such  as  of  the  fingers  and  hands  of  physicians,  surgeons, 
obstetricians,  and  nurses,  of  the  breast  of  wet  nurses  (s^•philitic  child), 
etc.;  and  it  may  also  be  transmitted  indirectly  by  means  of  divers 
fomites,  such  as  infected  drinking  and  eating  utensils,  pipes,  dental 
instruments,  clothing,  tattooing  instruments,  etc.,  and  formerly  by 
vaccine  virus  when  human  lymph  was  employed.  The  blood  and  the 
secretions  from  the  primary,  secondary,  and  tertiary  lesions  containing 
the  specific  infectious  agent  may  transmit  the  disease  if  they  come  in 
contact    with    an   abraded    skin   or  mucous   membrane.     The    normal 


SYPHILIS  181 

physiological  secretions,  such  as  the  milk,  tears,  sweat,  and  urine,  are 
ordinarily  non-infectious,  but  they  readily  become  infectious  through 
contamination  with  the  secretions  of  a  s}^hilitic  sore;  the  saliva  and 
the  semen  are  usually  infected  (through  contamination). 

Congenital  syphilis  may  be  transmitted  in  one  of  several  ways:  (1) 
By  the  father  (sperm  transmission),  the  mother  being  healthy.  This 
is  very  common,  the  semen  carrying  the  infectious  agent,  and  infecting 
as  it  fertilizes  the  ovum.  It  is  more  likely  to  occur  the  more  recent  the 
infection  in  the  father;  it  is  unlikely  after  the  lapse  of  three  or  four 
years,  if  the  man  has  been  efficiently  treated;  but  it  may  occur  even 
after  years  of  apparently  complete  recovery  and  entire  absence  of 
symptoms.  On  the  other  hand,  a  man  with  florid  sj'philis  may  beget 
a  healthy  child.  (2)  By  the  mother  (germ  transmission),  the  father 
being  healthy.  The  circumstances  influencing  the  likelihood  of  infection 
are  similar  to  those  that  obtain  in  the  father;  but  a  syphilitic  woman 
almost  always  transmits  the  disease  to  her  ofltspring,  and  this  form  of 
infection  is  much  more  fatal  to  the  foetus  than  is  the  paternal;  since 
not  only  is  the  ovum  diseased,  but  also  the  source  of  nourishment  of 
the  foetus.  A  mother  of  a  syphilitic  child,  though  herself  not  obviously 
syphilitic,  cannot  become  infected  (having  acquired  an  artificial  im- 
munity), as  is  well  expressed  in  Colles'  law:  A  child  born  of  a  syphilitic 
mother  who  is  without  obvious  venereal  symptoms,  and  which,  with- 
out being  exposed  to  any  infection  subsequent  to  its  birth,  shows  this 
disease  when  a  few  weeks  old,  will  infect  the  most  healthy  nurse, 
whether  she  suckle  it,  or  merely  handle  and  dress  it;  and  yet  this  child 
is  never  known  to  infect  its  own  mother,  even  though  she  suckle  it  while 
it  has  venereal  ulcers  of  the  lips  and  tongue.  (3)  By  both  parents 
being  syphilitic.  This  is  very  common,  one  parent  having  infected  the 
other — in  which  event  the  likelihood  of  infection  in  the  foetus  is  much 
enhanced.  (4)  By  intra-uterine  or  placental  transmission  of  the  infection. 
A  woman  infected  during  pregnancy  may,  by  way  of  placental  trans- 
mission, infect  her  foetus;  this  is  less  likely  to  occur  the  older  the  foetus 
at  the  time  of  infection,  and  it  is  uncommon  after  the  seventh  month; 
but  during  })irth  the  foetus  may  acquire  the  infection  from  vaginal 
lesions. 

A  person  having  acquired  syphilis  is  immune  to  a  second  infection, 
though  occasional  exceptions  to  this  rule  seem  to  be  observed;  and 
children  who  have  inherited  syphilis  are  immune  to  the  acquired  infec- 
tion (Prof eta's  law). 

Pathology. — The  primary  lesion,  or  chancre,  consists  of  serous  and 
cellular  infiltration  (lymphoid,  plasma,  epithelioid,  and  occasionally 
giant  cells),  especially  in  the  deeper  layers  of  the  skin  or  mucous  mem- 
brane about  the  capillaries  and  small  veins,  together  with  proliferation 
of  the  vascular  endothelium,  thromboses  of  the  small  vessels,  and 
hyperplastic  and  degenerative  changes  in  the  small  nerves.  Together 
these  constitute  a  firm,  hard,  reddish  papule — the  hard  chancre.  Soon, 
on  account  of  deficient  blood  supply  (due  to  the  thromboses),  liquefac- 


182  PROTOZOAN  INFECTIONS 

tion  necrosis  sets  in,  and  this,  involving  the  overlying  and  perhaps 
proliferated  epithelium,  leads  to  vesiculation  and  usually  ulceration — 
the  ulcer  being  circumscribed,  "scooped  out,"  and  indurated  at  the 
base  and  about  the  edges.  Ultimately  the  serous  and  cellular  infiltration 
subsides  and  is  removed;  fibroblasts  form  and  cicatrization  ensues.  The 
lymph  nodes  adjacent  to  the  primary  lesion,  and  later  the  other  lymph 
nodes  throughout  the  body,  become  enlarged  and  indurated  (buboes), 
in  consequence  of  serous  infiltration  and  cellular  proliferation,  and 
those  adjacent  to  the  chancre  sometimes  undergo  suppuration  in  con- 
sequence of  secondary  pyogenic  infection.  Later  all  the  lymph  nodes 
exhibit  more  or  less  well-marked  sclerosis.  The  cutaneous  and  the 
mucous  membrane  lesions  consist  of  proliferation  and  infiltration  of  the 
upper  layers  of  the  skin  and  the  mucosa,  in  some  cases  associated  with 
cellular  infiltration  of  the  rete  IMalpighii  and  proliferation  of  the  underly- 
ing bloodvessels.  The  characteristic  mucous  patch  (mouth,  genitals, 
anus)  and  the  similar  condyloma  (of  the  soft  and  usually  moist  skin  of 
the  perineum,  groins,  axillae,  between  the  toes,  etc.)  exhibit  lesions  quite 
like  those  of  the  chancre — cellular  infiltration  of  the  deeper  layers  of 
the  epithelium  and  elongation  of  the  papillee,  proceeding  to  necrosis 
and  exfoliation  of  the  superficial  layers.  Later  in  the  course  of  the 
disease  dift'use  indurative  changes  occur  in  the  bloodvessels  (arterio- 
sclerosis, atheroma);  these  lead  to  or  are  associated  with  indurative 
changes  in  the  organs  (liver,  spleen,  kidneys,  heart,  brain,  spinal  cord, 
meninges,  etc.).  At  the  same  time  characteristic  formations,  so-called 
gummas  (s}'philomas,  specific  granulation  tumors)  appear,  especially 
in  the  viscera,  bones,  periosteum,  etc.  These  vary  in  size  from  so-called 
miliary  gummas  to  formations  ten  to  fifteen  or  more  centimeters  in 
diameter.  They  are  firm,  nodular,  somewhat  elastic,  and  on  section 
gelatinous  (or  mucoid),  and  surrounded  and  pervaded  by  bands  of 
dense,  fibrous,  connective  tissue  that  also  sends  prolongations  into  the 
adjacent  tissue.  Occasionally  considerable  softening  occurs,  and  if 
the  gumma  be  situated  in  the  skin  or  the  mucous  membrane  small 
ulcers  may  form;  these  usually,  sooner  or  later,  cicatrize.  Micro- 
scopically, the  gumma  consists  of  epithelioid  and  round  cells  and 
some  giant  cells,  together  with  proliferation  of  the  vascular  endothelium, 
the  formation  of  new  bloodvessels,  and  a  general  tendency  to  sclerosis — 
although  softening  (mucoid  and  fatty  degeneration)  is  quite  common 
in  the  larger  gummas.  The  so-called  parasyphilitic  lesions  (syphilitic 
in  origin  but  not  in  nature)  exhibit  no  specific  features. 

Symptoms  of  Acquired  Syphilis.— The  period  of  incubation  varies 
from  two  to  five  weeks,  being  about  three  weeks  in  the  majority  of 
cases.  Usually  there  are  no  prodromal  symptoms,  the  first  indication 
of  the  infection  being  the  so-called  hard,  or  Hunterian,  chancre.  This 
develops  at  the  seat  of  inoculation — usually  in  men  on  the  prepuce 
or  glans  penis,  though  sometimes  in  the  urethra  (where  it  may  remain 
unobserved),  and  in  women  on  the  vulva,  the  vagina,  or  the  cervix 
of   the  uterus.     The  chancre,  however,  may  be  extragenital — on  the 


SYPHILIS  183 

anus,  rectum,  lips,  tonsils,  breast,  finger,  etc.  It  consists  of  a  firm, 
hard,  painless,  reddish  papule,  which  soon  exhibits  slight  central  necrosis 
and  ulceration,  and  may  discharge  a  small  amount  of  secretion,  which 
sometimes  dries  to  form  a  scab.  By  the  third  week  the  chancre  has 
become  characteristically  hard,  indurated,  and  cartilaginous;  but  this 
is  more  apparent  on  cutaneous  than  on  mucous  surfaces.  At  first  it 
evinces  no  tendency  to  heal;  but  in  most  cases  cicatrization  is  complete 
by  the  end  of  the  fifth  or  sixth  week,  although  it  may  be  much  delayed; 
the  scar,  as  a  rule,  remains  indurated  for  a  long  time.  During  the 
second  week  the  lymph  nodes  adjacent  to  the  primary  lesion  (usually, 
therefore,  the  inguinal  nodes)  become  enlarged,  hard,  and  indurated 
(syphilitic  bubo);  they  are  painless  unless  secondary  pyogenic  infections 
leading  to  suppuration  occur.  By  the  end  of  the  third  or  fourth  week 
the  lymph  nodes  in  general  (epitrochlear,  axillary,  cervical,  auricular, 
submaxillary,  etc.),  are  enlarged  and  indurated. 

The  period  prior  to  the  development  of  the  cutaneous  and  other 
so-called  constitutional  symptoms  is  usually  spoken  of  as  the  primary 
stage,  and  lasts  from  six  to  twelve  weeks.  With  the  onset  of  the  cutaneous 
manifestations  the  secondary  stage  is  said  to  begin;  this  lasts  from 
two  months  to  a  year  or  more,  and  is  sometimes  followed  after  a  variable 
and  uncertain  period  (often  of  apparently  good  health)  by  the  so-called 
tertiary  stage  (gummas,  certain  cutaneous  eruptions,  amyloid  degenera- 
tion, etc.);  but  no  sharp  line  of  demarcation  between  the  secondary 
and  the  tertiary  stage  can  be  drawn:  indeed,  certain  of  the  so-called 
tertiary  manifestations  sometimes  develop  unusually  early,  even  before 
the  chancre  has  healed.  Nor  is  it  correct  to  assume  constitutional 
involvement  only  with  the  onset  of  the  cutaneous  and  other  manifesta- 
tions of  the  so-called  secondary  stage — constitutional  involvement  is 
effected  even  before  the  maturation  of  the  chancre  (treponemse  may 
be  demonstrated  in  the  blood). 

General  Symptoms. — Slight  fever  is  not  uncommon  with  the  onset 
of  glandular  enlargement,  and  it  is  almost  always  present  when  the 
glandular  enlargement  has  become  universal.  In  other  cases  no  note- 
worthy fever  may  be  apparent  until  three  or  four  weeks  before,  or 
concurrently  with,  the  development  of  the  cutaneous  lesions.  This 
"fever  of  invasion"  (as  well  as  the  attacks  of  fever  that  may  occur  at 
any  time  during  the  secondary  or  tertiary  stages)  may  be  moderate 
(101°  F.)  or  sometimes  quite  high  (104°  F.  or  more);  and  it  may  be 
continuous  (when  it  is  likely  to  be  mild),  or  remittent  (usually),  or 
intermittent  (when  it  may  be  accompanied  by  chilly  sensations  or  chills). 
This  fever  may  be  mistaken  for  typhoid  fever,  malaria,  tuberculosis, 
sepsis,  rheumatism,  etc.  In  addition  to  the  fever,  evidences  of  general 
infection  are  seen  in  malaise,  languor,  prostration,  general  neuro- 
muscular pains,  bone  pains  (especially  tibia,  clavicle,  and  skull),  joint 
pains,  headache,  iritis  (exceedingly  painful),  coated  tongue,  poor 
appetite,  slight  enlargement  of  the  spleen,  and  anemia  (oligocythemia, 
disproportionate    ologochromemia,    and    lymphocytosis).     Late    in    the 


184  PROTOZOAN  INFECTIONS 

disease  aggravation  of  the  anemia,  cachexia,  and  amyloid  degeneration 
may  be  observed. 

Cutaneous  Lesions. — ^The  cutaneous  lesions  (syphilides),  usually 
looked  upon  as  marking  the  beginning  of  the  secondary  stage,  are 
characterized  by  their  polymorphism,  superficial  character,  general 
symmetry,  copper-colored  hue,  and  absence  of  itching.  Erythematous, 
papular,  pustular,  squamous,  and  tubercular  syphilides  may  be  dis- 
tinguished. The  commonest  and  the  earliest  is  the  roseola,  which 
develops  about  eight  to  ten  weeks  after  infection  and  consists  of  light 
reddish  or  rose-colored  (later  slightly  coppery),  roundish  or  ovoid  macules, 
varying  from  5  to  10  mm.  in  diameter,  and  irregularly  distributed 
on  the  thorax  and  abdomen,  sometimes  on  the  thighs  and  arms 
(especially  the  flexor  aspects),  and  rarely  on  the  face.  It  persists  for 
a  week  or  two  or  longer;  and  may  recur  frequently.  The  syphilitic 
roseola  may  be  accompanied,  and  is  often  followed,  by  papular  and 
pustular  syphilides,  such  as  the  so-called  lenticulopapular,  acneiform, 
varioliform,  echthymaform,  etc.  These  are  usually  distributed  in 
groups  over  the  trunk,  flexor  surfaces  of  the  extremities,  and  the  face, 
especially  the  forehead  (corona  veneris).  A  papulosquamous,  so-called 
psoriasiform  syphilide,  is  not  uncommon;  it  may  be  circumscribed 
or  widespread,  and  is  rather  common  on  the  palms  and  soles.  It  may 
be  distinguished  from  psoriasis  by  its  coppery  hue,  absence  of  silvery 
scales,  and  absence  of  bleeding  upon  removing  the  scales.  The  soft 
and  usually  moist  skin  of  the  perineum,  anus,  vulva,  groins,  axillae, 
angles  of  the  mouth,  between  the  toes,  etc.,  is  often  the  seat  of  character- 
istic condylomas — flat,  well-defined,  wart-like  growths.  Concurrently 
with  the  roseola  the  hair  usually  becomes  thinned,  lustreless,  and  falls 
out  (alopecia).  It  usually  returns  upon  appropriate  treatment,  except 
in  the  event  of  ulceration  and  cicatrization,  when  the  alopecia  is  perma- 
nent. Onychia  and  paronychia  are  rather  common  (more  common 
in  congenital  syphilis),  and  often  lead  to  brittleness  and  shedding  of 
the  nails.  Late  in  the  course  of  the  disease  different  gummatous 
lesions  of  the  skin  occur,  of  which  the  lupiform  syphilide  and  rupia  are 
the  most  important — since  they  give  rise  to  considerable  ulceration 
and  destruction  of  tissue.  Small  roundish  or  irregular  whitish  spots 
(leukoderma)  also  are  sometimes  observed,  especially  in  women  and 
about  the  neck;  they  are  usually  2  to  5  mm.  in  diameter,  but  they  may 
coalesce  to  form  larger  spots  or  bands  (collier  de  Venus),  or  they  may 
spread  over  a  greater  part  of  the  body. 

Mucous  Membrane  Lesions. — ^The  mucous  membranes  may  be 
involved  early  or  late,  and  the  lesions  may  be  erythematous,  papular, 
ulcerative,  or  gummatous.  Concurrently  with  the  cutaneous  rash, 
sometimes  earlier,  complaint  is  often  made  of  sore  throat,  and  on  inspec- 
tion the  pharyngeal,  faucial,  and  tonsillar  mucous  membrane  is  found 
swollen,  red,  and  hyperemic;  small  papules  soon  form,  and  the  super- 
ficial epithelium  becoming  opaque  and  cloudy,  and  later  ulcerated, 
gives  rise  to  the  characteristic  mucous  patch — a  moist,  whitish,  flat, 


SYPHILIS  185 

superficial,  somewhat  raised,  and  well-defined  area.  Siich  mucous 
patches  may  be  found  on  any  mucous  membrane  or  mucocutaneous 
junction  of  the  body,  although  they  are  most  common  in  the  fauces, 
pharynx,  uvula,  cheek,  tongue,  lips,  nose,  larynx,  anus,  vagina,  etc. 
Sometimes  these  patches  coalesce  or  spread  to  form  more  or  less  extensive 
serpiginous  ulcers,  especially  on  the  tonsil,  uvula,  soft  palate,  and 
pharynx.  Hypertrophy  of  the  papillae  of  the  tongue  is  common  early, 
and  gives  rise  to  papules  which  sometimes  become  necrotic  and  form 
small  ulcers,  especially  near  carious  teeth;  or  ichthyosis  may  supervene; 
or  the  tongue  may  become  atrophic,  and  the  base,  firm,  hard,  and  smooth 
(Virchow's  smooth  atrophy  of  the  base  of  the  tongue) — which  is  of 
considerable  diagnostic  significance  in  persons  over  fifty  years  of  age. 
Gummas  are  quite  common  in  the  mucous  membranes  and  submucous 
tissues.  In  the  tongue  they  not  infrequently  give  rise  to  extensive 
ulceration  and  loss  of  tissue,  and  they  have  often  been  mistaken  for 
carcinoma  (and  the  tongue  in  consequence  has  been  excised). 

Circulatory  System.— The  chief  lesions  consist  of  arteriosclerosis 
and  its  consequences,  notably  fibroid  degeneration  of  the  myocardium, 
aneurysm,  and  aortic  valve  disease,  all  of  which  are  discussed  under 
their  respective  headings.  A  special  type  of  arteriosclerosis  due  to 
syphilis  may  be  distinguished,  and  in  the  lesions,  especially  in  the  aorta, 
Treponema  pallidimi  may  be  found.  Occasionally  a  gumma  forms  in  the 
myocardium,  and  if  situated  in  the  pathways  of  the  bundle  of  His  may 
give  rise  to  heart  block.  Syphilitic  endocarditis  is  very  rare  (aside  from 
arteriosclerosis);  syphilitic  pericarditis  is  perhaps  more  common. 

Respiratory  System. — The  mucous  membrane  lesions  in  the  nose 
(syphilitic  rhinitis)  have  already  been  mentioned.  In  addition,  gummas 
may  occur,  comparatively  early.  Usually  they  involve  the  bone  before 
the  mucous  membrane;  they  give  rise  to  considerable  necrosis  and 
destruction,  to  the  occurrence  of  perforation  of  the  hard  and  the  soft 
palate  and  the  bones  and  cartilages  of  the  nose,  and  the  consequent 
development  of  the  so-called  saddle  nose  and  extreme  fetor  (ozoena). 
In  the  larynx,  in  addition  to  the  common  laryngitis,  gummas  may 
occur,  and  give  rise  to  ulceration  of  the  cartilages,  with  subsequent 
cicatrization  and  stricture.  Involving  first  the  epiglottis,  they  may 
cause  a  severe,  even  fatal,  oedema  of  the  glottis.  Similar  lesions  may 
occur  in  the  trachea  or  one  of  the  main  bronchi  (dyspnoea,  inspiratory 
stridor,  lessened  expansion  and  feebler  breath  sounds  on  the  aftected 
side);  bronchial  dilatation  may  occur  below  the  site  of  the  lesion. 
Syphilis  of  the  lung  is  very  rare:  it  may  occur  as  small  multiple  gummas, 
about  which  there  may  be  areas  of  bronchopneumonia;  or  it  may  lead  to 
an  interstitial  fibrosis,  developing,  as  a  rule,  from  the  root  of  the  lung 
(perhaps  very  rarely  from  the  pleura),  and  being  especially  conspicuous 
about  the  bronchi  and  the  bloodvessels;  the  bronchi  may  become 
dilated.  The  diagnosis  can  rarely  be  made,  although  it  may  be  sus- 
pected upon  the  development  in  a  known  syphilitic  subject  of  the  ])liysical 
signs    of   chronic    interstitial    pneumonitis    with    bronchiectasis    of    the 


186  PROTOZOAN  INFECTIONS 

lower  lobe,  and  the  absence  of  tubercle  bacilli  from  the  sputum;  but 
one  must  remember  that  tuberculosis  of  the  lungs  may  occur  in  a  syphilitic 
subject,  and  tubercle  bacilli  may  not  be  found  for  some  time.  A  positive 
Wassermann  reaction  may  be  of  diagnostic  assistance. 

Digestive  System. — Rarely  a  gumma  may  develop  in  the  oesophagus 
and  ultimately  lead  to  stricture.  An  occasional  syphilitic  ulcer  has 
been  observed  in  the  stomach,  but  otherwise  syphilis  of  the  gastro- 
intestinal tract  is  rare,  except  in  the  rectum.  Gummas  are  quite  common 
in  the  rectum,  especially  in  women.  They  develop  usually  just  above 
the  internal  sphincter,  and,  gradually  cicatrizing,  produce  a  stricture. 
The  symptoms  are  those  of  gradually  increasing  difficulty  in  evacuating 
the  bowels  and  narrowing  of  the  fecal  masses.  The  stricture  may  be 
recognized  by  palpation  and  protoscopic  examination,  and  may  be 
distinguished  from  carcinoma  by  its  being  firm  and  fibrous  rather 
than  a  more  or  less  exuberant,  centrally  ulcerated  mass,  and  by  the 
absence  of  the  carcinomatous  cachexia. 

Syphilis  of  the  liver  is  very  common.  Jaundice  is  not  uncommon 
at  the  time  of  development  of  the  cutaneous  rash  and  enlargement 
of  the  lymph  nodes;  it  is  likely  due  to  radicular  cholangitis.  Some- 
times a  type  of  acute  yellow  atrophy  supervenes.  In  the  tertiary  stage, 
the  lesions  may  consist  of:  (1)  Gummas,  which  may  be  single  or 
multiple;  usually  they  give  rise  to  a  large  protruding  tumor  in  or  near 
the  epigastrium,  together  with  local  pain  and  distress.  The  diagnosis 
is  facilitated  by  the  detection  of  evidences  of  syphilis  elsewhere.  Carci- 
noma may  be  eliminated  by  the  less  rapid  growth  or  stationary  condition 
of  the  enlargement  (growth  is  usually  rapid  and  progressive  in  car- 
cinoma), and  by  the  absence  of  the  general,  cachectic,  manifestations 
of  carcinoma.  In  some  cases,  however,  the  therapeutic  test  is  necessary 
to  establish  the  diagnosis.  The  presence  of  fever  may  suggest  liver 
abscess,  but  the  other  evidences  of  suppuration  are  usually  absent. 
Following  absorption  of  the  gumma  the  liver  becomes  more  or  less 
distorted  from  scar  formation.  (2)  Chronic  interstitial  hepatitis.  These 
cases  exhibit  the  common  manifestations  of  cirrhosis — enlargement 
of  the  liver  with  the  signs  of  portal  obstruction  and  ascites;  there  is 
likely  to  be  also  slight  jaundice  and  some  fever,  at  least  from  time  to 
time;  later  the  liver  may  decrease  in  size.  Perihepatitis  is  usually  asso- 
ciated, and  may  give  rise  to  palpable  and  audible  frictions.  The  lesions 
may  also  implicate  the  peritoneum  more  extensively.  (3)  Amyloid  dis- 
ease presents  the  symptoms  and  signs  mentioned  under  amyloidosis. 

Genito-urinary  System. — In  a  few  cases  an  acute  syphilitic  nephritis 
occurs  during  the  second  stage  of  the  disease;  death  may  ensue  soon, 
but,  as  a  rule,  recovery  follows  after  a  number  of  months,  although 
albuminuria  may  persist  for  a  long  time.  A  chronic  parenchymatous 
nephritis  may  be  associated  with  the  renal  and  other  lesions  of  amy- 
loidosis. Chronic  diffuse  indurative  (or  interstitial)  nephritis  is  a 
common  sequence  of  syphilis  and  the  arteriosclerotic  changes  that  it 
induces.     Miliary  or  larger  gummas  may  be  found  in  the  kidney,  espe- 


SYPHILIS  187 

cially  in  association  with  syphilis  of  the  liver.  The  testicle  may  become 
the  seat  of  gummas  or  of  progressive  fibrosis  (interstitial  orchitis). 
Abortion  and  repeated  abortion  is  common  in  syphilitic  women. 

Nervous  System. — The  lesions  of  the  brain  may  consist  of:  (1) 
Syphilitic  arteriosclerosis,  which  may  lead  to  aneurysm  and  rupture 
of  a  vessel  (apoplexy),  or  to  thrombosis  and  cerebral  softening.  (2) 
Gummas,  which  may  be  single  or  multiple,  and  vary  in  size  from  that 
of  a  pea  to  that  of  an  egg.  They  may  occur  in  any  part  of  the  brain, 
but  usually  develop  in  the  dura  mater  or  the  pia-arachnoid  at  the  base 
of  the  cerebral  hemispheres,  near  the  pituitary  body,  or  on  the  convexity 
of  the  frontal  convolutions.  When  the  meninges  are  involved,  a  sub- 
acute or  chronic  meningitis  with  much  thickening  results,  and  the 
lesions  are  likely  to  extend  along  the  nerve  sheaths  (especially  the 
oculomotor,  the  facial,  etc.).  The  symptoms  of  the  larger  gummas 
are  those  of  tumor  of  the  brain — especially  headache,  vomiting,  con- 
vulsions, optic  neuritis,  etc.,  together  with  various  localizing  symptoms 
depending  upon  the  situation  of  the  gumma.  (3)  Meningitis — which 
may  occur  without  definite  macroscopic  gummatous  formations,  although 
microscopic  gummas  are  almost  always  present.  This  is  common 
at  the  base  of  the  brain,  where  it  usually  implicates  one  or  more  of  the 
cranial  nerves,  especially  the  oculomotor,  the  trochlear,  the  abducens, 
and  the  trigeminal;  but  it  may  involve  also  the  cortex.  The  chief 
symptoms  consist  of  initial  headache,  which  may  be  local  or  general, 
and  constant  or  intermittent,  but  is  usually  worse  at  night;  vertigo, 
somnolence,  failure  of  mentality,  mental  depression,  sometimes  irri- 
tability, and  localizing  symptoms  depending  upon  the  cranial  nerves 
involved.  In  some  cases  there  is  eventually  coma  or  convulsions;  rarely 
these  may  be  the  major  initial  manifestations.  The  symptoms  due  to 
cortical  involvement  are  those  of  meningo-encephalitis,  which  gradually 
progress  to  well-defined  paretic  dementia. 

Spinal  cord  lesions  are  less  common  than  cerebral;  they  may  consist 
of  arterial  disease  (with  softening  of  the  cord);  or  gumma  (tumor  for- 
mation) of  the  meninges  or  the  cord;  or  meningitis  (which  usually  is 
irregularly  distributed,  although  it  involves  all  the  meninges  and  the 
spinal  cord  and  the  spinal  nerve  roots);  or  of  myelitis  and  secondary 
sclerosis.  The  so-called  parasyphilitic  (metasyphilitic)  diseases  involve 
the  nervous  system,  and  consist  of  tabes  dorsalis,  paretic  dementia, 
etc.  The  diagnosis  of  cerebrospinal  syphilis,  in  some  cases  readily 
made,  may  be  difficult;  the  symptoms  are  likely  to  be  variable,  multi- 
form, and  asymmetrical,  to  exhibit  combinations  of  spinal,  cerebral, 
and  meningeal  symptoms  not  readily  explainable  by  a  single  or  well- 
defined  lesion.  In  some  cases  resort  must  be  had  to  antisyphilitic 
treatment  to  settle  the  diagnosis. 

The  Bones,  Joints,  Burs.^,  and  Muscles. — Syphilitic  periostitis 
is  common,  and  gives  rise  to  local  pain,  often  worse  at  night,  tenderness, 
and  swelling.  Gummas  may  develop  in  the  periosteum  as  well  as 
in   the  deeper  structures,  reaching  even  to  the   medulla  and  causing 


188  PROTOZOAN  INFECTIONS 

considerable  destruction.  Occasionally  acute  or  chronic  synovitis  is 
observed;  or  a  syphilitic  osteo-arthritis  may  occur.  The  muscles  may 
be  the  seat  of  an  early  myositis,  or  of  a  later  gummatous  formation. 
Absorption  of  the  gumma  may  lead  to  more  or  less  loss  of  substance 
and  fibrosis.  The  syphilitic  bursopathy  of  Verneuil,  occurring  especially 
about  the  larger  joints  (knee,  elbow,  etc.),  is  a  rare  manifestation. 

Symptoms  of  Congenital  Syphilis. — ^Aside  from  the  primary  sore, 
congenital  syphilis  presents  all  the  manifestations  of  the  acquired 
disease.  The  child  at  birth  may  present  obvious  evidences  of  the 
disease,  or  it  may  appear  healthy,  the  symptoms  not  developing  until 
about  the  second  month;  in  other  cases,  the  symptoms  first  become 
obtrusive  about  puberty  (delayed  congenital  syphilis).  The  infant 
obviously  syphilitic  at  birth  is  poorly  nourished,  wizened,  old-looking; 
it  suffers  from  coryza  that  interferes  with  respiration  (whence  "snuffles") 
and  with  suckling;  the  lips  and  the  angles  of  the  mouth  are  fissured 
and  ulcerated,  and  blisters  are  present  on  the  hands,  wrists,  feet,  and 
ankles  (pemphigus  neonatorum).  The  liver,  spleen,  and  pancreas 
are  usually  enlarged;  the  lungs  are  heavy,  firm,  grayish  white,  and 
almost,  if  not  quite,  airless  (the  so-called  white  pneumonia  of  Virchow); 
and  the  ends  of  the  long  bones  commonly  reveal  an  osteochondritis 
that  may  lead  to  separation  of  the  epiphyses.  Hemorrhages,  sub- 
cutaneous, submucous,  umbilical,  occur  in  some  cases.  These  infants, 
as  a  rule,  soon  die;  foetuses  born  dead  reveal  the  same  changes. 

In  other  cases  the  infant  is  apparently  healthy  at  birth.  Usually 
early  in  the  second  month  the  sj-philitic  rhinitis  ("snuffles")  develops; 
the  discharge  may  be  serous,  or  purulent,  or  sanguinolent,  and  is  highly 
infectious.  Necrosis  and  ulceration  of  the  nasal  bones  and  cartilages 
may  ensue,  and  lead  to  falling  in  of  the  nose — the  so-called  saddle- 
nose;  or  the  lesions  may  spread  to  the  pharynx,  the  Eustachian  tube, 
and  the  middle  ear,  and  give  rise  to  otorrhoea  and  deafness.  Cutaneous 
lesions  quite  analogous  to  those  of  the  acquired  disease  develop ;  usually 
they  begin  about  the  genitals  and  buttocks,  but  tend  to  spread  over  the 
body.  The  most  common  is  a  yellowish  or  reddish-brown  erythema, 
but  the  lesions  may  be  also  papular,  eczematous,  or  pustular.  Fissures 
(ragades)  are  common  about  the  lips,  especially  at  the  angles  of  the 
mouth.'  Mucous  patches,  condylomas,  alopecia,  onychia,  dactylitis, 
iritis,  etc.,  also  occur;  the  liver  and  spleen  are  usually  enlarged; 
the  bones  about  the  fontanelle  and  elsewhere  may  be  thickened,  and 
the  epiphyses  may  be  enlarged.  Many  of  these  children  also  die;  but 
in  favorable  cases  and  under  appropriate  treatment,  the  symptoms 
subside  toward  the  end  of  the  first  year,  and  the  child  may  appear 
perfectly  healthy  until  about  puberty.  From  puberty  to  about  the 
twentieth  year  many  so-called  late  manifestations  of  congenital  syphilis 
occur.  As  a  rule,  growth  is  retarded,  and  the  child  appears  wizened 
and  prematurely  old;  the  skull  may  be  large  or  asymmetrical,  the 
nose  depressed,  the  lips  prominent,  and  scars  of  healed  fissures  may 
radiate  from  the  corners  of  the  mouth — appearances  which  of  them- 


SYPHILIS  ISO 

selves  suggest  the  disease.  The  teeth  are  Ukely  to  be  deformed,  and 
the  two  upper  central  incisors  may  be  short  and  broad,  peg-shaped 
(narrower  below  than  above),  and  reveal  a  single  notch  at  the  free  edge 
(Hutchison's  teeth).  Interstitial  keratitis  (ground  glass  opacity  of 
the  cornea),  usually  bilateral,  and  bilateral  deafness,  unassociated  with 
pain  or  discharge,  are  quite  common.  The  malformations  of  the 
teeth,  interstitial  keratitis,  and  deafness  constitute  Hutchison's  triad 
of  congenital  syphilis.  Bone  lesions  also  are  common — especially 
bilateral  gummatous  periostitis,  affecting  especially  the  tibiae,  but  also 
other  bones,  and  leading  to  permanent  thickenings  and  deformities. 
Joint  lesions  are  rare,  although  a  synovitis,  usually  symmetrical  and 
involving  the  knee  by  preference,  may  occur.  Gummas  in  different 
parts  of  the  body  and  amyloid  disease  are  rare  manifestations. 

Diagnosis. — In  some  cases  the  initial  lesion  is  so  characteristic 
as  to  admit  of  no  doubt  of  the  diagnosis;  in  other  cases  in  the  past, 
certainty  was  not  obtainable  until  the  development  of  enlarged  lymph 
nodes  and  the  cutaneous  rashes.  But  at  present  Treponema  pallidum 
may  be  readily  demonstrated  in  the  serum  of  the  chancre  (by  "dark- 
field"  illumination  or  by  staining),  as  well  as  in  a  section  excised  from 
the  chancre,  and  in  the  circulating  blood,  so  that  it  is  no  longer  necessary 
to  await  the  tedious  appearance  of  the  so-called  secondaries  to  make  a 
positive  diagnosis  and  institute  treatment.  In  older  cases  in  which 
the  diagnosis  is  uncertain,  aid  may  be  obtained  by  a  history  of  a  primary 
lesion  or  of  exposure  to  infection,  but  both  may  be  denied;  there  may 
be,  however,  a  history  of  sore  throat,  cutaneous  rashes,  alopecia  or 
iritis,  etc.,  and  in  women  of  repeated  abortions;  search  may  reveal 
the  scar  of  a  primary  lesion  or  of  other  syphilitic  lesions  elsewhere, 
or  copper-colored  cicatrices  on  the  legs  (not  always  syphilitic),  or  peri- 
osteal thickenings,  or  enlarged  lymph  nodes,  etc.  Congenital  syphilis 
in  early  infancy  is  readily  recognized  from  the  general  appearance  of 
the  child,  the  snuffles,  the  cutaneous  eruptions,  the  ragades  at  the  angles 
of  the  mouth,  the  condylomas,  enlarged  liver  and  spleen,  etc.  Snuffles 
and  a  rash  occurring  within  the  first  three  months  of  life  are  almost 
certainly  syphilitic.  There  may  be  also  a  history  of  syphilis  in  one  or 
l)oth  parents.  The  disease  manifesting  itself  about  puberty  may  be 
recognized  by  the  retarded  growth  and  general  appearance  of  the 
child,  Hutchison's  teeth,  usually  bilateral  keratitis,  bilateral  deafness, 
symmetrical  nodosities  on  the  bones,  etc.  In  any  case  of  supposed 
congenital  or  acquired  syphilis,  or  of  parasyphilitic  disease,  such  as 
tabes  dorsalis,  paretic  dementia,  arteriosclerosis,  aortic  valvular  disease 
of  the  heart,  etc.,  resort  may  be  had  to  the  Wassermann  reaction,  which 
seems  to  give  positive  results  in  80  to  90  per  cent,  of  the  cases.  Finally, 
in  doubtful  cases,  resort  may  be  had  to  the  therapeutic  test,  which, 
however,  is  by  no  means  infallible. 

Prognosis. — In  acquired  syphilis,  the  outlook  is  good  if  treatment 
is  instituted  early  and  carried  out  efhciently  and  for  a  sufficiently 
long  time — which  is  rarely  the  case.     Some  cases  are  unusually  virulent, 


190  PROTOZOAN  INFECTIONS 

and  more  or  less  rebellious  to  treatment;  and  in  other  cases  a  fatal 
acute  yellow  atrophy  of  the  liver  may  supervene.  Death  is  frequently 
due  to  tertiary,  gummatous  lesions,  and  to  related  disorders  due  to 
arteriosclerosis,  etc.  The  prognosis  in  the  parasyphilitic  diseases,  tabes 
dorsalis  and  paretic  dementia,  is  almost  hopeless  as  to  cure.  Congenital 
syphilis  may  lead  to  death  of  the  foetus  or  to  death  soon  after  birth, 
hemorrhages,  jaundice,  and  pemphigus  especially  being  bad  omens. 
The  ocular  and  aural  manifestations  developing  about  puberty  may 
be  more  or  less  permanent.  There  is  considerable  doubt  whether 
syphilis  can  be  transmitted  to  the  third  generation. 

Treatment. — The  only  efficient  method  of  prophylaxis  is  to  avoid 
the  sources  of  infection.  A  syphilitic  subject  should  be  told  of  the 
danger, of  transmitting  the  disease  by  kissing,  for  instance,  as  well  as 
by  contaminating  any  article  that  he  may  use,  such  as  table  utensils, 
pipes,  public  drinking  vessels,  personal  and  bed  linen,  towels,  etc. 
Physicians,  nurses,  midwives,  barbers,  chiropodists,  etc.,  should 
carefully  sterilize  all  instruments,  towels,  etc.,  that  have  been  used 
on  known  or  supposedly  syphilitic  persons.  A  syphilitic  infant 
may  be  nursed  by  its  mother,  but  should  not  be  given  to  a  healthy  wet 
nurse,  who  certainly  would  acquire  the  infection  from  the  infant.  From 
a  purely  medical  point  of  view,  altogether  aside  from  the  question  of 
morals  involved  in  exposing  an  innocent  and  unsuspecting  woman 
and  possible  children  to  the  likelihood  of  infection,  a  syphilitic  subject 
must  not  marry  until  at  least  four  years  have  elapsed  since  infection; 
the  first  two  years  must  have  been  devoted  to  persistent  and  efficient 
treatment,  and  during  the  second  two  years  the  subject  must  have  been 
entirely  free  from  symptoms;  otherwise  the  physician  must  prohibit 
the  marriage,  and  such  quasi  approval  as  he  may  give  should  be  always 
reserved,  since  even  after  apparently  efficient  treatment  infection  may 
be  transmitted,  and  late  results,  such  as  gummas,  tabes  dorsalis,  and 
paretic  dementia,  are  likely  to  ensue. 

Opinions  differ  as  to  the  propriety  of  excising  the  initial  lesion  with 
a  view  to  prevent  constitutional  symptoms.  Although  it  is  undoubtedly 
true  that  general  infection  has  occurred  by  the  time  the  chancre  has 
matured,  it  is  perhaps  possible  to  minimize  the  infection  by  early  remov- 
ing the  main  hatching  ground;  this,  however,  can  scarcely  be  proved, 
although  it  has  been  successful  in  the  ape.  Treponema  pallidum,  how- 
ever, should  first  be  demonstrated  in  the  chancrous  discharge.  If  not 
removed,  the  chancre  should  be  washed  with  an  antiseptic  solution,  such 
as  mercuric  bichloride  1  to  2000,  and  dusted  with  calomel ;  or  a  calomel 
ointment  (10  per  cent.),  or  mercurial  plaster,  may  be  applied. 

Internal  medication  should  be  commenced  as  soon  as  the  diagnosis 
is  certain,  and  not  sooner.  If  Treponema  pallidum  has  been  early  iden- 
tified, treatment  may  then  be  instituted;  otherwise,  one  should  await  the 
general  lymph-node  enlargement,  the  cutaneous  rash,  and  other  so- 
called  secondaries.  Mercury  is  the  sovereign  remedy,  and  may  be 
given  by  the  mouth,  by  inunction,   by  intramuscular  injection,  and 


SYPHILIS  191 

by  fumigation.  The  preferable  preparations  for  administration  by  the 
mouth  are:  Mercury  with  chalk  (containing  38  per  cent,  of  mercury), 
which  may  be  given  in  doses  of  1  grain  (0.06  gram),  with  or  without 
an  equal  amount  of  Dover's  powder  to  prevent  diarrhoea  in  those  sus- 
ceptible; the  protoiodide  (l  grain,  0.015  gram),  the  tannate  (^  grain, 
0.015  gram),  and  the  biniodide  (-^^  grain,  0.004  gram),  three  times  a 
day.  The  dose  may  be  increased  to  the  point  of  toleration  (abdominal 
pain,  diarrhoea,  tenderness  of  the  gums),  whereupon  the  dosage  should 
be  reduced  one-half,  and  continued  thereat  for  one  year,  provided  the 
general  health  of  the  patient  is  maintained.  Should  the  general  health 
fail,  the  mercury  should  be  stopped,  and  iron  and  tonics  substituted. 
Should  relapses  occur  while  taking  the  mercury,  the  dose  should  be 
increased,  or  another  method  of  administration  resorted  to.  During 
the  second  year,  in  the  absence  of  symptoms,  there  should  be  alternating 
periods  of  treatment  and  of  cessation  of  treatment  of  a  month  or  six 
weeks  each;  if  symptoms  are  present,  treatment  should  be  continuous, 
as  in  the  first  year,  and  the  alternate  periods  of  treatment  and  cessation 
thereof  should  be  resorted  to  in  the  third  year. 

In  cases  in  which  a  rapid  influence  is  desired,  inunctions  may  be 
resorted  to.  After  preliminary  cleansing,  1  dram  (4  grams)  of  the 
official  mercurial  ointment  (50  per  cent,  of  mercury),  or  an  equivalent 
amount  of  the  oleate  (10  per  cent,  of  mercury),  should  be  rubbed  into 
the  body  daily  (for  20  to  30  minutes)  on  six  consecutive  days;  on  the 
seventh  day  the  patient  should  have  a  warm,  cleansing  bath.  The 
skin  of  the  parts  selected  for  the  inunction  should  be  thin  and  as  free 
from  hair  as  possible:  the  inner  aspect  of  the  thighs,  the  sides  of  the 
chest  and  abdomen,  and  the  arms  are  six  serviceable  regions  that  may 
be  used  in  rotation.  When  the  inunction  is  done  by  some  one  other 
than  the  patient,  the  rubber  should  be  protected  by  gloves  or  he  should 
use  a  glass  rod  or  spatula.  The  treatment  should  be  continued  for  four 
or  five  weeks,  and  then  discontinued;  but  at  least  two  courses  of  such 
treatment  should  be  given  yearly  for  two  years,  or  longer  should  symp- 
toms recur.  Intramuscular  injections  are  exceedingly  valuable  in 
intractable  cases,  in  cerebrospinal  syphilis,  and  in  persons  who  dislike 
the  inconvenience  and  publicity  of  pills  and  inunctions.  One  may 
use:  (1)  The  insoluble  salts  of  mercury,  such  as  calomel,  1  grain 
(0.0(5  gram),  in  15  minims  (1  c.c.)  of  sterile  olive  oil;  gray  oil,  1  to  2 
minims  (0.06  to  0.12  c.c.)  diluted  with  olive  oil;  or  mercury  salicylate, 
10  minims  (0.60  c.c.)  of  a  10  per  cent,  suspension  in  paraffin  oil;  or 
(2)  the  soluble  salts  of  mercury,  of  which  the  bichloride  is  the  best, 
and  may  be  used  in  doses  of  ^  grain  (0.008  gram)  in  15  minims  (1  c.c.) 
of  sterile  physiological  saline  solution.  The  injections  should  be  made 
deep  into  the  buttock,  in  the  centre  of  a  line  running  from  the  anterior 
superior  spine  of  the  ileum  to  the  upper  end  of  the  intergluteal  fold. 
The  insoluble  salts  should  be  injected  once  a  week  for  twelve  to  fifteen 
weeks,  and  the  soluble  salts,  at  first  daily,  then  every  other  day,  and 
then  twice  a  week  until  about  forty  injections  have  been  made.     The 


192  PROTOZOAN  INFECTIONS 

injections  may  then  be  discontinued  for  a  month  or  two,  but,  as  in  the 
other  methods,  treatment  must  be  resorted  to  for  shorter  periods  for  at 
least  two  years,  and  again  if  any  symptoms  recur. 

In  the  late  or  tertiary  stage  of  the  disease  (visceral  and  bone  lesions) 
the  iodides  should  be  given,  either  alone  or  alternating  with  or  in  combi- 
nation with  mercury  (so-called  mixed  treatment).  The  iodide  may  be 
given  in  gradually  ascending  doses,  in  some  alkaline  water  or  milk; 
although  excellent  results  sometimes  attend  the  use  of  small  doses,  15 
grains  (1  gram)  daily,  it  is  wise,  as  a  rule,  to  give  large  doses  to  the 
point  of  toleration  (150  grains,  10  grams,  or  more  a  day).  One  may  give 
the  iodide  and  mercury  together,  as  in  the  following  prescription  (the 
arsenic  has  been  added  for  its  tonic  effect  and  to  prevent  acne,  coryza, 
and  other  manifestations  of  iodism,  but  it  may  be  omitted): 

I^ — Mercuric  bichloride 1  grain  0  6 

Potassium  iodide 3  drams  12  0 

Solution  of  potassium  arsenite 30  minims  2  0 

Compound  syrup  of  sarsaparilla 4  ounces  120  0 

Water  sufficient  to  make 8  ounces  250,0 — M. 

Sig. — One  tablespoonful  (15  c.c.)  in  water  three  times  a  day. 

The  iodides  should  be  continued  for  two  or  three  months,  then  inter- 
mitted for  a  month,  and  then  resumed,  alternating  thus  month  by  month 
for  a  year.  Mercury  is  sometimes  administered  also  by  fumigation 
(sublimation  of  calomel),  and,  rarely,  by  intravenous  injection.  iVt  all 
times  when  mercury  is  being  taken  the  greatest  care  must  be  exercised 
to  keep  the  mouth  clean,  by  frequent  use  of  the  toothbrush,  and  of 
solutions  of  potassium  chlorate  or  mild  antiseptics.  Alcohol  and 
tobacco  should  be  interdicted.  Mucous  patches  may  be  treated  with 
solid  silver  nitrate,  acid  nitrate  of  mercury,  etc.;  condylomas  about 
the  genitalia  by  cleansing  with  mercuric  bichloride,  1  to  2000,  and 
dusting  with  calomel;  scaly  lesions  on  the  hands,  feet,  etc.,  by  a  10 
per  cent,  ointment  of  ammoniated  mercury;  and  ulcerating  cutaneous 
gummatous  lesions  by  cleansing  and  the  application  of  mercurial  plaster. 
The  syphilitic  cachexia  should  be  treated  with  bitter  tonics,  iron,  quinine, 
strychnine,  syrup  of  iron  iodide,  cod-liver  oil,  arsenic,  the  lactophosphates, 
and  hypophosphites. 

Syphilitic  infants  are  best  treated  with  mercurial  ointment  (diluted 
with  an  equal  part  of  vaseline)  or  the  oleate  of  mercury  on  the  binder, 
or  by  administering  mercury  and  chalk,  \  grain  (0.03  gram),  three 
times  a  day.  The  later  lesions  occurring  about  puberty  may  be  treated 
with  mercury  and  the  iodides,  the  following  formula  being  serviceable: 

I^ — Mercuric  bichloride '  lo  grain  0  03 

Potassium  iodide IH  drams  6  0 

Tincture  of  iron  chloride 2  drams  8  0 

Syrup  of  lemon 2  ounces  60  0 

Water  suflScient  to  make 4  ounces  120  0 — M. 

Sig. — One  teaspoonful  (5  c.c.)  in  water  three  times  a  day. 


YAWS  193 

YAWS. 

(Framboesia.) 

Yaws  is  a  chronic,  infectious,  and  highly  contagious  disease,  caused 
by  Treponema  pertenuis  (Castellani),  and  characterized  by  a  papular 
rash  which  usually  develops  into  a  fungating,  granulomatous,  encrusted 
eruption. 

Etiology. — Yaws  is  widely  distributed  throughout  the  tropics,  espe- 
cially Africa,  Asia,  Central  and  South  America,  the  Pacific  Islands, 
and  the  West  Indies.  During  the  early  part  of  the  nineteenth  century 
it  was  exceedingly  common  among  the  slaves  of  our  southern  countries, 
but  has  now  practically  disappeared  from  the  land.  The  disease 
attacks  persons  of  all  ages,  but  children  are  most  susceptible.  Indeed, 
in  some  parts  of  the  West  Indies  and  in  Fiji  nearly  every  child  is  attacked, 
and  those  who  might  otherwise  escape  are  often  voluntarily  exposed  to 
infection  by  their  parents  under  the  impression  that  the  disease  is  a 
necessary  part  of  a  child's  training.  The  black  and  the  yellow  races 
are  more  susceptible  than  the  white.  One  attack  seems  to  confer  partial 
immunity.  The  disease  is  not  hereditary  or  congenital,  as  is  sj'philis, 
for  which  it  is  sometimes  mistaken. 

The  exciting  cause  of  the  disease  is  Treponema  pertenuis.  The  disease 
is  highly  contagious.  The  contagium  may  be  transmitted  directly,  that 
is,  from  the  sick  directly  to  the  well;  by  means  of  fomites,  such  as  articles 
of  domestic  use,  dishes,  etc.;  and  probably  also  by  insects;  but  an  open 
wound  or  abrasion  seems  rec|uisite  for  infection.  Mere  residence  in  an 
infected  locality  (a  house,  for  instance)  seems  to  have  sufficed  for  infec- 
tion, but  many  other  factors  must  be  considered  in  such  cases.  The 
infection  is  inoculable  into  lower  animals,  such  as  the  monkey. 

Symptoms. — The  period  of  incubation  varies  from  about  two  weeks 
(in  inoculation  cases)  to  as  much  as  six  months  (in  cases  otherwise 
acquired).  Prodromal  symptoms  are  usually  absent,  though  there  may 
be  for  several  days  malaise,  headache,  fever,  and  vague  neuromuscular 
pains.  The  disease  begins,  certainly  in  the  inoculation  cases,  and  usually 
also  in  other  cases,  with  the  development  of  a  papule  at  the  site  of  inocula- 
tion— usually  on  the  feet,  legs,  or  face.  At  the  end  of  a  week  this 
is  converted  into  an  ulcer,  which  at  the  end  of  another  week  heals  and 
leaves  a  superficial  cicatrix.  This  is  called  the  primary  eruption  or  sore. 
The  secondary  eruption,  which  may  occur  with  the  primary  eruption, 
or  be  delayed  for  two  weeks,  consists  of  pin-sized  papules  which  gradually 
increase  in  size  until  they  reach  that  of  a  pea  or  a  small  nut,  or,  by  conflu- 
ence, that  of  a  small  ap})le.  They  may  be  distributed  more  or  less 
widely  over  the  body,  but  are  found  most  commonly  at  or  about  the  muco- 
cutaneous junctions  and  on  the  limbs,  neck,  and  trunk;  the  hairy  scalp 
and  the  axilla  are  rarely  involved.  They  consist  largely  of  granulation 
tissue  and  inflammatory  overgrowth  of  the  papillary  layer  of  the  cutis 
and  the  Malpighian  layer  of  the  epidermis.  They  much  resemble 
13 


194  PROTOZOAN  INFECTIONS 

syphilitic  condylomas,  and  itch  considerably,  but  are  otherwise  painless. 
Their  epidermic  covering  becomes  thinner,  and  is  ruptured  or  shed, 
permitting  the  escape  of  a  whitish-yellow,  seropurulent  fluid  which  dries 
and  forms  crusts,  which  are  usually  quite  tough,  often  very  hard,  and 
adherent.  When  removed  they  reveal  irregular,  reddish  granulation 
tissue,  which  has  been  likened  to  a  raspberry,  whence  the  name  fram- 
boesia  (frambcesia,  raspberry).  The  yaw,  as  a  rule,  reaches  its  maximum 
development  in  about  two  weeks,  remains  stationary  for  about  two 
weeks,  and  then  begins  to  shrink.  The  crust  dries  up,  the  papillomatous- 
looking  granulation  tissue  is  gradually  converted  into  a  cicatrix,  which 
is  pale  in  the  negro,  pigmented  in  the  white  race,  and  surrounded  by  an 
area  of  increased  pigmentation. 

In  some  cases  the  primary  eruption  is  followed  by  one  or  more 
relapses,  associated  with  fever  and  severe  neuromuscular  pains  in  the 
back.  In  other  cases  the  yaw  itself  ulcerates,  but  may  heal  after  a 
time  with  considerable  cicatricial  contraction. 

Diagnosis. — ^The  disease  is  commonly  unmistakable,  but  care  must 
be  exercised  to  exclude  syphilis,  verruga,  leprosy,  tuberculosis,  and 
epithelioma.  Treponema  pertenuis  may  be  demonstrated  in  the  lesions, 
especially  the  papillomatous  skin  lesions. 

Prognosis. — The  duration  of  yaws  is  from  a  few  weeks  to  several  years. 
In  most  cases  recovery  ensues.  Young  children,  however,  and  older 
persons  the  subject  of  divers  constitutional  diseases,  may  succumb. 

Treatment. — Attention  to  general  hygienic  measures  is  imperative — 
isolation,  fresh  air,  good  food,  suitable  clothing  (to  obviate  cold  and 
chill),  and  daily  warm  baths.  The  ulcerated  areas  should  be  treated 
antiseptically  and  with  stimulants,  such  as  copper  sulphate,  silver  nitrate, 
chromic  acid,  etc.  Potassium  iodide  internally  is  believed  to  be  of  much 
value  in  effecting  the  disappearance  of  the  local  lesions.  Mercury 
is  sometimes  used,  but  often  avoided,  as  tending  to  do  harm.  The 
bitter  tonics  and  iron,  arsenic,  and  quinine  are  useful  as  general 
measures. 

TRYPANOSOMIASIS. 

(Sleeping  Sickness;  African  Lethargy;  Tsetse  Fly  Disease.) 

Trypanosomiasis  is  a  chronic,  specific,  infectious  disease  caused  by 
Trypanosoma  gambiense,  and  characterized  by  fever,  weakness,  lassitude, 
emaciation,  and  eventually  by  protracted  lethargy — sleeping  sickness. 

Etiology. — Sleeping  sickness  is  known  to  have  existed  for  the  last  one 
hundred  years  on  the  west  coast  of  Africa,  and  recently  has  been  reported 
inland.  It  affects  the  white  as  well  as  the  colored  race,  and  it  is  common 
at  all  seasons.  The  specific  exciting  cause  is  Trypanosoma  gambiense, 
which  is  transmitted  by  a  tsetse  fly,  Glossina  palpalis,  which  Koch 
believes  becomes  infected  by  feeding  on  infected  crocodiles,  and  which 
probably  serves  as  an  alternate  host;  that  is,  the  parasite  probably  under- 
goes some  phase  of  development  in  the  fly. 


KALA-AZAR  195 

Symptoms. — The  period  of  incubation  is  probably  from  two  to  three 
weeks.  In  the  early  stage  of  the  disease,  which  varies  in  duration  from 
about  three  to  as  much  as  three  years,  the  only  symptom  of  marked  con- 
stancy is  enlargement  of  the  lymph  nodes,  but  there  may  be  also  irregular 
fever,  rapid  pulse,  mental  hebetude,  slight  anemia,  and  some  loss  of 
weight.  This  stage  gradually  merges  into  the  second  stage,  that  of 
sleeping  sickness.  The  patient  becomes  definitely  dull,  listless,  and 
apathetic;  the  pulse  becomes  rapid  (120  or  more  per  minute)  and  weak; 
the  temperature  becomes  irregular,  often  rising  as  high  as  101°  or  102°  in 
the  evening;  indefinite  pains  are  complained  of  in  the  head  and  through- 
out the  body;  patches  of  erythema  or  of  oedema  may  develop  on  the  skin. 
There  is  gradual  loss  of  strength  in  the  arms  and  legs,  associated  with 
tremors,  as  well  as  with  tremors  of  the  tongue.  The  patient  lies  most  of 
the  time  in  a  lethargic  state  and  becomes  emaciated.  Finally,  during 
the  last  two  or  three  weeks  of  life  the  temperature  falls  below  normal, 
and  the  patient  ultimately  dies  in  coma. 

Diagnosis. — The  diagnosis  may  be  made  tentatively  from  a  considera- 
tion of  the  symptomatology  and  possible  etiological  factors,  and  positively 
on  finding  Trypanosoma  gambiense  in  the  enlarged  lymph  nodes 
(aspiration  of  some  fluid  therefrom  with  a  hypodermic  needle  and  syringe), 
circulating  blood,  or  cerebrospinal  fluid.  Darling  has  described,  as 
occurring  upon  the  Isthmus  of  Panama,  a  fatal  infection  resembling  kala- 
azar,  that  he  has  named  Histoplasma  capsulatum,  and  due,  as  he 
believes,  to  an  organism  resembling  Leishmania  donovani. 

Prognosis. — The  disease  is  invariably  fatal. 

Treatment. — Prime  importance  must  be  attached  to  avoiding  the 
tsetse  fly,  and  searching  out  and  destroying  its  breeding  places.  Treat- 
ment is  unavailing,  arsenic  being  the  only  drug  apparently  capable  of 
producing  any  good  effects,  and  it  only  prolongs  life.  The  ordinary 
preparations  or  atoxyl  may  be  used.  They  have  sometimes  been  com- 
bined with  aniline  preparations,  such  as  trypanroth,  with  asserted  good 
results.     Hopes  are  entertained  of  the  production  of  an  efficient  serum. 


KALA-AZAR. 

(Tropical  Spleiwmegahj;  Tropical  Cachexia;  Dum-duni  Fever;  Piroplasinosis.) 

Kala-azar  is  a  chronic,  specific,  infectious  disease  caused  by  Leishmania 
donovani,  and  characterized  by  intermittent  or  remittent  fever,  marked 
and  progressive  anemia  and  emaciation  and  enlargement  of  the  spleen 
and  tiie  liver.  A  similar  organism,  described  as  Leishmania  infantum 
(Pianese  and  NicoUe),  has  been  found  in  certain  types  of  infantile  splenic 
anemia. 

Etiology. — Kala-azar  was  formerly  believed  to  be  indigenous  in  the 
lowlands  of  India,  but  it  is  now  known  to  occur  in  many  regions  of  the 
Orient.  How  the  disease  is  transmitted  is  not  definitely  known.  Patton 
has  studied  the  flagellated  stage  of  I>eishmania  donovani  in  the  bed-bug 


196  PROTOZOAN  INFECTIONS 

(Cimex  rotundatiis),  but  whether  this  is  a  transmitting  agent  has  not  yet 
been  determined. 

Symptoms. — ^The  period  of  incubation  is  not  definitely  known,  but  it 
may  be  less  than  ten  days  (Manson).  The  onset  of  the  disease  is  usually 
abrupt — chills,  fever  (104°  to  106°),  vomiting,  and  rapid  enlargement  of 
the  spleen  and  liver.  The  fever,  though  somewhat  irregular  in  type, 
remains  high  for  a  few  days  to  six  weeks,  and  then  subsides  by  lysis  to 
normal  or  subnormal;  recurrences  are  common,  and  a  low  grade  contin- 
ued fever  may  super\'ene.  Profound  debility,  emaciation,  and  anemia 
(rarely  less  than  2,500,000  erythrocytes)  and  marked  leukopenia  (involving 
especiallv  the  polynuclear  neutrophiles)  ensue.  The  skin  becomes  pecu- 
liarly pigmented — of  an  earthy  gray  or  drab  color;  and  subcutaneous 
hemorrhages  and  dropsical  effusions  may  develop  in  the  skin  and  the 
serous  sacs.  The  disease  lasts  for  several  months,  as  a  rule,  but  may 
be  prolonged  to  one  or  even  two  years. 

Diagnosis. — ^The  diagnosis  is  suggested  by  continued  fever,  enlarge- 
ment of  the  spleen,  leukopenia  (relative    lymphocytosis),  and  is  con- 
firmed by  detecting  Leishmani  donovani  in  the  blood  (especially  in  the 
leukocytes)  or  in  the  tissues. 

Prognosis. — Death  occurs  in  about  96  per  cent,  of  the  cases — from 
exhaustion,  or  intercurrent  infections,  such  as  chronic  diarrhoea,  etc. 

Treatment. — The  treatment  is  purely  hygienic,  dietetic,  and  sympto- 
matic. Removal  from  infected  regions  and  isolation  of  the  patient  are 
advisable. 

ORIENTAL  SORE.  ^ 

(Tropical  Ulcer;  Delhi  Boil.) 

Oriental  sore  is  a  chronic,  specific,  granuloma  that  occurs  endemically 
in  certain  tropical  and  subtropical  countries,  is  caused  by  Leishmania 
tropica  (Helcosoma  tropicum,  Wright),  and  is  characterized  by  a  nodule, 
which  breaks  down  and  forms  an  indolent  ulcer. 

Etiology. — How  the  exciting  cause  of  the  disease  is  transmitted  is 
not  known,  but  the  bite  of  an  insect  or  infection  of  an  already  existing 
wound  is  usually  postulated.  Age,  sex,  race,  and  occupation  are  devoid 
of  etiological  significance.     One  attack  seems  to  confer  immunity. 

Symptoms. — ^The  disease  begins  with  a  small,  red  spot,  resembling 
a  mosquito  bite,  in  the  centre  of  which  a  small  nodule  or  papule  soon 
forms.  The  surface  becomes  covered  with  fine  scales  that  form  a  crust, 
which,  when  removed  or  separated  spontaneously,  leaves  a  shallow, 
painless  ulcer,  that  may  itch  considerably.  About  this  similar  ulcers 
develop,  and  by  coalescence  of  many,  a  single  ulcer,  often  an  inch  in 
diameter,  results.  In  some  cases  there  is  only  one,  sometimes  two  ulcers, 
whereas  in  other  cases  there  may  be  as  many  as  twenty.  After  the  lapse 
of  from  two  to  twelve  months,  healing  begins.  The  resulting  cicatrix 
may  occasion  considerable  deformity,  especially  if  on  the  face.  Occa- 
sionally the  nodule  does  not  ulcerate,  but  merely  desquamates  at  the 


MALARIAL  INFECTIONS  197 

end  of  several  months.  The  general  health  is  little,  if  at  all,  disturbed. 
Enlargement  of  the  lymph  nodes,  lymphangitis,  phlebitis,  erysipelas, 
abscesses,  and  gangrene  are  sometimes  encountered  as  complications, 
and  may  result  in  death. 

Diagnosis. — The  diagnosis  suggested  by  the  symptoms,  is  confirmed 
by  detecting  the  specific  cause. 

Prognosis.— The  specific  lesion  itself  rarely  leads  directly  to  death, 
but  the  prognosis  as  to  cure  is  unfavorable. 

Treatment. — Cauterization  of  the  specific  lesion  is  recommended  by 
some  observers.  At  all  events  it  should  be  dressed  antiseptically. 
Change  of  climate  and  tonics  are  said  to  be  useful  in  some  cases. 


MALARIAL  INFECTIONS. 

(Afjue;  Intermittent  Fever;  Remittent  Fever;  Pernicious  Remittent  Fever;  Bilious 

Remittent  Fever;  Estivo-autuinnal  Fever;  Paludism;  Suiamp  Fever; 

Marsh  Fever.) 

The  malarial  infections  comprise  a  group  of  specific  infectious  dis- 
eases, caused  by  Plasmodium  malariae  (Hsemamoeba  malariae,  Laveran), 
and  variously  characterized  by  intermittent  or  remittent  fever,  enlarge- 
ment of  the  spleen,  the  presence  of  the  specific  microorganism  in  the 
circulating  blood,  and  sometimes  by  certain  so-called  pernicious  mani- 
festations or  a  chronic  cachexia. 

Etiology. — The  malarial  infections  are  widely  disseminated  throughout 
all  parts  of  the  world.  Though  especially  prevalent  in  tropical  and  sub- 
tropical regions,  they  frequently  prevail  extensively  in  the  temperate 
zones;  but  a  noteworthy  diminution  in  the  prevalence  of  the  infections 
is  found  to  follow  intelligent  agricultural  pursuits,  efiicient  drainage,  and 
other  sanitary  measures  commonly  introduced  by  the  more  enlightened 
people.  On  the  contrary,  the  infections  not  infrequently  break  out 
among  laborers  engaged  in  constructing  railroads,  canals,  fortifications, 
and  other  operations  connected  with  upturning  the  soil.  These  and 
other  etiological  (telluric  and  atmospheric)  factors,  such  as  comparativelv 
high  atmospheric  temperature  and  humidity,  are  of  influence  only  in 
so  far  as  they  favor  the  growth  and  development  of  the  Anopheles  mos- 
quito— the  essential  factor  in  disseminating  the  infections.  The  mos- 
quito fructifies  and  flourislies  best  at  a  temperature  of  75°  F.,  or  over 
— whence  the  malarial  infections  are  most  common  in  tropical  and  sub- 
tropical regions,  and  in  temperate  zones  during  the  summer.  Pools  of 
stagnant  water  are  essential  for  the  breeding  of  mosquitoes — whence 
malarial  infections  are  common  in  the  neighborhood  of  earth-cutting 
operations  accompanied  by  the  formation  of  holes  and  surface  irregulai- 
ities  wherein  water  collects  and  stagnates,  and  in  the  neighborhood  of 
low  marsh  lands,  swamps,  and  old  river  beds,  where  the  water  affords 
the  necessary  medium  and  the  abundant  vegetation  additional  protection 
for  tlie  developing  larvae.     The  malarial  infections  are  less  common  at 


198  PROTOZOAN  INFECTIONS 

high  than  at  low  ahitudes,  because  the  mosquitoes,  as  a  rule,  do  not 
fly  high;  nor  do  they  fly  far  (200  to  300  yards),  although  they  may  be 
carried  long  distances  by  winds;  and  the  proverbial  insalubriousness  of 
the  night  air  is  attributable  to  the  fact  that  the  malaria-bearing  mosquito 
(Anopheles)  peregrinates  only  at  night. 

In  this  country  the  malarial  infections  at  present  are  endemic  along 
the  Gulf  of  Mexico  and  the  Mississippi  River  and  in  the  States  adjacent 
thereto,  and  they  are  rather  common  in  the  Middle  and  Southern  States . 
that  border  the  Atlantic  Ocean.  They  are  much  less  common  than 
formerly  in  the  central.  New  England,  and  Northwestern  States ;  and  the 
Hudson,  the  Delaware,  and  the  Schuylkill  valleys,  formerly  much  in- 
fected, are  now  comparatively  free.  The  infections  are  uncommon  in 
Canada.  Many  of  the  Central  and  South  American  States,  especially 
those  along  the  coasts,  are  markedly  infected.  The  British  Isles  are 
practically  uninfected.  The  valleys  of  lower  Russia,  the  Balkan  prov- 
inces, Italy,  and  India  present  many  foci  of  infection,  and  along  the 
coast  of  Africa  the  most  malignant  forms  of  the  infections  are  endemic. 

Age,  sex,  and  race  are  devoid  of  etiological  significance.  The  sup- 
posed relative  immunity  of  the  adult  negro  of  South  Africa  has  been 
found  to  be  due  to  a  relative  immunity  acquired  during  childhood,  when 
the  disease  is  very  common,  though  often  masked.  Occupation  is  of 
significance  only  in  that  laborers  on  railroads,  in  swamps,  etc.,  and 
soldiers,  fishermen,  farmers,  etc.,  are  more  exposed  to  the  likelihood  of 
being  bitten  by  infected  mosquitoes. 

The  essential  etiological  factor,  then,  is  infected  mosquitoes.  Thus  far 
only  mosquitoes  of  the  genus  Anophelinse  have  been  found  to  be  malaria- 
bearing  hosts,  and  of  the  one  hundred  and  fifty  or  more  species,  forty 
have  been  proved  by  experiment  to  be  active  infectious  agents.  The  most 
common  and  important  are:  Anopheles  maculipennis  (also  called  quad- 
rimaculatus,  and  claviger — the  most  common).  Anopheles  punctipennis. 
Anopheles  crucians,  and  Anopheles  argyritarsis.  Fortunately  in  the 
temperate  zone  the  common  mosquito  is  not  Anopheles,  but  Culex — 
which  does  not  transmit  malaria  (though  it  does  transmit  filarial  disease). 
The  two  may  be  distinguished  by  the  fact  that  the  palpi  of  the  adult  Culex 
are  very  short,  while  those  of  Anopheles  are  almost  if  not  quite  as  long 
as  the  proboscis;  the  wings  of  Anopheles  are  distinctly  mottled  (brownish), 
while  those  of  Culex  are  not  (aside  from  the  veins) ;  Culex  while  resting 
has  its  body  nearly  parallel  with  the  surface  (wall)  and  its  posterior 
pair  of  legs  turned  up  over  its  back,  while  Anopheles  rests  with  its  body 
almost  at  right  angles  (45  degrees  or  more)  to  the  wall  and  its  posterior  pair 
of  legs  usually  against  the  wall  or  hanging  downward.  Anopheles  is 
a  rural  insect,  breeding  especially  in  shallow  pools,  irrigating  ditches, 
and  the  still  edges  of  running  streams,  often  remote  from  human  habita- 
tions; Culex  is  a  city  beast,  breeding  in  tanks,  cisterns,  and  stagnant 
pools  of  water  near  or  in  houses.  The  males  of  all  mosquitoes  have 
feathered  antennae  (woolly  heads),  while  the  females  have  not. 

The  mosquito,  like  other  insects,  passes  through  the  stages  of  ovum, 


MALARIAL  INFECTIONS  199 

larva,  pupa,  and  imago  (adult  insect).  Depending  upon  the  genus, 
and  the  environmental  conditions,  such  as  season,  temperature,  stillness 
of  the  water,  food,  etc.,  the  cycle  of  development  from  ovum  to  imago 
takes  from  ten  days  to  three  or  four  weeks.  The  male  mosquito  thrives 
on  the  juices  of  plants,  whereas  the  female  mosquito  feeds  mostly  upon 
the  blood  of  vertebrates,  a  meal  of  which  is  said  to  be  essential  to  the 
deposition  of  eggs.  These,  as  a  rule,  are  deposited  on  the  surface  of 
still  water,  and  they  vary  in  number  with  the  species:  Anopheles  and 
Stegomyia  deposit  40  to  50  ova,  singly  or  in  small  groups,  each  ovum 
resting  on  its  side;  Culex  deposits  300  to  400  ova,  in  large,  coherent 
masses,  the  individual  ova  being  on  end.  The  ova  are  very  resistant, 
and  may  mature  even  after  several  months  of  drying.  In  from  twelve 
hours  to  three  or  four  days,  depending  upon  the  temperature  of  the  water 
and  the  air,  the  ova  develop  to  larvae — minute,  whitish  or  brownish, 
worm-like  bodies  that  hang  below  the  surface  of  the  water  and  exhibit 
an  active  wiggling  motion,  whereby  (about  once  a  minute)  they  come  to 
the  surface  to  breathe,  through  a  respiratory  tube  that  projects  from  the 
last  abdominal  segment.  The  larvse  may  remain  capable  of  maturation 
after  several  months  of  unfavorable  environmental  conditions,  even 
freezing  in  ice.  After  existing  in  the  larval  stage  for  about  one  week 
(Culex  and  Stegomyia)  to  two  weeks  (Anopheles),  during  which  time 
several  moultings  occur,  the  pupse  appear — distinguishable  from  larvse 
chiefly  by  the  greater  size  of  the  thoracic  segment,  but  also  by  their  dis- 
position to  float  on  the  water  (being  lighter  than  water).  At  the  end  of 
from  two  days  (Culex  and  Stegomyia)  to  five  days  (Anopheles),  the  imago 
or  adult  insect  emerges  from  the  pupal  shell.  The  first  deposition  of 
eggs  occurs  about  twenty  days  later,  and  recurs  at  intervals  of  several 
days — each  female  mosquito  being  said  to  give  rise  to  at  least  twelve 
generations  in  a  season.  The  Anopheles  mosquito  becomes  infected 
with  the  malarial  parasite  by  sucking  the  blood  of  a  malarious  subject. 

Plasmodium  Malari^e  in  Man. — Craig  distinguished  four  distinct 
species:  Plasmodium  vivax  (Grassi  and  Feletti),  the  tertian  parasite; 
Plasmodium  malarise  (Marchiafava  and  Celli),  the  quartan  parasite; 
Plasmodium  falciparum  (Blanchard),  the  tertian  estivo-autumnal  para- 
site; and  Plasmodium  falciparum  quotidianum  (Craig),  the  quotidian 
estivo-autumnal  parasite.  Each  species  passes  through  two  different 
cycles  of  development,  the  one  in  man,  the  other  in  the  mosquito. 

The  Tertian  Parasite. — ^The  tertian  parasite  is  seen  in  its  earliest 
stage  within  the  infected  erythrocyte  as  a  small  (2//  in  diameter),  round- 
ish, hyaline,  unpigmented,  and  actively  ama'boid  body — proti'uding 
and  retracting  pseudopodia.  This  increases  in  size  and  soon  accumulates 
a  number  of  fine,  reddish-brown  pigment  granules  which  it  has  elaborated 
from  the  hemoglobin  of  the  infected  erythrocyte,  and  which,  reflecting  the 
amoeboid  movement  of  the  parasite,  appear  actively  motile.  ^Vhen 
almost  or  quite  full  grown  the  parasite  is  roundish,  distinctly  outlined, 
actively  amoeboid,  and  contains  motile  pigment  granules  which  are 
usually  distributed  rather  dift'usely  (sometimes  in  small  clumps)  througii- 


200  ■  PROTOZOAN  INFECTIONS 

out  the  parasite;  what  are  usually  described  as  a  nucleus  and  a  nucleolus 
may  be  distinguished  in  stained  specimens.  The  containing  erythrocyte 
is  much  swollen  and  pale.  At  the  end  of  thirty-six  hours,  as  maturity  is 
reached,  scarcely  any  of  the  distended  erythrocyte  (which  may  be  almost 
twice  the  normal  size)  is  visible,  the  amoeboid  motion  has  lessened,  and 
the  pigment  granules,  much  increased  in  number,  tend  to  collect  in  the 
centre  of  the  parasite.  Soon  radial  striations  appear  and  divide  the 
parasite  into  from  twelve  to  twenty-four  (an  average  of  sixteen)  segments, 
which  contain  no  pigment  and  are  arranged  usually  in  two  rows,  one 
toward  the  periphery  and  the  other  toward  the  centre,  though  they  may 
be  arranged  irregularly.  Toward  the  end  of  forty-eight  hours  the  ery- 
throcyte has  been  entirely  destroyed,  and  segmentation  of  many  of  the 
parasites  (sporocytes)  occurs;  the  free  segments,  liberated  in  the  blood 
stream,  float  about  as  unpigmented  bodies,  and  soon  re-infect  other 
erythrocytes  and  again  pass  through  this  so-called  asexual  cycle  of  de- 
velopment. Some  parasites,  however,  do  not  undergo  segmentation, 
but  persist  as  large  parasites  with  actively  motile  pigment  granules — the 
sexually  differentiated  microorganisms  (gametocytes)  designed  for  the 
sexual  cycle  of  development  in  the  mosquito.  Remnants  of  the  mother 
parasites,  consisting  mainly  of  inanimate  bodies  and  pigment,  are  ab- 
sorbed by  the  leukocytes  and  the  vascular  endothelium,  and  thus  removed 
from  the  circulation.  The  malarial  paroxysms  (chill  and  fever)  occur  at 
the  time  of  segmentation  (liberation  of  toxins)^thus  at  intervals  of 
forty-eight  hours  (every  third  day).  In  some  cases  a  double  tertian 
infection  occurs,  and  segmentation  of  the  different  sets  of  parasites  occur- 
ring on  alternate  days,  a  malarial  paroxysm  occurs  every  day  (quotidian 
malarial  fever). 

The  Quartan  Parasite. — In  general  the  quartan  parasite  resembles 
the  tertian,  but  it  presents  certain  noteworthy  differences.  In  its 
early  stages  the  quartan  parasite  is  smaller  than  the  tertian  and  has  a 
more  definite  contour;  its  amoeboid  movements  are  more  sluggish;  the 
pigment  granules  are  coarse,  rod-like  in  shape,  and  deep  brown  or 
blackish  in  color;  and  the  containing  erythrocyte  does  not  increase  in 
size,  but  remains  normal,  or  perhaps  decreases  in  size,  and  becomes 
darker,  yellowish,  yellowish  green,  or  brassy  in  color.  As  the  parasite 
increases  in  size,  the  amoeboid  movement  gradually  ceases,  so  that  when 
full-grown  (toward  the  end  of  seventy-two  hours),  the  parasite  is  entirely 
motionless,  distinctly  outlined,  and  completely  fills  the  containing 
erythrocyte.  Throughout  most  of  its  life  cycle  the  pigment  granules  are 
distributed  around  the  periphery  of  the  parasite,  but  toward  the  end  of 
seventy-two  hours  these  tend  to  collect  in  the  centre  to  form  a  star- 
shaped  mass  radiating  from  the  centre.  Segmentation  occurs  as  in  the 
tertian  organism,  but  the  segments  are  more  distinctly  outlined  than  in 
the  tertian  parasite,  they  are  fewer  in  number  (six  to  twelve),  and  they  are 
arranged  regularly  around  the  pigment  (so-called  daisy  or  marguerite 
forms).  Like  the  tertian  organism,  some  of  the  quartan  parasites  do  not 
undergo  segmentation,  but  persist  to  undergo  the  mosquito  phase  of 


MALARIAL  INFECTIONS  201 

development.  The  malarial  paroxysms  (chill  and  fever)  occur  concm- 
rently  with  segmentation — about  every  seventy-two  hours  (every  fourth 
day).  Double  or  even  triple  infections  with  the  quartan  parasite  may 
occur,  giving  rise  to  a  malarial  paroxysm  on  each  of  two  succeeding  days 
with  a  free  day,  or  to  a  daily  paroxysm. 

The  Estivo-autumnal  Parasite. — Two  types  of  the  estivo-autumnal 
parasite  may  be  distinguished,  the  quotidian  and  the  tertian.  The 
quotidian  estivo-autumnal  parasite  is  seen  in  its  earliest  stages  in  the  in- 
fected erythrocyte  as  a  small,  round,  hyaline  or  ring-shaped  body 
(signet  ring),  with  indistinct  outlines,  and  markedly  amoeboid  (rapid  but 
not  wide  movements).  The  containing  erythrocyte  is  usually  smaller 
than  normally,  greenish  or  brassy  in  color,  and  sometimes  contains  two 
or  even  three  parasites.  Some  of  the  parasites  become  pigmented,  in 
some  cases  apparently  only  those  in  the  organs  (the  spleen  and  the  bone 
marrow),  those  in  the  circulating  blood  remaining  unpigmented;  the 
pigment  at  first  consists  of  fine,  dust-like  particles,  slightly  motile  and 
arranged  usually  about  the  periphery;  as  the  parasite  grows  the  pigment 
tends  to  collect  in  the  centre  and  then  becomes  motionless.  AMien  full 
grown  the  parasite  is  scarcely  more  than  one-fourth  or  one-third  the 
size  of  a  normal  erythrocyte  (distinction  from  the  ordinary  tertian  and 
quartan  parasite).  Segmentation  occurs  (in  the  organs  rather  than  in 
the  circulating  blood)  at  the  end  of  twenty-four  hours,  and  often  quite 
obviously  within  the  erythrocyte;  six  to  eight  spores  are  formed.  The 
tertian  (so-called  malignant)  estivo-autumnal  parasite  differs  from  the 
quotidian  parasite  in  that  the  ring  form  is  larger,  more  irregular  in 
outline,  more  sharply  defined,  and  more  refractile;  it  requires  forty- 
eight  hours  to  complete  its  cycle  of  development;  the  pigmented  stage 
lasts  twenty-four  hours  or  more,  and  during  this  time  the  parasite  is 
actively  amoeboid  and  the  pigment  exhibits  a  characteristic  oscillatory 
movement  not  seen  in  the  quotidian  parasite;  and  when  full  grown  the 
parasite  fills  one-half  or  two-thirds  of  the  infected  erythrocyte.  This 
parasite  difters  from  the  ordinary  tertian  organism  in  being  smaller 
(at  corresponding  stages  of  development);  in  sometimes  assuming  ring 
forms  and  giving  rise  to  crescents;  in  the  more  scanty  and  less  active 
pigment;  in  occasioning  shrinkage  (rather  than  swelling)  of  the  infected 
erythrocyte;  and  in  giving  rise  to  a  less  number  of  spores  (eight  to  fifteen). 
Segmentation  occurs  in  the  internal  organs,  and  often  intermittently — 
whence  the  irregularity  of  the  clinical  manifestations.  In  both  varieties 
of  estivo-autumnal  infection,  at  the  end  of  about  a  week,  other  character- 
istic parasites  (with  coarse,  centrally  situated,  pigment  granules)  appear 
in  the  blood — crescent-shaped,  spindle-shaped  (cigar-shaped),  and  sphe- 
roid (or  ovoid)  l)odies.  These  do  not  sporulate,  but  represent  sexually 
differentiated  forms  (gametocytes)  designed  for  the  life  cycle  of  the 
parasite  in  the  mosquito.  The  quotidian,  as  contrasted  with  the  tertian, 
crescent  is  smaller,  shorter,  and  plumper;  its  extremities  are  rounded 
(never  pointed);  its  protoplasm  is  less  granular;  and  its  pigment  is  le.ss 
in  amount.     The  estivo-autumnal  parasites  give  rise  to  the  more  severe 


202  PROTOZOAN  INFECTIONS 

malarial  infections,  to  many  latent  or  masked  infections,  and  to  the  so- 
called  pernicious  or  malignant  infections,  especially  common  in  tropical 
and  subtropical  regions;  but  the  ordinary  tertian  or  quartan  infections 
may  become  pernicious. 

Plasmodium  Malari^e  in  the  Mosquito. — When  a  mosquito  of 
the  genus  Anopheles  bites  a  malarious  subject,  it  sucks  into  its  stomach 
blood  containing  the  sexually  differentiated  forms  of  the  malarial  parasite 
(gametocytes) — large  spheroidal  non-sporulating  forms  in  the  tertian 
and  the  quartan  infections,  and  crescents  and  spheroid  (or  ovoid)  forms 
in  estivo-autumnal  infections.  These  develop  into  flagellating  and  non- 
flagellating  spheres,  the  former  representing  male  elements  (micro- 
gametocytes)  and  the  latter  female  elements  (macrogametocytes). 
The  flagella  (microgametes)  are  cast  off  by  the  male  elements,  and  pene- 
trating fertilize  the  female  body  (macrogamete).  The  impregnated 
female  parasite  now  penetrates  the  wall  of  the  midgut  of  the  mosquito 
and  continues  its  development  in  the  muscular  coat,  in  which,  at  the  end 
of  two  days,  minute,  refractile,  and  pigmented  spheres  may  be  found. 
These  rapidly  increase  in  size  and  become  encapsulated.  At  the  end 
of  a  week  they  may  have  attained  a  diameter  of  70/<,  and  they  contain 
a  large  number  of  delicate  spindle-shaped  filaments,  about  14/i  in  length 
(sporozoites).  The  mother  cell  (zygote)  soon  ruptures,  setting  free 
an  enormous  number  of  sporozoites,  which  speedily  accumulate  in  the 
salivary  glands  of  the  mosquito,  and  are  inoculated  into  man  through 
the  proboscis  of  the  mosquito  when  next  it  bites.  The  sporozoites  soon 
develop  into  young  hyaline  forms,  and,  invading  the  erythrocytes,  pass 
through  the  asexual  cycle  of  development  and  give  rise  to  the  clinical 
manifestations  of  malaria.  Fertilization  of  the  macrogamete  may  also 
be  studied  on  the  warmed  stage  under  the  microscope,  as  was  originally 
observed  by  W.  G.  MacCallum. 

Pathology. — The  most  striking  lesions  in  the  acute  infections  consist 
of  destruction  of  the  erythrocytes  and  certain  resultant  changes.  The 
blood  as  a  whole  is  hydremic,  the  erythrocytes  are  decreased  in  number 
(due  to  direct  destruction  and  probably  also  in  consequence  of  a  toxin 
produced  by  the  parasites);  the  color  index  is  reduced,  and  granular 
degeneration  and  polychromatophilia  occur;  the  mononuclear  leukocytes 
are  increased;  many  of  the  polynuclear  leukocytes  are  much  pigmented; 
and  free  pigment  is  found  in  the  plasma.  The  spleen  is  enlarged;  the 
capsule  is  tense  and  may  rupture;  many  infected  erythrocytes  are  found 
in  the  pulp;  and  considerable  pigment  is  free  and  enclosed  within  macro- 
phages. The  liver  is  enlarged,  and  hyperemic,  and  may  reveal  foci  of 
necrosis  due  usually  to  capillary  thromboses;  the  capillaries  may  contain 
many  parasites.  The  kidneys  are  often  swollen  and  may  show  some 
cloudy  swelling,  and  may  reveal  pigmented  leukocytes  and  parasites, 
acute  nephritis  is  not  uncommon  in  estivo-autumnal  infections.  The 
bone  marrow  often  contains  many  segmenting  parasites.  In  pernicious 
infections  hemoglobinemia  and  parenchymatous  hemorrhages  are  com- 
mon, and  the  capillaries  throughout  the  body  (brain,  gastro-intestinal 


MALARIAL  INFECTIONS 


20c 


tract,  kidneys,  etc.)  may  be  found  packed  with  parasites.  In  chronic 
malaria  there  is  usually  a  high-grade  anemia;  great  enlargement,  indura- 
tion, and  pigmentation  of  the  spleen  (ague  cake) ;  enlargement,  pigmenta- 
tion of  the  endothelial  and  Kupffer's  perivascular  cells,  and  occasion- 
ally cirrhosis  of  the  liver;  enlargement  and  pigmentation  of  the  kidneys; 
pigmentation  of  the  gastro-intestinal  mucous  membrane,  especially  of 
the  solitary  glands  and  Peyer's  patches ;  and  in  the  bone  marrow  replace- 
ment of  the  fat  by  proliferated  marrow  cells,  new  bloodvessels,  and  pig- 
mentation. 

Symptomatology. — The  following  clinical  types  of  the  malarial  infec- 
tions may  be  distinguished :  (1)  Tertian  infection;  (2)  quartan  infection ; 
(3)  estivo-autumnal  infections;  and  (4)  chronic  malarial  cachexia. 
The  tertian  and  the  quartan  infections  comprise  the  regularly  intermittent 
fever  of  the  older  writers,  and  the  estivo-autumnal  infections  the  irregular, 
remittent,  continued,  and  pernicious  fevers. 


Fig.  4 


The  temperature  in  tertian  malarial  infection  (Craig). 


Tertian  Infection. — Tertian  malarial  infection  is  characterized 
by  a  so-called  malarial  paroxysm,  consisting  of  chill,  fever,  and  sweat, 
recurring  at  intervals  of  forty-eight  hours  (every  third  day),  corresponding 
with  the  life  cycle  of  the  tertian  parasite  (Fig.  4).  The  period  of  incuba- 
tion is  not  definitely  known;  it  is  said  to  vary  from  thirty-six  hours  (experi- 
mentally) to  twenty  days.  Prodromal  symptoms,  consisting  of  malaise, 
headache,  restlessness,  yawning,  stretching,  loss  of  appetite,  etc.,  usually 
precede  for  several  days  the  definite  malarial  paroxysm.  The  initial 
manifestation  of  the  paroxysm,  the  chill,  is,  as  a  rule,  sudden  in  onset,  and 
it  is  usually  severe,  the  entire  body  being  more  or  less  violently  agitated. 
The  skin  is  pale,  cold,  cyanosed,  and  presents  the  peculiar  appearance 
described  as  goose-flesh  (cutis  anserina).  The  patient  complains  bitterly 
of  the  violent  agitation  and  cold,  and  seeks  to  mitigate  his  distress  by 
additional  bedclothes,  and  hot  water  bottles.  His  discomfort  is  sometimes 
increased  by  nausea  and  vomiting  and  intense  headache  (congestion 
of  the  cerebral  vessels).     The  pulse  is  frequent,  and  often  hard  and 


204  PROTOZOAN  INFECTIONS 

irregular;  and  the  urine  may  be  increased  in  amount.  The  chilhng  of 
the  body  is  superficial  only,  since  with  the  advent  of  the  chill  (if  not  pre- 
viously) the  temperature  begins  to  rise,  and  at  the  height  of  the  chill  the 
rectal  (or  the  axillary)  temperature  may  be  103°  to  106°  F.  or  more.  This 
so-called  cold  stage  lasts  for  from  fifteen  minutes  to  an  hour,  and  is 
succeeded  by  the  hot  stage.  The  patient  begins  to  complain  of  alternat- 
ing sensations  of  heat  and  cold,  until  gradually  the  subjective  sensation 
of  cold  disappears  and  the  surface  of  the  body  becomes  intensely  hot, 
whereupon  he  complains  as  much  of  the  heat  as  he  did  of  the  cold. 
The  face  is  flushed,  the  conjunctivae  injected,  the  general  integument 
congested;  the  pulse  becomes  full,  bounding,  and  perhaps  dicrotic; 
the  respirations  are  quickened;  throbbing  headache  and  thirst  are  often 
marked;  and  in  severe  infections  stupor  and  delirium  may  supervene. 
Cutaneous  eruptions — erythema,  urticaria,  and  herpes — often  develop, 
labial  herpes  being  quite  as  common  as  in  pneumonia.  During  this 
stage  the  temperature  reaches  its  highest  point — 105°  to  106°  F.  or  more, 
though  occasionallv  it  mav  be  onlv  104°  F.  The  hot  stage  lasts  for  from 
one  to  three  or  four  hours  or  more,  and  ends  abruptly  with  a  sudden 
fall  of  the  temperature  to  normal  (intermittent  fever)  and  a  profuse 
sweat.  The  perspiration  usually  begins  on  the  forehead  and  face  and 
soon  involves  the  entire  body,  and  has  been  said  to  have  a  characteristic 
sperm-like  odor;  the  pulse  becomes  slower  and  weaker;  the  headache 
and  other  subjective  complaints  cease;  considerable  urine  may  be 
voided;  and  the  patient  often  falls  into  a  sleep  from  which  he  awakens 
several  hours  later  much  refreshed,  though  often  somewhat  exliausted. 
The  sweating  stage  lasts  usually  from  one  to  three  hours. 

The  average  duration  of  the  tertian  malarial  paroxysm  is  from  ten 
to  twelve  hours;  it  may  be  less  when  mild,  and  it  is  sometimes  very  severe 
and  much  prolonged.  One,  two,  or  all  three  stages  may  be  much 
shortened  or  abortive.  Frequently,  especially  in  primary  attacks  and 
in  children,  there  is  not  a  distinct  chill,  but  only  chilliness,  or  merely 
pallor  and  cyanosis  in  children;  or  the  hot  stage  alone  may  be  present, 
the  sweating  being  slight;  or  the  fever  may  escape  observation — where- 
upon the  infection  is  likely  to  go  unrecognized. 

During  the  paroxysm  the  spleen  becomes  enlarged  and  palpable,  and 
may  remain  so.  The  skin  may  present  a  peculiar  lemon-yellow  tint — due 
to  a  rapidly  developed  anemia,  a  form  of  hemolytic  jaundice,  or  abnor- 
mal deposition  of  pigment.  A  dry  bronchitis,  diarrhoea  and  other 
intestinal  symptoms,  etc.,  are  not  uncommon  concomitant  symptoms, 
and  suggest  special  localizations  of  the  toxic  process. 

In  some  cases  the  paroxysms  occur  not  every  other  day,  but  daily 
(quotidian  intermittent  fever):  cases  of  double  tertian  infection  in 
which  the  two  sets  of  parasites  mature  on  alternate  days.  After  persist- 
ing for  several  weeks,  the  malarial  paroxysms  frequently  tend  to  cease 
spontaneously,  but  in  this  event  recurrence  is  very  likely.  When 
neglected  the  infection  may  become  chronic  (malarial  cachexia),  or 
rarely  pernicious. 


MALARIAL  INFECTIONS 


205 


Quartan  Infection. — Quartan  malarial  infection  is  characterized 
by  malarial  paroxysms  (chill,  fever,  and  sweat)  recurring  at  intervals  of 
seventy-two  hours  (every  fourth  day) — corresponding  with  the  life  cycle 
of  the  quartan  parasite  (Fig.  5).  In  the  event  of  a  double  quartan  infec- 
tion a  paroxysm  occurs  on  each  of  two  successive  days  and  is  followed 
by  a  free  day;  in  the  event  of  a  triple  infection  a  paroxysm  occurs  daily 
(quotidian  fever).  As  a  rule,  the  paroxysms  in  quartan  infection,  as 
contrasted  with  tertian  infection,  are  more  severe,  though  they  are  shorter 
(usually  less  than  ten  hours);  nervous  symptoms,  such  as  headache, 
restlessness,  etc,  are  more  pronounced;  delirium  is  more  likely  to  occur; 
and  the  tendency  toward  perniciousness  is  somewhat  more  marked. 
Otherwise  there  is  but  little  difference  in  the  clinical  manifestations  of 
the  two  forms  of  infection. 


Fig.  5 


The  temperature  in  quartan  malarial  infection.       (Craig.) 

EsTivo-AUTUMNAL  INFECTIONS. — These  are  most  common  in  tropical 
and  subtropical  regions,  where  they  prevail  throughout  the  year,  but  they 
are  also  rather  prevalent  in  the  temperate  zones,  especially  during  July, 
August,  September,  and  October  (whence  the  name).  As  a  rule,  they  are 
more  severe  than  the  ordinary  tertian  and  quartan  infections,  and  they 
are  more  likely  to  become  pernicious.  The  following  varieties  may  be 
differentiated:  (1)  Tertian  estivo-autumnal  infection  (the  most  com- 
mon); (2)  quotidian  estivo-autumnal  infection;  (3)  pernicious  estivo- 
autumnal  infection,  of  which  the  comatose,  the  algid,  and  the  hemor- 
rhagic forms  are  the  most  common. 

Tertian  Estlvo-didumudl  Infection. — The  prodromal  symptoms,  as 
a  rule,  are  similar  to  those  of  the  ordinary  tertian  and  quartan  infections. 
The  cold  stage  does  not  last  more  than  a  half  hour,  and  there  is  usually 
chilliness  rather  than  a  distinct  chill;  but  the  patient  complains  of  head- 
ache, pain  in  the  back  and  legs,  nausea,  and  perliaps  vomiting;  he  is 
much  depressed  mentally,  and  he  may  be  slightly  stuporous  or  even 
delirious;  the  skin  and  mucous  membranes  are  cyanosed;  the  pulse  is 
frequent,  weak,  and  irregular;  the  respirations  are  rapid  and  shallow; 


206 


PROTOZOAN  rXFECTIOXS 


and  the  internal  temperature  is  elevated  (Fig.  6).  At  the  onset  of  the  hot 
stage,  the  temperature  has  reached  103°  to  104°  F. ;  whereupon  it  oscillates 
slightly  for  several  hours,  then  falls  a  degree  or  two  or  three  (pseudo- 
crisis),  rises  again,  perhaps  higher  than  it  was  previously  (precritical 
rise),  and  finally  falls  rapidly  to  normal  or  below  (true  crisis).  The  entire 
fever  period  is  much  longer  than  in  ordinary  tertian  infections,  and  may 
last  twenty,  thirty,  or  even  forty  hours.  Concurrently  with  the  crisis 
the  patient  sweats,  but  the  sweating  is  usually  much  less  marked  than  in 
ordinary  tertian  infections.  In  many  cases  the  paroxysms  reciu'  regularly 
every  forty-eight  hours,  corresponding  with  the  life  cycle  of  the  parasite — 
a  fact  not  sufficiently  recognized;  but  in  many  cases  the  manifestations 
are  quite  irregular.  The  temperature  may  rise  slowly  or  fall  by  lysis; 
and  it  frequently  becomes  remittent  or  continuous  in  consequence  of 
anticipation  (overlapping)  or  retardation  of  the  paroxysms  (especially 


Fig.  6 


The  temperature  in  tertian  estivo-autumnal  malarial  infection. ^(Craig.) 

common  in  estivo-autumnal  infections),  reduplications  of  the  paroxysms 
due  to  double  or  mixed  infections,  etc. ;  and  sometimes  there  is  a  moderate 
degree  of  fever  between  irregularly  recurring  paroxysms  attended  by 
more  marked  fever.  In  consequence,  the  infection  has  been  and  fre- 
quently is  mistaken  for  t\^hoid  fever:  a  coated  tongue,  enlarged  spleen, 
bronchitis,  tympanites,  and  diarrhoea  alternating  with  constipation, 
increase  the  diagnostic  difiiculties — whence  the  ill-advised  term,  t^'pho- 
malarial  fever.  The  patient  is  depressed,  even  prostrated,  and  complains 
of  divers  subjective  complaints,  not  only  during  the  paroxysms,  but  also 
between  them.  Frequently  the  fever  subsides  at  the  end  of  a  week  or 
ten  days,  but  it  may  continue  much  longer.  In  severe  infections,  loss  of 
appetite,  nausea,  bilious  vomiting,  and  jaundice,  suggest  the  designations 
bilious  remittent  fever,  gastrobilious  fever,  jungle  fever,  etc.  These 
often  assume  pernicious  tendencies. 

Quotidian  estivo-uutummd  infection  frequently  cannot  be  differenti- 
ated clinically  from  the  tertian  estivo-autumnal  infection,  but,  as  a  rule, 
it  is  characterized  by  more  severe  chilly  sensations  or  distinct  chills 
and  more  marked  sweating  (though  neither  is  as  marked  as  in  the  ordinary 


MALARIAL  INFECTIONS 


207 


tertian  and  quartan  infections);  the  paroxysms  recur  daily,  the  fever 
rising  rapidly  to  103°  or  104°  F.,  and  falling  suddenly  within  six  or  eight 
hours  to  normal  (Fig.  7) ;  but  the  paroxysms  frequently  become  prolonged 
to  twelve,  sixteen,  or  twenty-four  hours  (due  to  irregular  generation  of 
parasites) — whence  a  remittent  or  continued  fever  results  (especially  in 
pernicious  cases).  Postponement  of  the  paroxysms  occurs  in  cases 
tending  to  spontaneous  recovery. 


Fig.  7 


The  temperature  in  quotidian  estivo-autumnal  malarial  infection.      (Craig.) 

Pernicious  Estivo-autumnal  Infections. — Depending  upon  the  special 
prominence  of  certain  symptoms,  many  varieties  of  pernicious  estivo- 
autumnal  infections  have  been  described,  such  as  comatose,  delirious, 
convulsive,  syncopal,  paralytic,  algid,  gastro-intestinal,  bilious,  choleraic, 
dysenteric,  cardialgic,  hemorrhagic,  hemoglobinuric,  pneumonic,  etc.; 
but  these  represent  variations  in  degree,  rather  than  differences  in  kind. 
The  so-called  comatose,  the  algid,  and  the  hemorrhagic  forms  are  the 
most  common  and  merit  special  mention. 

The  comatose  (the  most  common)  form  is  due  usually  to  the  tertian 
estivo-autumnal  parasite,  and  is  characterized  by  symptoms  of  intense 
cerebral  congestion  (intimately  associated  with  thrombi  of  parasites  in 
the  cerebral  capillaries  and  necrotic  and  other  changes  about  them). 
At  the  onset  there  is  often  a  chill  and  fever,  as  in  other  malarial  infections, 
though  nervousness  and  mental  depression  (rarely  slight  delirium)  maybe 
early  obtrusive  features.  Soon  the  patient  becomes  stuporous  and  then 
comatose.  The  coma  may  come  on  with  the  first  paroxysm,  or  not  until 
the  second  or  third  (or  later),  and  although  it  may  be  precetled  by  mental 
disturbance,  it  may  develop  suddenly,  persist,  and  lead  to  death  within 
several  hours  or  two  or  three  days.  On  the  other  hand,  the  coma 
may  intermit,  that  is,  develo])  with  the  rise  of  the  tem])erature  and  clear 
up  when  the  fever  falls — in  which  event  it  rarely  lasts  more  than  twelve 
to  twenty-four  hours;  but  a  second  or  third  attack  may  prove  fatal. 
The  fever  is  high,  but  it  may  be  as  low  as  101°  F.;  the  face  is  fliished,  or 


208  PROTOZOAN  INFECTIONS 

subicteric  or  leaden,  if  anemia  is  present;  the  pulse  is  slow  and  full  at 
first,  but  it  soon  becomes  weak  and  irregular;  the  spleen  is  enlarged;  the 
pupils  may  be  equally  contracted,  or  unec[ually  contracted  or  dilated; 
muscular  twitchings  are  common;  and  the  sphincters  may  become 
paralyzed. 

The  algid  form  (congestive  chills)  is  characterized  by  nausea,  vomit- 
ing, and  purging,  leading  to  collapse  and  simulating  the  algid  stage  of 
cholera.  Usually  there  is  no  chill,  but  chilliness  is  complained  of;  the 
internal  temperature  may  become  considerably  or  moderately  elevated, 
but  it  is  not  infrequently  subnormal;  the  pulse  is  rapid,  weak,  and  ir- 
regular; the  general  integument  and  the  visible  mucous  membranes  are 
pale  and  livid,  and  the  skin  is  covered  with  a  profuse  clammy  sweat; 
the  eyes  are  sunken,  the  pupils  dilated,  and  the  Hippocratic  facies  de- 
velops. The  urine  is  often  lessened  in  amount  or  suppressed,  and  jaun- 
dice and  grave  nervous  spuptoms  may  supervene  (simulating  yellow 
fever).  The  patient  may  die  within  a  few  hours,  or  at  the  end  of 
several  days,  from  profound  asthenia. 

The  hemorrhagic  form  is  characterized  by  bleeding  from  the  mucous 
membranes  of  the  body  (mouth,  stomach,  intestine,  rectum,  vagina, 
etc.),  or  into  the  skin  and  the  interstices  of  the  body;  but  special  interest 
attaches  to  a  peculiar  hemorrhagic  form  of  the  infection  known  as 
blackwater fever,  hemoglobinuric  fever,  or  malarial  hemoglobinima.  This 
is  rather  common  in  our  own  Southern  States,  and  in  Central  America, 
Italy,  and  Africa.  It  usually  follows  estivo-autumnal  infections,  but 
it  has  been  observed  after  ordinary  tertian  and  quartan  infections.. 
Apparently  it  occurs  only  in  persons  who  have  had  repeated  attacks  of 
malaria  and  have  become  anemic  or  cachectic.  The  parasites,  as  a  rule, 
are  present  in  the  blood  before  the  onset  of  the  attack,  but  during  the 
attack  they  are  often  absent.  The  immediate  cause  of  the  attack  is  not 
known :  those  who  have  seen  the  disorder  are  not  agreed  as  to  whether 
or  not  quinine  is  of  significance  in  provoking  the  attack;  but  there  is 
some  evidence  that  c[uinine  is  of  etiological  importance  in  some  cases, 
and  it  often  appears  to  be  harmful  if  administered  during  the  attack 
when  the  parasites  are  absent  from  the  blood  (said  to  be  referable  to  a 
hemolytic  action  of  the  quinine  on  the  erythrocytes).  In  some  cases 
the  patient  gives  a  history  of  a  few  days  of  intermittent  or  remittent 
fever  with  increasing  biliousness,  then  a  sudden  chill  and  bloody  urine; 
in  other  cases,  especially  those  that  develop  late  in  the  fall  or  winter,  there 
may  have  been  for  some  time  irregular  outbreaks  of  malaria,  then  the 
prodromal  symptoms  of  another  attack  followed  by  the  bloody  urine 
(said  by  some  observers  to  be  provoked  by  the  quinine  taken  to  ward 
off  the  impending  paroxysm).  The  urine  contains  methemoglobin, 
hemoglobin,  hematin,  degenerated  erythrocytes,  leukocytes,  biliary 
coloring  matter,  tube  casts,  and  considerable  albumin.  In  favorable 
cases  the  urine  becomes  clear  in  from  three  or  four  hours  to  three  or 
four  days;  but  the  other  malarial  manifestations  may  continue.  In 
other  cases  the  hemoglobinuria  recurs  periodically.     Death  may  occur 


MALARIAL  INFECTIONS  209 

on  the  first  clay  from  marked  toxemia  and  coma,  or  it  may  occur  later 
from  the  effects  of  the  blood  destruction,  suppression  of  the  urine  and 
uremia,  and  general  exhaustion. 

Chronic  Malarial  Cachexia. — ^This  is  a  condition  of  pronounced 
anemia  with  enlarged  spleen  that  develops  in  those  the  subjects  of  long- 
continued  malarial  infection.  The  symptoms  are  those  common  to 
high  grade  anemia — asthenia,  breathlessness,  palpitation  of  the  heart, 
and  slight  oedema  about  the  ankles.  In  addition  there  is  a  subicteric  hue 
to  the  skin  or  a  yellowish-brown  pigmentation;  the  spleen  is  enlarged; 
hemorrhages  may  occur  into  the  retina  and  elsewhere  (especially  the 
gastro-intestinal  tract);  and  the  patient  is  subject  to  irregular  attacks  of 
fever  of  variable  duration  with  intervening  periods  of  apyrexia. 

Latent  and  Masked  Malarial  Infections. — ^These  are  by  no 
means  uncommon,  and  though  usually  due  to  the  estivo-autumnal  para- 
site, they  may  be  due  to  the  ordinary  tertian  or  quartan  parasite.  These 
infections,  though  they  often  manifest  a  noteworthy  periodicity,  simulate 
a  wide  variety  of  disorders,  such  as  neuralgia  (supra-orbital,  occipital, 
intercostal,  sciatica,  etc.),  paresthesias,  anesthesias,  paralyses,  hemi- 
plegia, ataxia,  amaurosis,  deafness,  etc.,  and  certain  gastro-intestinal 
disorders,  such  as  gastro-enteritis,  dysentery,  etc.  In  many  of  the 
cases  the  parasite  may  be  found  in  the  blood;  in  other  cases,  the  symp- 
toms subside  promptly  upon  the  administration  of  quinine.  Tubercu- 
losis, dysentery,  cardiac  degeneration,  cirrhosis  of  the  liver,  nephritis, 
orchitis,  parotitis,  gangrene  of  the  skin,  etc.,  have  been  observed  as  com- 
plications or  sequels  of  malarial  infections. 

Diagnosis. — ^The  ordinary  tertian  and  quartan  infections  are  usually 
recognizable  from  the  clinical  manifestations,  but  the  diagnosis  is  easily 
rendered  certain  by  a  microscopic  examination  of  the  blood.  This 
should  not  be  neglected  in  any  case  in  the  diagnosis  of  which  malaria 
enters  as  a  possibility.  In  the  event  of  more  continued  fever,  it  may  be 
necessary  to  exclude  typhoid  fever,  tuberculosis,  pyogenic  infections 
(especially  acute  ulcerative  endocarditis),  etc.  Typhoid  fever  may  be 
excluded  by  the  absence  of  the  Gruber-Widal  reaction,  the  presence  of 
malarial  parasites  in  the  blood,  and  the  response  of  the  symptoms 
to  quinine;  in  fact,  that  fever  that  does  not  respond  to  quinine  within 
four  or  five  days  may  be  said  not  to  be  malaria.  Tuberculosis  may 
be  excluded  by  the  history  of  the  patient,  the  associated  general  symp- 
toms, the  physical  signs,  the  presence  of  tubercle  bacilli  in  the  sputum  or 
cerebrospinal  fluid  (or  choroid  tul)ercles),  and  the  absence  of  malarial 
parasites  in  the  blood,  and  the  non-response  of  the  symptom.s  to  ({uinine. 
Most  of  the  pyogenic  infections,  of  which  ulcerative  endocarditis  is  a 
type,  are  attended  by  leukocytosis  (which  is  absent  in  malaria),  they  do 
not  respond  to  quinine,  and  malarial  parasites  are  not  found  in  the  blood. 

Prognosis. — In  the  ordinary  tertian  and  quartan  infections  the  prog- 
nosis is  good;  the  disorders  are  quite  amenable  to  treatment.  The 
prognosis  is  also  relatively  good  in  many  of  the  latent  and  masked 
infections,  though  they  may  last  a  long  time.     But  the  outlook  is  very  bad 

14 


210  PROTOZOAN  INFECTIONS 

in  many  of  the  estivo-autumnal,  especially  the  pernicious,  infections — 
the  mortality  being  very  high. 

Treatment. — Prophylaxis. — The  malarial  infections  may  be  prevented 
by  protecting  all  persons  from  the  bites  of  mosquitoes.  In  malarious 
districts  the  windows  and  doors  of  all  houses  should  be  screened,  and 
additional  protection  should  be  afforded  by  surrounding  the  beds  with 
mosquito  netting,  especially  the  beds  of  malarious  subjects  (to  prevent 
infection  of  uninfected  mosquitoes).  Furthermore,  the  breeding  places 
of  mosquitoes  should  be  destroyed  by  filling  up  and  draining  swamps, 
and  preventing  stagnation  of  surface  water.  Larv^se  should  be  de- 
stroyed by  coating  the  surface  of  all  stagnant  pools  with  kerosene  (one 
ounce  to  each  fifteen  square  feet  of  water) — whereby  the  larvae  are  de- 
prived of  oxygen;  this  should  be  repeated  every  three  or  four  weeks. 
Small  fish  also  are  of  service  in  destroying  the  larvae.  Oil  of  pennyroyal 
or  of  eucah^tus  (which  is  obnoxious  to  mosquitoes)  may  be  smeared 
on  the  hands  by  those  obliged  to  work  out  of  doors  in  malarious  districts. 
Five  to  ten  grains  (0.3  to  0.6  gram)  of  cjuinine,  once  or  twice  a  week,  is 
also  of  service  in  warding  off  malarial  attacks. 

Quinine  is  a  specific  remedy  and  the  only  drug  that  really  can  be 
depended  upon.  Following  ancient  custom,  it  is  wise  to  deplete  the  liver 
and  to  unload  the  bowels  by  a  preliminary  dose  of  calomel  (10  grains, 
0.6  gram),  followed  by  a  saline.  Since  the  quinine  is  most  efficacious 
when  the  parasites  are  free  in  the  blood  plasma,  rather  than  when  they 
are  within  the  erythrocytes,  it  is  desirable  to  have  an  adequate  amount 
of  quinine  in  the  circulation  at  the  time  of  sporulation.  Therefore, 
four  to  six  hours  before  the  expected  paroxysms  in  tertian  and  quartan 
infections,  15  to  30  grains  (1  to  2  grams)  of  quinine  bisulphate  or 
bihydrochlorate  should  be  given  in  solution  (or  in  capsule  or  cachet,  but 
not  in  pill  form,  since  the  pills  often  do  not  dissolve).  If  administered 
only  shortly  before  the  paroxysm  the  quinine  will  not  prevent  it,  but 
will  exert  a  deleterious  effect  on  the  parasites  and  prevent  a  recurrence. 
After  the  initial  dose,  it  is  wise  to  continue  the  quinine  in  from  10  to  20 
grain  (0.6  to  1.3  gram)  doses  for  several  days,  and  then  in  5  grain  (0.3 
gram)  doses  daily  for  a  week,  and  thereafter  at  intervals  of  a  week  for 
a  month.  In  estivo-autumnal  infections,  similar  doses,  as  a  rule,  are 
effectual,  but  in  severe  infections  larger  doses  (up  to  60  grains,  4  grams, 
or  more,  daily)  may  be  required.  In  pernicious  types  of  the  infection 
it  is  often  necessary  to  bring  the  system  rapidly  under  the  effects  of  the 
cjuinine,  in  which  event  it  should  be  administered  hypodermicly  or 
intravenously:  15  to  30  grains  (1  to  2  grams)  of  the  bihydrochlorate,  or 
of  the  hydrochlorate  of  quinine  and  urea,  in  2  drams  (30  c.c.)  or  more 
of  physiological  saline  solution;  if  necessary,  this  may  be  repeated  every 
two  to  four  hours.  During  the  attack  of  blackwater  fever,  quinine  should 
not  be  administered,  but  it  may  be  given  in  the  intervals  if  parasites  are 
found  in  the  blood.  No  really  efficient  substitute  for  quinine  has  been 
discovered;  methylene  blue  is  a  poor  substitute,  but  may  be  given  in 
doses  of  1  to  4  grains  (0.06  to  0.25  gram)  when  quinine  cannot  be  taken. 


DISTOMATOSIS  211 

During  the  malarial  pai'bxysms  the  patient  should  be  made  as  com- 
fortable as  possible — hot  water  bags  during  the  cold  stage,  and  tepid 
sponging  and  cooling  drinks  (ku'ing  the  hot  stage.  Unduly  severe  parox- 
ysms should  be  controlled  by  an  opiate.  If  necessary,  the  circulation 
should  be  supported  by  stimulants^ — strychnine  and  alcohol.  Vomiting 
may  be  controlled  by  counterirritation  to  the  epigastrium,  cracked  ice, 
sips  of  hot  water,  spirit  of  chloroform,  a  small  amount  of  dry  champagne, 
cerium  oxalate  and  bismuth,  etc. 

Many  latent  and  masked  infections  are  immediately  relieved  by  one 
or  two  large  doses  of  quinine;  others  require  the  prolonged  use  of  the 
drug.  Warburg's  tincture  is  sometimes  efficacious.  In  chronic  malarial 
cachexia,  removal  to  a  non-malarious  region,  preferably  at  a  high 
altitude,  arsenic  (Fowler's  solution  or  arsenous  acid),  small  doses  of 
quinine  and  iron,  or  Warburg's  tincture  will  be  found  efficacious. 


METAZOAN  INFECTIONS. 


DISTOMATOSIS. 

(Distomiasis;  Trematode  Infections;  Fluke  Infections.) 

In  man  there  are  four  important  clinical  forms  of  distomatosis — pul- 
monary, hepatic,  intestinal,  and  venal  or  hemal  distomatosis. 

Pulmonary  Distomatosis  (Lung-fluke  Disease);  Paragonimiasis; 
Parasitic  Hemoptysis. — Pulmonary  distomatosis  occurs  principally  in 
Japan  and  China,  but  also  in  the  United  States,  the  Philippines,  and 
Formosa.  The  parasite,  Paragonimus  (Distoma)  westermanii,  is  an  oval 
spinose  fluke,  somewhat  pinkish  in  color,  and  measuring  from  7.5  to  16 
mm.  long,  4  to  8  mm.  broad,  and  2  to  5  mm.  thick.  The  original  host  has 
not  been  determined  with  certainty,  but  the  organism  has  been  found  in 
man,  cats,  dogs,  swine,  etc.  The  source  of  infection  in  man  is  not  known, 
but  it  is  probably  contaminated  food  or  water.  The  adult  parasites  are 
found  in  cysts  in  the  lungs,  pleura,  brain,  liver,  abdominal  cavity,  etc. 
The  symptoms  consist  of  cough,  yellowish,  reddish,  or  rusty-brown 
sputum,  in  which  ova  (smooth,  oval  organisms,  (SO  to  100  /i  in  length, 
by  40  to  GO  /i  in  breadth)  may  })e  found,  often  in  great  abundance  (12,000 
daily).  In  some  cases  attacks  of  more  or  less  severe  hemoptysis  occur. 
The  liver,  brain,  eyelids,  etc.,  may  become  involved,  and  death  not 
infref|uently  results. 

Hepatic  Distomatosis  (Liver-fluke  Disease.). — Six  difl'erent  species 
of  flukes  have  been  found  in  connection  with  hepatic  distomatosis:  (1) 
Opisthorchis  sinensis  (Distoma  sinense),  the  most  important,  the  cause 
of  Asiatic  opisthorchiasis  or  Japanese  liver-fluke  disease.  The  organism 
is  an  elongate,  lanceolate,  non-spinose  trematode,  9.7  to  20  mm.  long  and 
2  to  5  mm.  l)road;  it  is  of  a  reddish  color  and  very  transparent.     Its  chief 


212  METAZOAN  INFECTIONS 

anatomical  characteristic  is  the  branched  condition  of  the  testicles. 
The  eggs  are  dark  brown  in  color,  have  a  well-defined  operculum,  and 
measure  24  to  30  by  15  to  17.5  ix.  Man,  cats,  and  dogs  appear  to  be  nor- 
mal hosts.  Infection  seems  to  be  accj[uired  from  swallowing  the  free 
cercaria  or  indirectly  from  eating  an  infected  water  animal  (snail,  fish,  etc.) 
or  food  contaminated  by  infected  water.  (2)  Opisthorchis  felineus,  the 
cause  of  Siberian  opisthorchiasis  or  Siberian  liver-fluke  disease.  Cases 
in  man  have  been  reported  in  Siberia  and  Prussia.  The  organism  is  a 
lanceolate,  non-spinous  trematode,  8  to  18  mm.  long  and  1.25  to  2.5  mm. 
broad;  the  testicles  are  lobate,  but  not  branched.  The  eggs  are  yellow- 
ish brown,  oval,  have  a  well-defined  operculum,  and  one  side  flatter  than 
the  other,  and  measure  26  to  30  by  11  to  15  /i.  The  cat,  dog,  fox,  and 
glutton  are  natural  hosts.  Infection  seems  to  be  acquired  from  eating 
raw  fish.  (3)  Opisthorchis  noverca,  the  cause  of  Indian  opisthorchiasis 
or  Indian  liver-fluke  disease,  which  is  very  rare.  (4)  Dicrocoelium 
lanceatum,  the  cause  of  dicrocoeliasis  (lancet-fluke  infection).  The 
organism  is  a  lancet-shaped  trematode,  4  to  9  mm.  long  and  2  to  4  mm. 
broad.  The  eggs  are  dark  brown  and  thick  shelled,  have  a  distinct 
operculum,  and  measure  38  to  45  by  20  to  30  /i.  Cattle  and  sheep  are 
normal  hosts.  The  infection  is  rare  in  man,  and  probably  always 
accidental.  (5)  Fasciola  hepatica,  the  cause  of  fascioliasis.  The 
organism  is  a  broad  flattened,  oval  trematode,  IS  to  30  mm.  long  and 
4  to  13  mm.  broad.  The  eggs  are  yellowish  or  brownish  in  color,  130 
to  145  by  70  to  90  /x,  and  they  have  a  distinct  operculum.  Cattle,  goats, 
and  sheep  are  normal  hosts;  snails  are  the  intermediate  host.  Infection 
is  acquired  by  swallowing  the  encysted  cercaria.  The  infection  is  rare 
in  man.  (6)  Fasciola  hepatica,  or  an  organism  allied  thereto,  is  said  to 
be  the  cause  of  a  disease  known  as  halzoun  in  Liban,  Syria.  .  These  liver 
flukes  enter  the  bile  ducts  and  cause  (mechanically  and  by  irritation) 
stoppage  of  these  passages.  In  early  cases  the  liver  is  enlarged  and 
hyperemic;  in  protracted  cases  it  may  be  normal  or  lessened  in  size,  and 
there  may  be  some  sclerosis.  The  symptoms  consist  principally  of 
enlargement  and  tenderness  of  the  liver,  preceded,  attended,  or  followed 
by  diarrhoea  (irregular  and  intermittent),  with  dark,  sometimes  bloody 
stools,  occasionally  slight  fever  (100°).  Night  blindness,  intermittent 
ascites,  anasarca,  and  epistaxis  may  occur.  Anemia  and  emaciation 
supers^ene,  and  finally,  after  more  or  less  improvement  and  relapses 
(diarrhoea,  etc.),  the  patient  usually  dies.  The  ova  are  readily  found  in 
the  stools.  Preventive  measures  comprise  destruction  of  infected  animals 
and  their  excreta,  the  use  in  infected  localities  of  boiled  water  and  thor- 
oughly cooked  food,  and  removal  from  infected  regions.  There  is  no 
efficient  treatment. 

Intestinal  Distomatosis  (Intestinal  Fluke  Disease). — Intestinal 
distomatosis  in  man  may  be  caused  by:  (1)  Fasciolopsis  buskii,  the  largest 
and  most  important;  it  measures  27  to  37  mm.  in  length,  5.5  to  14  mm. 
in  breadth,  and  1.5  to  2  mm.  in  thickness.  It  occurs  especially  in  Asia, 
and  is  distinguishable  from  Fasciola  hepatica  by  its  large  acetabulum 


DISTOMATOSIS  213 

and  simple  intestine.  Infection  is  said  to  cause  indigestion,  nausea, 
headache,  and  diarrhoea  with  bloody  stools.  The  ova  which  may  be 
found  in  the  stools  measure  120  to  130  by  77  to  80  /i.  Thymol  and 
calomel  are  said  to  be  capable  of  expelling  the  parasite.  (2)  Fasciolopsis 
rathonisi  (reported  once  in  Asia).  (3)  Heterophyes  heterophyes,  a 
minute  harmless  trematode  found  in  the  small  intestine  of  man,  dogs, 
and  cats.  (4)  Gastrodiscus  hominis  (found  in  the  cecum  and  colon  of 
man  in  India).  (5)  Cladorchis  (Watsonius)  watsoni  (reported  once  in  a 
negro  boy  in  Africa). 

Venal  Distomatosis  (Blood-fluke  Disease,  Bilharziosis;  Egyptian 
Hematuria;  Endemic  Hematuria;  Bilharzian  Hematuria;  Bilharzia 
Disease). — Blood-fluke  infection  in  man  may  be  due  to:  (1)  Schistosoma 
haematobium  (Bilharz),  the  African  blood  fluke,  of  which  the  male  is  4  to 
15  mm.  long  and  1  mm.  broad,  and  the  female  (carried  in  the  gynecophoric 
canal  of  the  male)  longer  and  filiform.  The  eggs  are  135  to  160  by  55  to 
66  fi,  provided  with  a  terminal  spine,  but  no  operculum.  (2)  Schistosoma 
japonicum  (Katsurda),  the  Asiatic  blood  fluke,  of  which  the  male  is 
7  to  12  mm.  long,  and  0.53  to  0.8  mm.  broad;  the  female  is  8  to  12  mm. 
long.  The  eggs  are  60  to  90  by  30  to  50  n,  and  are  not  provided  with  a 
terminal  spine  or  an  operculum.  The  source  of  infection  is  not  definitely 
known,  although  there  is  increasing  evidence  that  it  occurs  through  the 
skin;  drinking  water  cannot  be  eliminated;  some  observers  believe  that 
the  urethra  and  the  anus  may  be  the  infectious  atria.  The  young 
worms  live  in  the  veins  of  the  liver;  the  eggs  are  deposited  in  various 
organs  (liver,  intestine,  bladder),  and  escape  from  the  body  with  the  urine 
and  feces.  One-half  of  the  people  of  Egypt  are  believed  to  be  infected ; 
the  males  more  than  the  females,  and  the  rural  rather  than  the  urban 
population.  The  symptoms,  (usually  preceded  by  a  period  of  incubation 
of  four  or  five  months)  may  be  chiefly  urogenital,  consisting  of  irritability 
of  the  bladder,  hematuria,  pains  in  the  lumbar  region,  left  iliac  fossa, 
thigh,  or  vulva,  either  spontaneous  or  on  micturition;  or  they  may  be 
chiefly  rectal,  consisting  of  bloody  stools,  diarrhoea,  and  perhaps  pro- 
lapse of  the  rectum.  Secondarily  cystitis,  vesical  calculus,  urinary 
fistulas,  nephritis,  vaginal  and  rectal  growths  may  develop.  The  patient 
l)ecomes  anemic  and  debilitated,  and  after  a  year  or  two  may  die,  often 
from  some  intercurrent  infection.  The  diagnosis  is  readily  made  by 
examining  the  urine  and  feces  for  the  ova ;  in  some  cases  it  may  be  neces- 
sary to  examine  scrapings  from  the  bladder  or  the  rectal  wall  to  detect 
the  parasites.  The  frocpiosis  in  mild  infections  is  favorable,  although 
relapses  are  common.  The  treatment  is  largely  symptomatic  and  pallia- 
tive. Good  results  are  said  to  follow  the  use  of  male  fern  (15  grains,  1 
gram,  thrice  daily),  methylene  blue  (3  grains,  0.2  gram,  thrice  daily), 
santonin,  quinine,  etc.  In  rectal  infections,  local  sedatives,  as  in  dys- 
enterv,  often  mitigate  the  suft'ering. 


214 


METAZOAN  INFECTIONS 


TENIASIS. 

(Cestode  Infection;  Hydatid  Disease.) 

Teniasis  may  occur  in  one  of  two  forms:  (1)  Intestinal  infection  with 
the  adult  cestode — tapeworm;  and  (2)  somatic  infection  with  the  larval 
cestode. 

Intestinal  Teniasis  (Tapeworm  Infection)  .—Stiles  states  that,  so 
far  as  established,  man  seems  to  be  the  normal  and  sole  host  for  the 
sexual  stage  of  at  least  two  large  tapeworms.  Taenia  saginata  and  Taenia 
solium.  Man,  together  with  the  dog,  probably  forms  the  normal  host 
for  a  third  large  tapeworm,  Dibothriocephalus  latus.  In  common  with 
rats  and  mice,  man  seems  to  have  become  a  normal  host  for  the  dwarf 
tapeworm,  Hymenolepis  nana,  although  it  has  not  been  definitely 
established  that  the  worm  in  man  is  exactly  identical  with  that  of  the 
rodents.  Occasionally,  though  rarely,  as  accidental  host,  man  harbors 
the  double-pored  tapeworm,  Digylidium  caninum,  of  dogs  and  cats, 
the  flavopunctate  tapeworm,  Hymenolepis  diminuta,  of  rats,  and  the 
lanceolate  tapeworm,  Hymenolepis  lanceolata,  of  ducks  and  geese. 
Other  rarer  examples  of  tapeworm  infection  in  man  have  also  been 
reported. 


Fig.  8 


Fig.  9 


Gravid  segment  of  Taenia 
saginata,  showing  the  lateral 
branches  of  the  uterus,  en- 
larged.    (Stiles.) 


Gravid    segment   of    Taenia  solium,   showing    the   lateral 
branches  of  the  uterus,  enlarged.    (Stiles.) 


Tcenia  saginata  (mcdiocanellata)  the  fat,  unarmed,  or  beef  (beef- 
measle)  tapeworm,  is  the  commonest  tapeworm  in  North  America. 
It  may  attain  a  length  of  4  to  10  meters;  the  head,  which  may  measure 


TENIASIS 


215 


2  mm.  in  breadth,  is  larger  than  that  of  Taenia  solium,  it  is  square-shaped, 
and  has  four  large  sucking  disks,  but  no  hooklets.  There  may  be  as 
many  as  a  thousand  segments;  only  two  ovaries  are  found  in  each  mature 
segment;  the  uterus  in  the  gravid  segments  has  15  to  35  slender  dicho- 
tomous  lateral  branches  each  side  of  and  shorter  than  the  median  stem 
(Fig.  8);  genital  pores  lateral  (marginal),  irregularly  alternate;  terminal 
segments  attain  a  length  of  16  to  25  mm.,  and  a  breadth  of  4  to  7  mm.; 
the  eggs  are  provided  with  a  thick,  dark,  radially  striated  embryophore 
(so-called  shell),  and  measure  30  to  40  by  20  to  30  /i.  Cattle  become 
infected  by  swallowing  the  embryo  with  food  or  water  which  has  become 
contaminated  by  infected  human  feces.  Man  acquires  the  infection  by 
eating  beef,  especially  the  tongue  and  the  muscles  of  mastication,  in- 
fected with  Cysticercus  bovis. 


Fig.  10 


Gra\nd  segment  of  Dibothriocephalus  latus,  showing  the  rosette  uterus  in  the  median  line.     X  6. 

(Leuckart.) 

Taenia  solium,  the  armed  or  pork-measly  tapeworm,  is  most  common  in 
Europe  and  Asia.  Usually  it  does  not  attain  a  length  of  more  than  2 
to  3.5,  sometimes  6  to  8  meters;  the  head  is  armed  with  a  rostellum 
bearing  a  double  row  of  hooks,  of  larger  and  smaller  size,  22  to  32  in 
number;  genital  pores  lateral  (marginal)  irregularly  alternate;  mature 
segments  contain  three  ovaries,  due  to  the  fact  that  the  ovary  on  the  pore- 
side  of  the  segment  is  divided;  the  segments  may  attain  10  to  12  mm.  in 
length  by  5  to  6  mm.  in  breadth;  800  to  900  segments  may  be  present; 
in  gravid  segments,  the  median  uterine  stem  possesses  7  to  15  lateral 
dichotomous  branches  on  each  side  (Fig.  9);  "eggs"  (embryophore)  are 
very  similar  to  those  of  Taenia  saginata,  and  measure  31  to  36  pt  in  dia- 
meter. Hogs  become  infected  by  eating  infected  human  feces;  and  man 
becomes  infected  by  eating  undercooked,  underpickled,  or  undercured 
pork  or  wild  boar  meat,  infected  with  Cysticercus  cellulosse. 

Dibothriocephalus  latus,  the  broad,  or  fish  tapeworm,  is  cosmopolitan 
in  its  geographical  distribution,  but  is  most  common  in  the  vicinity  of 
large  bodies  of  water.  It  attains  a  length  of  2  to  9  or  10  meters,  and  a 
maximum  breadth  of  20  mm.;  it  is  usually  grayish  yellow  to  brownish 
in  color,  and  composed  of  3000  to  4200  segments,  which  are  usually 
broader  than  long,  especially  in  the  anterior  two-thirds  of  the  strobila; 
the  posterior  segments  become  quadrate  or  even  longer  than  broad,  and 


216  METAZOAN  INFECTIONS 

are  especially  characterized  by  the  rosette  spot  (uterus)  in  the  centre 
(Fig.  10);  the  genital  pores  are  ventromedian;  the  eggs  measure  68  to 
71  by  45  p.,  have  a  distinct  operculum,  and  are  laid  during  segmentation. 
Infection  in  man  is  acquired  by  eating  raw  or  underdone  fish,  especially 
pike,  ling  or  turbot,  perch,  and  salmon,  in  the  muscles  and  organs  of 
which  the  larval  stage  of  the  parasite  (a  "  plerocercoid")  may  be  found. 

Hymenolepsis  nana,  the  dwarf  tapeworm,  the  smallest  tapeworm 
known  for  man,  is  more  or  less  cosmopolitan  in  its  geographical  distribu- 
tion; it  is  5  to  45  mm:  long  and  0.5  to  0.9  mm.  in  maximum  breadth,  and 
is  composed  of  100  to  200  segments;  the  rostellum  is  armed;  there  are 
three  testicles  to  each  segment;  the  genital  pores  are  unilateral;  the  eggs 
have  two  distinct  membranes,  the  outer,  30  to  60  /x  in  diameter,  and  the 
inner,  16  to  34  /i  in  diameter,  and  present  at  each  pole  a  more  or  less 
conspicuous  mammillate  projection  provided  with  filamentous  appen- 
dages. The  source  of  infection  in  man  is  not  definitely  known,  but  there 
is  reason  to  believe  that  it  occurs  from  food  infected  by  the  excrement  of 
rats  and  mice  infected  with  Hymenolepsis  nana  fraterna  (Stiles).  Stiles 
believes  that  autoinfection  is  highly  probable. 

S3miptoms. — The  symptoms  of  teniasis  are  quite  variable,  depending 
upon  the  species  of  tapeworm  present,  the  number  of  parasites,  and  the 
age  and  general  and  nervous  condition  of  the  person  infected.  Often  there 
are  no  symptoms,  the  parasite  being  an  accidental  finding  in  the  stools. 
The  appetite  is  variable;  salivation  may  occur;  nausea,  vomiting,  and  a 
feeling  of  faintness  may  be  present.  Abdominal  pains  are  common. 
They  may  be  colicky  or  gastralgic  in  character,  of  varying  intensity,  and 
may  be  referred  to  different  parts  of  the  body.  They  may  be  intermittent, 
and  may  be  increased  by  certain  foods  (herring,  onions,  and  sour  food), 
or  decreased  by  a  diet  of  milk,  eggs,  and  oily  food.  Anemia  is  usually 
not  marked  in  Taenia  solium  infection ;  it  is  more  marked  in  Taenia  sagi- 
nata  infection,  and  still  more  marked  in  Dibothriocephalus  latus  infec- 
tion. Unequal  pupils,  disorders  of  vision,  headache,  tinnitus  aurium, 
itching  and  dryness  of  the  nose,  epistaxis,  and  puruitus  may  be  obser^^ed. 
Emaciation  and  loss  of  strength  sometimes  supervene  in  cases  of  long 
standing. 

Diagnosis. — ^The  diagnosis  is  readily  made  from  finding  segments  of 
the  parasite  in  the  stools,  in  the  absence  of  which  the  disease  at  the  most 
can  be  merely  suspected. 

Treatment. — Prophylaxis  is  of  the  greatest  importance;  all  meat  at 
abattoirs  should  be  carefully  inspected,  and  that  used  for  food  should 
always  be  thoroughly  cooked  (which  kills  the  parasites);  infected  stools 
also  should  be  subject  to  incineration.  With  a  view  to  cause  expulsion 
of  the  tapeworm,  the  patient  for  a  day  or  two  should  have  the  bowels 
thoroughly  evacuated  by  means  of  saline  cathartics;  he  should  eat  very 
little  (mostly  fluids),  and  from  about  six  o'clock  in  the  evening  nothing 
whatever,  this  with  a  view  to  uncover  the  parasite,  permit  ready  access 
thereto  by  the  \'ermifuge,  and  favor  relinquishment  of  the  hold  of 
the  parasite  to  the  mucous  membrane.     In  the  morning  one  may  give 


TENIASIS  217 

1  to  2  drams  (4  to  8  grams)  of  the  oleoresin  or  the  ethereal  extract  of  male 
fern,  and  in  about  two  hours  a  saline  cathartic  (not  castor  oil — which 
leads  to  absorption  of  the  male  fern  and  toxic  symptoms) ;  to  an  emulsion 
of  the  male  fern  one  may  add  2  minims  (0.12  gram)  of  croton  oil.  Or 
one  may  use  a  decoction  of  pomegranate  root:  three  ounces  (100  grams) 
of  the  bark  to  10  ounces  (300  grams)  of  water,  should  be  reduced  to  one 
half  this  amount  by  evaporation,  and  this  taken  in  divided  doses  within 
two  to  three  hours.  The  active  principle  pelletierine  may  be  given  in 
doses  of  6  to  10  grains  (0.4  to  0.6  gram);  it  also  should  be  followed  in  an 
hour  by  a  saline  cathartic.  Decorticated  pumpkin  seed,  kooso,  kamala, 
santonin,  thymol,  etc.,  have  also  been  recommended.  Often  a  large 
part  of  the  worm  is  brought  away,  but  the  head  remains ;  whereupon  the 
worm  continues  to  grow.  Attempts  to  remove  it  should  be  made  again 
at  the  end  of  a  month  or  two,  when  segments  again  appear  in  the  stools. 

Somatic  Teniasis. — Infection  with  the  larval  stage  of  tapeworms 
may  be  due  to:  (1)  Echinococcus  granulosa  (hydatid  disease);  (2) 
Cysticercus  cellulosse,  the  larval  Taenia  solium;  and  (3)  Sparganum 
mansoni  and  Sparganum  proliferum. 

Echinococcus  granulosa  (Taenia  echinococcus)  is  one  of  the  smallest 
tapeworms;  it  is  composed  of  a  head  with  twenty-eight  to  fifty  hooks,  a 
short  neck,  and  three  or  four  segments;  the  first  segment  is  immature, 
the  second  is  mature,  and  the  last  is  gravid  and  composes  about  one  half 
of  the  total  length  (2.5  to  5  mm.)  of  the  worm.  The  larval  stage  is  the 
largest  cestode  known — the  echinococcic  hydatid;  a  subspecies  is  known 
as  Echincoccus  multilocularis.  The  gravid  terminal  segment  of  the 
tapeworm  is  discharged  in  the  feces  of  the  dog,  and  the  egg  gains  access 
to  the  intermediate  host  (sheep,  cattle,  hogs,  man,  etc.)  through  con- 
taminated food  or  drinking  water,  or,  in  the  case  of  man,  possibly  also 
from  hands  soiled  while  petting  dogs.  Upon  arriving  in  the  stomach, 
the  oncosphere  (six-hooked  embryo)  escapes  from  the  shell  and,  by  means 
of  its  hooks,  bores  its  way  to  various  parts  of  the  body,  especially  to  the 
liver.  Here  it  comes  to  rest,  and  increasing  gradually  in  size  it  presents 
a  thick  outer  cuticle  and  an  inner  parenchymatic  layer  surrounding  a 
cavity  containing  fluid.  An  outer  connective  tissue  cyst  is  furnished  by 
the  host.  Brood  capsules  arise  from  the  parenchymatic  layer  and  hang 
into  the  cavity;  heads  form  in  these  brood  capsules.  Daughter  and  even 
granddaughter  cysts  may  form  and  fall  into  the  cavity  of  the  mother 
cyst  (so-called,  endogenous  echinococcus,  common  in  man),  or  these 
daughter  cysts  may  pass  outside  the  mother  cyst  in  the  surrounding  tissue 
(exogenous  echinococcus,  uncommon  in  man).  Iceland  is  the  home  of 
the  echinococcic  infection,  but  it  occurs  in  all  parts  of  the  world,  although 
it  is  rather  rare  in  this  country.  The  infection  is  most  common  in  the 
liver  (56  per  cent.),  in  the  lung  (S  per  cent.),  and  in  the  kidneys  (7  per 
cent.);  but  it  may  occur  in  any  part  of  the  body. 

Symptoms. — The  symptoms  consist  of  a  slowly  growing  tumor,  which 
may  attain  very  large  dimensions.  The  tumor  may  be  more  or  less 
elastic,  and  may  manifest  on  percussion  a  so-called  hydatid  thrill  or 


218  METAZOAN  INFECTIONS 

fremitus.  The  nature  of  the  growth  may  be  revealed  by  detecting 
booklets  in  the  fluid.  Sugar  in  the  fluid  also  is  suggestive.  A  AA'asser- 
mann  and  a  precipitin-reaction  test  have  been  suggested. 

Treatment. — ^The  treatment  is  surgical. 

Cysticercus  celluloscB,  the  larval  form  of  Taenia  solium,  is  an  elliptical 
translucid,  bladder-like  structure,  6  to  12  mm.  long  by  5  to  10  mm.  broad, 
with  a  white  spot  at  its  equator,  due  to  the  invaginated  head.  The 
disorder  to  which  it  gives  rise,  cysticercosis,  is  characterized  by  the 
presence  of  the  parasite  in  the  subcutaneous  tissues,  muscles,  brain, 
spinal  canal,  eye,  heart,  lymph  nodes,  etc.  It  takes  about  three  months 
for  the  parasite  to  develop  from  the  six-hooked  embryo  (onchosphere)  to 
the  bladder  worm  stage,  which  may  live  in  man  as  long  as  twenty  years. 
The  symptoms  vary  with  the  location  and  the  number  of  parasites 
(sometimes  several  thousand).  In  slight  infections  there  may  be  no 
symptoms;  in  severe  infections,  involving  the  brain  there  may  be  head- 
ache, visual  disturbances  (ophthalmoscopic  examination  may  reveal 
the  parasite),  mental  disorders,  dizziness,  paralyses,  convulsions,  etc. 
There  is  no  effective  medical  treatment,  although  some  good  results 
with  male  fern  have  been  reported.  From  accessible  regions  (the  eye, 
for  instance),  the  parasite  may  be  removed  surgically. 

Sparganum  mansoni,  a  larval  bothriocephalide  tapeworm,  has  been 
rarely  found  in  man  (Japanese)  in  the  peritoneal  cavity,  eye,  urethra,  etc. 
Sparganum  proliferum  has  been  reported  once. 


NEMATHELMINTHIASIS. 

(Roundworm  Infection.) 

Uncinariasis  (Ankylostomiasis;  Hookworm  Disease;  Miner's 
Anemia;  Egpytian  Chlorosis). — Uncinariasis  is  common  in  tropical  and 
subtropical  countries.  It  is  estimated  that  90  per  cent,  of  the  rural  popu- 
lation of  Florida,  and  30  to  80  per  cent,  of  the  miners  of  Germany  are 
infected;  but  the  disorder  occurs  also  in  miners  and  others  who  are  close 
in  contact  with  the  soil  in  more  temperate  zones.  There  are  two  para- 
sites: (1)  Necator  americanus  (Uncinaria  americana,  Stiles),  the  New 
World  hookworm,  a  cylindrical  worm,  5  to  11  mm.  long,  and  possessed 
of  a  dorsal  and  a  ventral  pair  of  lips  at  the  mouth,  a  prominent  dorso- 
median  buccal  tooth,  and  four  buccal  lancets;  in  the  male,  the  dorsal 
ray  of  the  bursa  divides  at  the  base  and  each  branch  possesses  two  tips; 
in  the  female  the  vulva  is  the  anterior  half  of  the  body;  the  eggs  are  thin- 
shelled,  64  to  72  fx  long,  by  36  to  40  /i  broad;  they  are  oval  with  some- 
what bluntly  rounded  poles.  (2)  Ankylostoma  duodenale  (Uncinaria 
duodenalis,  Dubini),  the  Old  World  hookworm,  is  8  to  18  mm.  in  length 
and  possesses  in  its  mouth  two  pairs  of  strong,  curved,  ventral  teeth,  and 
one  pair  of  knob-like  dorsal  teeth;  the  dorsomedian  tooth  of  the 
buccal  capsule  is  nil  or  practically  so;  a  pair  of  ventral  lancets  is 
present  in  the  buccal  cavity;  in  the  male,  the  dorsal  ray  of  the  l)ursa  is 


NEMATHELMINTHIASIS  219 

divided  two-thirds  its  length  from  the  base,  and  each  branch  is  subdivided 
into  three  tips;  in  the  female  the  vulva  is  in  the  caudal  half  of  the  body; 
the  eggs  measure  52  to  61  /x  in  length  and  42  to  38  /j.  in  breadth;  they  are 
oval  and  have  bluntly  rounded  poles.  Both  parasites  inhabit  the  small 
intestine,  especially  the  jejunum  and  ileum,  but  also  the  duodenum  and 
occasionally  the  stomach.  Infection  may  occur  (1)  through  the  skin, 
whence  the  larvae  reach  the  circulatory  system  and  eventually  gain  the 
small  intestine;  and  (2)  by  way  of  the  digestive  tract  with  contaminated 
food  or  water  or  dirt  on  the  hands.  The  eggs  are  oviposited  in  the 
intestine  of  the  patient,  but  do  not  develop  until  after  they  escape  with 
the  feces.  The  conspicuous  lesions  consist  of  general  anemia,  deficient 
coagulability  of  the  blood  (due  to  a  toxin  produced  by  the  hookworm), 
and  catarrh  of  the  intestinal  tract. 

Sjmaptoms. — The  symptoms  vary  with  the  severity  of  the  infection. 
Ova  may  be  present  in  the  stools  without  noteworthy  symptoms.  The 
chief  manifestations  consist  of  gastro-intestinal  irritability,  such  as  poor 
appetite,  nausea,  vomiting,  epigastric  distress,  flatulence,  etc.;  slight 
fever;  and  in  advanced  cases  secondary  anemia,  with  high  leukocytosis 
and  eosinophilia.  The  patient  tires  readily  and  complains  of  lassitude. 
The  liver  and  spleen  may  become  enlarged;  the  heart  may  become  weak 
and  dilated,  and  oedema  may  develop.  The  diagnosis  is  readily  made 
by  finding  the  worms  or  the  ova  in  the  stools.  The  outlook  is  favorable 
in  early  cases,  but  the  mortality  is  about  30  per  cent. 

Treatment. — Efforts  should  be  made  to  minimize  and  prevent  the 
infection  by  insisting  upon  the  wearing  of  shoes  in  infected  regions, 
examining  the  stools  of  persons  in  infected  regions,  and  carefully  destroy- 
ing contaminated  stools,  and  disinfecting  privies.  The  patient  should 
be  put  on  a  fluid  diet  for  a  day;  in  the  evening  he  should  take  a  saline 
cathartic,  but  no  food.  In  the  morning  an  adult  should  be  given  30  to 
45  grains  (2  to  3  grams)  of  thymol  (in  cachets  with  an  equal  amount  of 
milk  sugar) ,  and  at  the  end  of  three  or  four  hours  (earlier  if  symptoms 
of  intoxication  develop),  he  should  take  another. saline  cathartic.  This 
may  be  repeated  at  the  end  of  a  week  if  worms  or  ova  are  still  present. 
Beta-naphthol  and  male  fern  also  have  been  recommended.  The  anemia 
requires  the  use  of  iron. 

Strongyloidosis. — Infection  with  Strongyloides  stercoralis  is  common 
in  tropical  and  subtropical  zones  (75  per  cent,  of  the  anemias  of  India); 
but  it  occurs  also  elsewhere,  including  the  United  States.  Infection 
may  occur  through  the  skin,  or  by  means  of  contaminated  food  or  water. 
The  parasite  apparently  may  be  harmless,  or  it  may  set  up  an  intestinal 
catarrh  and  diarrh(x?a.  The  diagnosis  may  be  made  by  finding  the  ova 
in  the  stools.  Thymol,  as  in  uncinariasis,  is  the  best  treatment,  but  it  is 
not  always  efficacious,  since  the  parasite  may  burrow  into  the  tissues. 

Ascariasis  (Eelworm  Infection). — Infection  with  Ascaris  lumbri- 
coides  (Linnteus)  is  widespread,  but  is  most  common  in  warm  climates. 
It  may  occur  at  any  age,  but  is  most  frerpient  in  children.  Several  or 
many   worms   may  be   j)n'S(Mit    in   the   one  case.      The    male  parasite 


220  MeTA^OAN  INPECTIONS 

measures  15  to  17  even  25  cm.  in  length  and  about  3  mm.  in  diameter;  the 
female,  20  to  40  cm.  in  length  and  5  cm.  in  diameter,  and  is  oviparous; 
they  are  grayish  to  reddish  yellow  in  color;  the  anterior  end  is  provided 
with  three  lips;  the  eggs  are  50  to  75  by  36  to  55  n,  unsegmented  when 
oviposited,  and  provided  with  a  thick  mamillate  covering,  frequently 
tinged  yellow  when  found  in  the  feces.  The  parasites  live  in  the  small 
intestine.  Development  is  direct,  without  an  intermediate  host.  Infec- 
tion is  acquired  by  contaminated  drink,  fruit,  hands,  etc. ;  the  fly  may 
be  an  active  agent  in  transmitting  the  infection.  The  embryo  being 
swallowed  develops  directly  into  the  adult  worm.  Symptoms  may  be 
entirely  in  abeyance,  or  there  may  be  various  ill-defined  gastro-intestinal 
manifestations,  or  nervous  symptoms  in  children,  and  eosinophilia.  The 
disorder,  of  course,  is  recognized  when  a  worm  is  passed  by  the  rectum 
or  is  vomited.  In  other  cases  the  ova  may  be  found  in  the  stools.  The 
best  treatment  consists  of  the  use  of  santonin,  ^  to  1  grain  (0.03  to.  0650 
gram)  to  a  child,  2  to  3  grains  (0.13  to  0.20  gram)  to  an  adult,  with  or 
followed  by  calomel,  and  later  a  saline  cathartic.  This  may  be  repeated 
on  the  third  and  the  fifth  day.  Thymol  and  oil  of  chenopodium  also 
have  been  recommended. 

Oxyuriasis  (Pinworm  Infection;  Threadworm  Infection;  Seatworm 
Infection). — Infection  with  Oxyuris  (Oxyurias)  vermicularis  (Linneeus) 
is  widespread,  and  very  common  in  children  and  women.  Few  or  many 
worms  may  be  present  in  the  one  individual.  The  parasite  is  small, 
white,  and  round,  and  measures  3  to  5  mm.  (male)  to  10  mm.  (female) 
in  length  and  0.16  to  0.6  mm.  in  diameter;  the  male  has  but  one  spicule; 
the  female  is  provided  with  a  relatively  long,  sharply  pointed  tail;  the 
vulva  is  in  the  latter  half  of  the  anterior  of  the  body;  two  uteri  are  present 
filled  with  numerous  eggs;  these  eggs  are  50  to  52  by  16  to  24  p.,  and  have 
a  thin  shell  and  a  dorsal  surface  much  more  convex  than  the  ventral. 
The  fertilized  females  wander  to  the  cecum,  and  later  when  gravid  to 
the  colon.  Infection  is  acquired  by  auto-infection  (infecting  the  finger 
nails  by  scratching  the  anus  to  relieve  irritation  occasioned  by  worms 
wandering  from  the  rectum — the  worm  is  thus  often  crushed);  from  a 
bed-fellow,  or  a  nurse,  or  the  bedclothes;  or  from  infected  food  or  drink. 
Flies  possibly  transmit  the  infection  to  food,  etc.  Development  is  direct 
— ^without  an  intermediate  host.  Symptoms  may  be  entirely  in  abeyance 
— in  slight  infections.  In  severe  or  heavy  infections,  gastro-intestinal 
symptoms  are  common,  especially  foul  breath,  abdominal  distress, 
nausea,  vomiting,  diarrhoea,  etc.,  as  well  as  nervous  symptoms,  such  as 
headache,  restlessness,  etc.  The  anus  is  often  markedly  irritated, 
and  itches  and  burns,  from  out-wandering  of  the  female  parasite; 
these  may  invade  the  vagina,  even  the  uterus  and  the  peritoneal  cavity. 
The  diagnosis  is  readily  made  from  detecting  the  worms  in  the  stools  or 
about  the  anus,  or  from  finding  the  ova  in  the  stools.  The  best  treatment 
consists  of  santonin  and  calomel,  as  mentioned  under  ascariasis.  Thy- 
mol, beta-naphthol,  and  a  bitter  infusion,  such  as  gentian,  have  also  been 
recommended.     In  addition,  with  a  view  to  rid  the  rectum  of  worms,  one 


NEMATHELMINTHIASIS  '         221 

should  use  daily,  for  a  week  or  ten  days,  enemas  of  an  infusion  of  quassia, 
or  turpentine  and  water,  or  saline  solution,  etc.  The  itching  about  the 
anus  may  be  relieved  by  belladonna  or  zinc  oxide  ointment. 

Trichocephaliasis  (Whipworm  Infection). — Infection  with  Trichuris 
trichiuria  (Linnseus)  is  widespread,  and  occurs  in  man,  apes,  etc. 
The  parasite  has  the  general  form  of  a  whip;  the  male  measures  40  to 
45  mm.  and  the  female  45  to  50  mm.  in  length;  the  eggs  measure  5Q  to 
54  by  21  to  23  p.,  and  are  of  a  yellowish  or  dark  brown  color,  with  un- 
segmented  protoplasm  and  a  peculiar  light  spot  at  each  pole  resembling- 
apertures.  The  parasites  inhabit  the  cecum,  but  may  be  found  in  the 
appendix,  colon,  and  ileum.  Symptoms,  as  a  rule,  are  entirely  in  abey- 
ance. In  some  cases  a  more  or  less  well-marked  secondary  anemia 
results.  Appendicitis  is  said  to  have  been  provoked  by  the  worms, 
which  also  have  been  credited  with  transporting  infecting  bacteria 
(typhoid  bacilli).  The  diagnosis  is  readily  made  by  finding  the  worms 
or  the  eggs  in  the  feces.  The  treatment  is  unsatisfactory:  thymol  and 
male  fern  have  been  recommended,  as  well  as  benzine  internally  and 
irrigations  of  the  colon  with  benzine,  1  dram  (4  c.c.)  to  a  quart  (liter) 
of  warm  water. 

Acanthocephaliasis. — Infection  with  Acanthocephali  (thorn-headed 
worms)  is  of  very  little  importance  in  human  medicine. 

Trichinosis  (Trichiniasis) . — Infection  with  Trichinella  spiralis  is 
widespread,  and  is  found  in  man,  hogs,  wild  boars,  rats,  dogs,  and  cats. 
Stiles  states  that  three  stages  of  the  parasite  should  be  clearly  held  in 
mind:  (a)  The  adults  live  in  the  duodenum  and  jejunum;  the  males 
measure  1.4  to  1.6  mm.  in  length  by  40 /x  in  diameter,  while  the  females 
are  3  to  4  mm.  long  by  60  ix  thick;  they  are  circular  on  cross  section,  and 
appear  as  minute  thread-like  objects;  the  oesophagis  is  supported  by  a 
single  row  of  cells  known  as  the  cell-body;  the  male  is  without  spicules; 
the  female  is  viviparous,  the  vulva  being  situated  about  one-fifth  the 
length  of  the  body  from  the  mouth.  The  males  die  shortly  after  copula- 
tion. The  females  may  remain  for  a  few  weeks  in  the  lumen  of  the  intes- 
tine, or  they  bore  into  the  lymphatic  spaces  of  the  intestine  where  they 
live  about  five  to  seven  weeks  and  deposit  their  numerous  young,  about 
1500  or  more  per  female;  (&)  embryos,  which  measure  about  90  to  100  // 
in  length  by  6  //  in  breadth;  these  wander,  either  with  the  lymph  or  with 
the  blood,  less  frequently  actively,  to  the  striated  muscles;  they  begin 
to  reach  the  muscles  about  the  tenth  day  after  infection;  they  enter  the 
muscle  fibers  and  there  develop  into  (c)  encysted  larvae;  these  cysts  vary 
somewhat  in  size,  but  are  usually  about  400  by  250  p..  The  encysted 
larvae  may  remain  alive  in  the  muscles  for  years,  cases  being  reported 
for  as  long  periods  as  twenty  to  thirty-one  years.  The  encysted  worm 
(the  "fleshworm")  is  the  infecting  stage,  found  in  the  hog;  upon  being 
swallowed  in  raw  or  rare  pork,  the  cyst  is  destroyed,  the  larvae  pass  from 
the  stomach  to  the  small  intestine  and  develop  within  about  two  days 
or  less  to  the  adults;  the  latter  copulate  and  may  have  embryos  in  the 
uterus  within  less  than  a  week  after  infection.     Man  becomes  infected 


222  METAZOAN  INFECTIONS 

from  eating  pork;  hogs,  from  eating  uncooked  swill  containing  scraps 
of  pork,  or  swine  offal  at  country  slaughter  houses,  or  rats;  and  rats, 
from  eating  one  another,  scraps  of  pork  in  houses  or  meat-shops,  and 
swine  offal  at  country  slaughter  houses. 

Symptoms. — ^The  symptoms  may  be  slight  and  escape  observation. 
Typical  cases  present  Rupprecht's  three  more  or  less  well  defined  periods, 
corresponding  to  the  three  stages  of  the  parasite  and  their  respective 
location:  (1)  The  period  of  ingression,  marked  by  predominance  of 
gastro-intestinal  symptoms — anorexia,  nausea,  vomiting,  diarrhoea 
(usually  profuse),  sometimes  succeeded  by  constipation,  recurrent 
abdominal  pains,  vague  pains  in  the  muscles,  a  primary  and  transient 
oedema  of  the  eyelids  (about  the  eighth  day),  etc.  (2)  The  period  of 
digression,  marked  often  by  rather  abrupt  onset  about  the  ninth  to  the 
fourteenth  day  (rarely  later),  fever,  pain  and  tenderness  of  the  muscles 
(especially  the  biceps  and  the  gastrocnemius),  which  become  firm  and 
resistent,  especially  on  motion;  this,  as  a  rule,  is  exceedingly  painful, 
and  may  inhibit  mastication,  phonation,  the  movements  of  the  eyes, 
respiration;  indeed,  dyspnoea  may  become  extreme  and  be  associated 
with  more  or  less  violent  asthmatic  paroxysm.  There  is  a  marked 
leukocytosis  (upw^ard  of  30,000)  and  a  notable  esosinophilia  (often  50 
per  cent,  of  the  leukocytes).  (3)  The  period  of  regression,  marked  by 
exaggeration  of  all  the  symptoms;  a  second  oedema,  especially  of  the 
head  ("big  head"),  may  develop;  anemia,  emaciation,  and  a  cachexia 
may  supervene;  or  the  parasites  become  encysted,  the  symptoms  lessen, 
and  the  patient  recovers. 

Diagnosis. — ^The  diagnosis  may  often  be  suspected  from  the  fever, 
transient  oedema  of  the  eyelids,  and  sore  muscles.  These  with  marked 
eosinophilia  make  the  evidence  almost  if  not  quite  conclusive.  In  addi- 
tion one  should  search  for  a  source  of  infection,  examine  suspected  pork 
for  encysted  larvse;  and  examine  the  patient's  stools  and  blood  for  the 
adult  worms,  and  a  piece  of  excised  muscle  (gastrocnemius  or  deltoid) 
for  the  encysted  larvae. 

Prognosis. — ^The  outlook  depends  upon  the  severity  of  the  infection. 
In  general  it  is  good,  better  in  children  than  in  adults.  The  mortality 
does  not  average  over  5  per  cent.,  although  in  some  local  epidemics  it 
may  be  very  high. 

Treatment. — ^The  infection  may  be  prevented  by  thorough  inspection 
of  pork  at  abattoirs,  and  by  thoroughly  curing  and  cooking  all  pork 
before  it  is  eaten.  If  the  infection  is  discovered  or  suspected  early,  the 
patient's  gastro-intestinal  tract  should  be  thoroughly  evacuated— by 
gastric  lavage,  and  by  calomel  and  saline  cathartics.  Perhaps  thymol 
and  beta-naphthol  also  might  prove  of  service.  Glycerin  in  large 
amounts  has  been  recommended,  in  the  hope  that  on  account  of  its 
hygroscopic  properties  it  may  destroy  the  worms.  Otherwise  the  treat- 
ment is  symptomatic:  hot  applications  or  baths  and  morphine  to  relieve 
the  pain,  whiskey  for  its  general  supportive  effect,  etc.  There  is  no 
known  remedy  that  affects  the  parasite  in  the  muscles. 


NEM  ATH  ELMINTHI ASIS  223 

Dracunculosis  (Dracontiasis ;  Guineaworm  Infection;  Medina- 
worm  Infection). — Infection  with  Dracunculus  medinensis  (Linnseus)  is 
distinctly  an  Old  World  disorder,  but  occasional  cases  are  observed  in 
this  country.  The  parasite  is  whitish  or  yellowish,  50  to  80  or  more 
cm.  in  length,  and  0.5  to  1.7  mm.  in  diameter;  its  anterior  end  is  bluntly 
rounded,  with  a  small  terminal  mouth  and  six  papillae.  The  uterus  is 
enormously  developed  and  filled  with  sharp-tailed  embryos,  0.5  to  0.75 
mm.  long  by  0.17  mm.  in  maximum  diameter.  Infection  is  probably 
acquired  through  the  drinking  water;  possibly  by  way  of  the  skin.  After 
copulation  the  male  probably  dies,  and  the  female  wanders  to  the  sub- 
cutaneous tissues.  The  symptoms  consist  of  the  production,  by  the 
gravid  parasite,  of  a  small,  painful,  blister-like  swelling,  particularly  on 
the  feet  and  ankles;  this  ruptures,  leaving  an  ulcer,  at  the  base  of  which 
the  head  of  the  parasite  may  be  seen ;  chills,  fever,  nausea,  and  vomiting 
may  occur.  Healing  does  not  ensue  until  the  parasite  has  been  expelled. 
The  treatment  consists  of  the  injection  into  the  ulcer  of  mercuric 
bichloride  (1  to  1000)  or  excision  of  the  parasite. 

Filariasis. — Many  filarial  infections  have  been  reported  in  man,  but 
major  interest  centres  in  Filaria  bancrofti  (Filaria  nocturna,  Manson). 
The  infection  occurs  in  tropical  and  subtropical  countries,  but  isolated 
cases  have  been  observed  in  many  regions  of  the  temperate  zone.  The 
adult  parasite,  which  occurs  only  in  man,  is  a  whitish  or  brownish, 
transversely  striated  worm,  44  to  95  mm.  long  by  0.1  to  0.26  mm.  in 
diameter;  the  male  has  two  spicules,  0.2  and  0.6  mm.  long,  an  anogenital 
pore,  138  mm.  from  the  tail;  renal  papillae  are  uncertain,  but  apparently 
there  are  three  pairs  of  postanal  papillae;  the  vulva  of  the  female  is 
0.66  to  1.2  mm.  from  the  head,  the  anus  225  fx  from  the  tip  of  the  tail; 
viviparous.  The  larvae,  which  occur  in  a  number  of  mosquitoes  (Ano- 
pheles, Culex,  Panoplites),  are  300  to  340  /x  long  by  6.6  to  8.5  or  11  ^  in 
diameter,  and  are  provided  with  a  sheath  and  sharply  pointed  tail. 
They  are  found  in  the  circulating  blood,  and  they  show  a  more  or  less 
marked  periodicity  in  that  they  are  much  more  numerous  during  the 
night,  but  if  sleep  is  reversed  to  the  day-time,  the  periodicity  also  is 
reversed.  Mosquitoes,  while  biting  patients,  swallow  these  larvae,  which 
then  undergo  development  in  the  muscles,  and  finally,  after  fourteen  to 
seventeen  days,  or  by  lower  temperature,  up  to  thirty-five  to  forty-one 
days  from  the  time  of  infection,  the  worms  reach  a  stage  in  which  they 
are  transmitted  to  man  during  the  bite  of  the  mosquito.  Manson  states 
that  the  organism  may  produce  abscess,  lymphangitis,  varicose  groin- 
glands,  varicose  axillary  glands,  lymph  scrotum,  cutaneous  and  deep 
lymphatic  varix,  orchitis,  chyluria,  elephantiasis  of  the  leg,  scrotum, 
vulva,  arm,  mamma,  etc.,  chylous  dropsy  of  the  tunica  vaginalis,  chylous 
ascites,  and  chylous  diarrhoea.  The  blood  may  reveal  a  lymphocytosis 
(up  to  40  per  cent.)  and  an  eosinophilia  (up  to  18  per  cent.).  The 
diagnosis  may  be  made  by  finding  the  larval  filaria  in  the  blood,  urine, 
or  chylous  accumulations.  Preventive  measures  comprise  killing  and 
avoiding  mosquitoes.     The  older  view  that  the  infection  was  acquired 


224  METAZOAX  IXFECTIONS 

from  the  drinking  water  suggested  its  being  boiled,  but  this  view  has  been 
abandoned.  As  far  as  is  known,  medicinal  treaiment  is  without  much 
avail,  although  good  results  are  said  to  have  attended  the  use  of  thymol, 
ichthyol,  etc.  The  patient  should  receive  supportive  treatment,  and  it  is 
perhaps  wise  to  limit  the  fluid  intake  and  give  purgatives  from  time  to 
time.     Surgical  intervention  is  indicated  in  some  cases. 

Filaria  loa  (diurna,  jManson)  is  a  small  threadworm  that  circulates  in 
the  blood  during  the  day,  inhabits  the  connective  tissues  throughout  the 
body,  and  is  thought  to  be  the  cause  of  so-called  Calabar  swellings. 

Filaria  perstans,  of  which  only  the  larvee  are  known,  is  smaller  than 
Filaria  loa,  and  is  said  by  JManson  to  be  the  cause  of  craw-craw,  a  papulo- 
pustular  eruption  of  the  West  Coast  of  Africa;  but  like  other  filarise  it 
frequently  is  found  in  the  blood  in  the  absence  of  noteworthy  symptoms. 

Anguillula  aceti  (the  vinegar-eel)  and  Leptodera  pellio  have  been 
found  in  the  human  bladder  and  vagina;  and  Dicotophyme  renale,  the 
giant  strongyle,  or  canine  kidney-worm,  has  occasionally  been  found  in 
man. 

AGARIASIS. 

{Acarine  Infections.) 

Ixodiasis  Tick  (Infection). — ^There  are  two  families  of  ticks 
(Ixodoidse) — Argasidae,  in  which  the  head  is  subterminal  in  the  adult; 
and  Izodidee,  in  which  the  head  is  terminal  in  the  adult.  The  impor- 
tant species  are  Ornithodorus  moubata,  the  agent  active  in  transmitting 
Spirochseta  duttoni,  the  cause  of  African  tick  fever  (relapsing  fever); 
Dermacentor  venustus.  Banks  (andersoni,  Stiles),  and  Dermacentor 
modestus  (Banks),  the  agent  active  in  transmitting  the  cause  of  Rocky 
^Mountain  spotted  fever,  or  tick  fever  (which  should  not  be  confounded 
with  the  African  tick  fever);  and  Boophilus  annulatus,  the  agent  active 
in  transmitting  the  cause  of  Texas  fever.  These  and  other  ticks  cling 
tenaciously  to  the  skin,  but  on  covering  them  with  oil  or  vaseline  (thus 
closing  their  breathing  spaces)  they  release  their  hold  and  drop  off. 

Sorcoptic  Acariasis  (Sarcoptic  Itch). — Infection  with  Sarcoptes 
scabiei  is  universal,  involving  man  and  animals.  The  parasite, 
as  it  occurs  in  man,  is  whitish  yellow,  round  to  oval,  with  transverse 
rows  of  small  spines,  and  a  number  of  longer  bristles;  the  male  measures 
0.2  to  0.3  by  0.145  to  0.190  mm.,  and  the  female,  0.33  to  0.45  by  0.25  to 
0.35  mm.;  they  bore  irregular  galleries,  0.5  mm.  to  4  to  5  cm.  or  more 
ia  length,  in  the  epidermis,  especially  on  portions  of  the  body  where  the 
skin  is  thin  and  soft,  as  on  the  flexor  surface  of  the  carpus,  between  the 
fingers,  in  the  groins,  at  the  knee,  on  the  penis,  breast,  etc.,  and  at  points 
subject  to  pressure,  as  at  the  waistband.  The  female  is  found  at  the 
blind  end  of  the  gallery;  she  deposits  her  eggs  (15  to  50  in  nuniber)  and 
feces  as  she  progresses.  The  eggs  measure  140  a  and  hatch  in  four  to 
eight  days;  the  parasite  becomes  mature  twenty-eight  days  after  birth. 
The  male  dies  shortly  after  copulation.     Infection  takes  plac^  directly 


PARASITIC  INSECTS  225 

from  person  to  person  through  prolonged  contact,  indirectly  through 
bedclothes,  towels,  clothes,  etc.,  or  by  direct  contact  in  handling  animals. 
The  main  symptoms  consist  of  itching,  increased  by  heat,  exercise,  and  rest 
in  bed ;  and  a  papular,  vesicular,  or  pustular  eruption,  the  result  partly  of 
scratching  and  partly  of  the  mechanical  and  chemical  irritation  provoked 
by  the  parasite.  The  diagnosis  is  readily  made  by  detecting  the  galleries 
with  the  female  at  the  end.  The  treatment  consists  of  thorough  cleansing 
of  the  affected  part  with  green  soap  and  hot  water;  and  thorough  inunc- 
tion with  mercurial  ointment,  sulphur  ointment,  or  a  compound  naphthol 
ointment  (naphthol,  15;  prepared  chalk,  10;  green  soap,  50;  lard,  100; 
Kaposi).  After  the  ointment  has  been  allowed  to  act  for  four  or  five 
hours,  the  patient  should  take  a  warm  bath  and  put  on  clean  non- 
infected  clothes. 

Other  mites  may  cause  various  disorders,  such  as  Demodex  foUicu- 
lorum,  which,  invading  the  hair  follicles,  may  set  up  nodular  formations; 
Leptus  americanus  (irritans,  autumnalis),  the  harvest  mite,  known  also 
as  the  red  bug,  the  harvest  bug,  or  the  jigger,  which,  burrowing  into  the 
skin  of  workers  in  the  field  in  summer,  may  set  up  considerable  irritation, 
and  Pediculoides  ventricosus,  the  cause  of  grain  or  straw-bed  itch. 


PARASITIC  INSECTS. 

Phthiriasis  (Pediculosis). — There  are  three  varieties  of  pediculidse — 
Pediculus  humanus  (capitis),  the  head  louse;  Pediculus  corporis  (vesti- 
menti),  the  body  louse;  and  Phthirius  pubis,  the  pubic  louse.  They 
are  found  only  in  persons  of  uncleanly  habits.  They  cause  irritation 
and  itching  and  eczematous  and  pustular  eruptions.  The  treatment 
consists  of  cutting  the  hair  and  saturating  the  infected  parts  with  kero- 
sene, or  with  carbolic  lotions  (2  per  cent.),  which  are  more  destructive  to 
the  eggs  (nits).  Mercurial  ointment  is  serviceable  in  the  event  of  pubic 
infection. 

Fleas. —  Sarcopsylla  penetrans  (the  burrowing  flea,  jigger  flea, 
chigger)  may  burrow  into  the  skin  of  the  feet,  but  also  elsewhere,  and  set 
up  considerable  irritation,  suppuration,  and  ulceration.  It  should  be 
taken  out  with  a  sharp  knife;  chloroform  or  mercurial  ointment  may  be 
applied.  Of  jumping  fleas,  there  are  two  that  may  attack  man — Pulex 
irritans,  the  common  or  house  flea,  and  Ctenocephalus  canis,  the  cat  and 
(log  flea.  These  may  act  as  ectoparasites,  biting  man;  as  an  intermediate 
host  for  certain  tapeworms;  or  as  disseminators  of  plague.  The  house 
should  be  rid  of  fleas  by  sulphur  fumigation,  sprinkling  about  pyrethrinn 
powder,  or  washing  the  floors  with  benzine  or  hot  soapsuds. 

Bed-bugs. — Two  types  of  bed-bugs  infect  dwellings — Cimex  lectu- 
larius,  the  common  bed-bug,  and  Conorhinus  sanguisuga,  the  Mexican 
bed-bug.  Stiles  recommends  fumigation  with  flowers  of  sulphur,  2 
pounds  to  1000  cubic  feet  of  space,  as  the  best  method  of  ridding  a  house 
of  these  pests. 
15 


226  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

Myiasis. — Compsomyia  macellaria  may  deposit  its  eggs  in  wounds. 
The  larva,  known  as  the  screw-worm,  issues  within  a  few  hours,  and  may 
burrow  into  the  tissues.  Intestinal  infection  also  may  occur.  Many 
other  dipterous  insects,  mosquitoes,  flies,  beetles,  etc.,  are  of  much  and 
increasing  medical  importance,  not  so  much  because  of  the  disorders 
that  they  may  engender  per  se,  but  on  account  of  the  divers  sorts  of  infec- 
tion that  they  transmit.  They  are  of  special  importance  in  tropical  and 
subtropical  countries,  where  the  control  of  many  of  the  known  and  un- 
known or  ill-understood  infections  unquestionably  depends  upon  a  study 
of  the  life  habits  and  other  biological  characteristics  of  various  sorts  of 
insects  that  undoubtedly  act  as  transmitting  agents. 


INFECTIONS  OF  UNKNOWN  OE  DOUBTFUL 

ETIOLOGY. 


VARIOLA. 

{Smallpox;  Varioloid.) 

Variola  is  an  acute,  specific,  infectious,  and  highly  contagious  disease, 
characterized  by  high  fever,  usually  of  sudden  onset  and  of  characteristic 
course,  and  an  eruption  consisting  successively  of  macule,  papule,  vesicle, 
pustule,  and  crust. 

Etiology. — Variola  occurs  at  all  ages  (in  the  case  of  pregnant  women 
sometimes  implicating  the  foetus),  and  affects  all  races,  and  the  sexes 
indiscriminately.  It  usually  prevails  epidemically,  especially  during 
the  late  fall,  the  winter,  and  the  spring;  but  sporadic  cases  are  often 
encountered.  One  attack  usually  confers  immunity,  but  undoubted  cases 
of  second  and  even  third  attacks  have  been  reported.  Some  few  persons 
are  apparently  naturally  immune. 

The  exciting  cause  of  the  disease  has  not  been  isolated  with  certainty 
—although  a  number  of  supposedly  causative  microorganisms  have  been 
described.  Recently  some  interest  has  been  shown  in  the  supposed 
etiological  significance  of  a  protozoon,  Cytoryctes  variolse,  described 
originally  by  Guarnieri,  later  studied  by  Wasielewski,  and  more  recently 
investigated  by  Councilman,  Magrath,  and  Brinckerhoff — who,  to- 
gether with  Calkins,  describe  what  they  believe  to  be  its  life  history. 
The  streptococcus  may  be  isolated  from  most  of  the  lesions  (primary, 
or  essential,  and  complicating),  and  seems  to  bear  some  relation  to  at 
least  certain  phases  of  the  disease.  The  contagium  is  present  in  the  blood 
of  the  patient,  the  emanations  and  exhalations,  the  secretions  and  ex- 
cretions, and  especially  the  dried  crusts.  The  disease  is  highly  con- 
tagious throughout  its  entire  course  (possibly  even  before  the  occurrence 
of  the  eruption).     Practically  all  persons  exposed  are  attacked,  unless 


VARIOLA  227 

they  are  immune  naturally  (very  rare),  by  a  previous  attack,  or  by 
vaccination.  Infection  is  transmitted  by  direct  contact  or  proximity, 
by  a  third  person,  or  by  fomites,  especially  clothes  and  house  furnishings, 
to  which  the  contagium  clings  with  extreme  pertinacity,  and  for  a  long 
time.  Recrudescence  of  the  disease  from  year  to  year  in  places  where  it 
has  been  for  a  time  endemic  can  almost  always  be  attributed  to  such 
fomites,  or  to  an  ill-defined  case.  The  question  of  the  aerial  convection 
of  the  infection  is  still  debated,  though  certain  facts  speak  in  favor  of  it. 
An  initial  mild  case,  or  even  varioloid,  may  be  the  starting  point  of  a 
virulent  and  widespread  epidemic.     Infection  is  acquired  by  inhalation. 

Pathology. — According  to  Councilman,  Magrath,  and  Brinckerhoff,  the 
specific  lesion  of  variola  (which  is  limited  to  the  skin  and  the  mucous  mem- 
brane of  the  soft  palate,  pharynx,  and  oesophagus)  consists  of  a  focal, 
vacuolar  degeneration  of  the  stratified  epithelium  accompanied  by  serous 
exudation  and  the  formation  of  a  reticulum — which  when  fully  developed 
constitute  the  characteristic  muitilocular  pock,  or  pustule.  In  the  skin 
the  lesions  begin  with  degeneration  of  the  cells  of  the  lower  layers  of  the 
epidermis,  accompanied  by  exudation,  at  first  serous,  later  more  or  less 
cellular,  the  products  of  which  are  contained  within  the  spaces  of  a  reticu- 
lum formed  by  the  degenerated  cells.  The  exudate  increases  in  amount 
and  the  spaces  of  the  reticulum  enlarge  until  its  fibers  finally  rupture, 
and  the  lesion  becomes  a  filled-out  pustule.  This  development  may 
take  place  wholly  within  the  epidermis,  and  the  fluid  contents  of  the  pock 
be  separated  from  the  corium  by  comparatively  intact  cells ;  or  the  corium 
may  form  the  bottom  of  the  pustule,  in  which  case  there  is  usually  necro- 
sis of  the  papillary  border.  (Edema,  cellular  infiltration,  and  hemor- 
rhage of  the  corium  may  occur.  The  subsidence  and  repair  of  the  lesion 
are  accomplished  by  the  removal  of  the  fluid  portion  of  the  exudate 
by  absorption  and  drying,  and  by  the  regeneration  of  the  epidermis, 
in  the  course  of  which  the  residual  mass  of  degenerated  epithelial  cells, 
leukocytes,  and  debris,  enclosed  between  two  layers  of  horny  epidermis, 
the  old  and  the  newly  formed,  is  exfoliated.  The  lesions  of  the  mucous 
membrane  are  proportionate  in  extent  and  severity  to  those  of  the  skin, 
but  on  account  of  the  absence  of  a  horny  layer  of  epithelium  the  degener- 
ated epithelial  cells  are  cast  off,  and  the  vesicle  within  the  epidermis 
is  rarely  seen,  the  pustule  never.  According  to  Councilman,  Magrath, 
and  Brinckerhoff  the  specific  parasite  of  variola  is  found  chiefly  in 
the  cells  of  the  rete  mucosum — its  younger  or  cytoplasmic  form  in  the 
protoplasm  of  the  epithelial  cells  of  early  lesions  and  of  such  of  the  older 
lesions  as  are  extending;  its  intranuclear  form,  for  the  most  part,  in 
more  advanced  lesions.  According  to  the  same  authors,  a  constant,  well- 
marked,  and  well-nigh  characteristic  lesion  consists  of  proliferation  within 
the  hematopoietic  organs,  giving  rise  in  the  spleen,  the  lymph  nodes,  and 
the  bone  marrow  to  the  formation  of  mononuclear,  basophilic  cells  (which 
enter  the  circulation  in  large  numbers),  and  in  the  lymph  nodes  and  the 
marrow  to  phagocytic  endothelial  cells.  Focal  and  interstitial  cellular 
infiltration    with    mononuclear    basophilic    cells    occurs    constandy    in 


228  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

the  testicle,  and  usually  in  the  kidney,  the  liver,  and  the  adrenal  glands; 
in  the  testicle  (in  consequence  of  pressure  and  thrombosis)  it  causes 
focal  nercosis — apparently  specific  to  variola.  Focal  degeneration, 
toxic  rather  than  anemic,  and  leading  to  necrosis,  at  times  with  hemor- 
rhage, and  accompanied  by  focal  formation  of  phagocytic  cells,  is 
present  in  the  blood-forming  cells  of  the  bone  marrow,  and  constitutes 
a  lesion  almost  pathognomonic.  Diffuse  toxic  degeneration  is  present 
in  the  liver  (where  it  is  more  marked  than  in  any  other  infectious  disease), 
the  kidney,  the  adrenal  gland,  and  the  testicle.  Toxic  inhibition  of  cell 
differentiation  is  present  in  the  bone  marrow  (absence  of  complete 
transformation  of  antecedent  cells  into  polynuclear  leukocytes)  and  in 
the  testicle  (absence  of  spermatogenesis).  The  paucity  of  polynuclear 
leukocytes  in  the  specific  lesions,  in  the  focal  degenerations,  and  in  the 
bone  marrow  is  so  constant  and  so  pronounced  as  to  render  it  a  strik- 
ing peculiarity  of  the  disease.  The  common  secondary  infections,  due 
commonly  to  pyococci,  do  not  differ  pathologically  from  similar  lesions 
occurring  under  different  circumstances. 

Symptoms. — ^The  period  of  incubation  is  usually  twelve  days,  though 
it  varies  from  seven  to  fifteen  days,  and  is  commonly  unattended  by  note- 
worthy prodromal  symptoms  (occasionally  malaise).  The  onset  is 
usually  abrupt  and  quite  characteristic,  consisting  of  severe  chills,  high 
fever  (103°,  104°,  even  106°  F.),  severe  lumbar  pains,  headache,  and 
vomiting — which  of  themselves,  in  the  presence  of  an  epidemic,  suggest 
the  disease.  Repeated  chills  or  chilliness  may  occur  within  the  first 
twenty-four  hours.  In  children  a  convulsion  not  infrecjuently  replaces 
the  initial  chill.  In  addition  to  the  foregoing,  in  the  early  days  of  the 
disease,  the  patient  is  nervous  and  restless,  his  face  is  flushed,  his  eyes 
bright,  and  his  skin  hot  and  dry,  though  in  some  cases  there  is  frequent 
and  rather  profuse  perspiration;  he  complains  of  thirst,  anorexia,  and 
usually  of  constipation  (though  diarrhoea  may  be  present  in  children); 
the  pulse  is  rapid  (100  to  140)  and  frequently  dicrotic,  and  a  systolic 
murmur,  attributable  to  cardiac  dilatation,  sometimes  develops;  catar- 
rhal inflammation  of  the  conjunctivse  and  of  the  respiratory  tract  (nose, 
throat,  larynx,  and  bronchi)  is  rather  common;  and  in  many  cases  by 
the  second  or  third  day  vertigo,  stupor,  or  more  or  less  delirium  has 
developed.  In  severe  cases  coma  and  delirium  may  be  initial  symptoms. 
On  the  second  day  of  the  disease,  in  from  one-sixth  to  one-fourth  of  the 
cases,  so-called  initial  or  prodromal  rashes  appear — measly,  scarlatini- 
form,  or  petechial.  Petechise  may  occur  either  alone  or  with  the  measly 
or  the  scarlatinif orm  rash.  These,  which  often  are  quite  indistinguishable 
from  the  ordinary  rashes  of  measles  and  scarlatina,  may  be  widespread, 
but  they  are  usually  localized  to  or  involve  especially  the  lower  half  of  the 
abdomen,  the  outer  aspect  of  the  chest,  the  extensor  and  inner  surfaces 
of  the  thighs  and  arms,  and  the  natural  folds  of  the  body — the  groins, 
axillas,  elbows,  etc.  They  usually  fade  at  the  end  of  twenty-four  to 
thirty-six  hours — except  the  petechi^e. 

The  period  of  invasion  lasts  three  days,  at  the  end  of  which  time, 


VARIOLA 


229 


that  is,  on  the  evening  of  the  third  day  or  the  morning  of  the  fourth, 
the  temperature  dechnes,  the  lumbar  pains  and  the  headache  abate,  the 
general  condition  of  the  patient  improves  markedly,  and  the  true  vari- 
olous rash  appears.  In  mild  cases  the  temperature  may  fall  rapidly  to 
the  normal;  in  severe  cases  this  also  may  happen,  but  often  the  tem- 
perature, although  it  lessens  with  the  outbreak  of  the  rash,  does  not 
approach  the  normal  until  after  the  lapse  of  twenty-four  to  forty-eight 
hours  (Fig.  11).  The  rash  develops  first  on  the  forehead  near  or  in  the 
hairy  scalp  and  on  the  wrists,  and  then  gradually  spreads  over  the 
entire  body  and  sometimes  to  the  mucous  membranes  in  contact  with 
the  air  (mouth,  nose,  conjunctiva,  pharynx,  larynx.  Eustachian  tube, 
trachea,  oesophagus,  anus,  vagina,  urethra).  It  is,  how^ever,  always 
more  marked  on  the  face,  scalp,  wrists,  hands,  and  fingers,  and  is  less 
where  the  initial  rashes  were  most  marked.     It    consists  at   first   of 


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Smallpox  in  an  un vaccinated  man,  aged  thirty-seven  years,  showing  the  temperature  of  the 
initial  stage,  the  secondary  or  suppurative  fever,  and  a  later  irregular  fever,  due  to  abscesses  and 
cellulitis;  recovery.      (Welch  and  Schamberg.) 


small  reddish,  or  rose-colored,  macules,  which  on  the  first  day  give 
rise  to  papules  that  are  quite  hard,  "shotty,"  and  attended  by  intense 
itching.  Sometimes  they  may  be  felt  before  they  can  be  seen.  The 
papules  gradually  enlarge,  and  at  the  end  of  two  days  (the  fifth  or  sixth 
day  of  the  disease)  become  vesicles — spherical,  elevated,  multilocular, 
and  containing  clear  serum.  By  the  following  day  well-marked  central 
depression  (umbilication)  of  the  vesicles  is  usually  apparent.  By  the 
eighth  day  the  first  pocks  have  become  pustules,  and  by  the  tenth  or 
eleventh  day  pustulation  is  usually  complete — the  pocks  have  become 
larger,  have  lost  their  umbilication,  the  contained  fluid  has  become 
turbid  (purulent),  and  they  are  surrounded  by  a  halo  of  inflammation. 
Concurrent  with  the  pustulation,  the  fever  returns — so-called  secondary 
or  suppurative  fever,  which  may  reach  104°  or  105°  F.,  or  more;  the 
general  .symptoms  become  aggravated;  pain,  tenderness,  and  itching- 
become  almost  intolerable,  and  the  areas  of  skin  intervening  between 


230  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

the  pocks  become  often  extremely  swollen  and  oedematous,  so  that  the 
patient  presents  a  most  repulsive  appearance;  the  cervical  lymph  nodes 
are  usually  much  enlarged,  and  the  spleen  palpable ;  leukocytosis  devel- 
ops; albumin  and  casts  are  present  in  the  urine  in  about  two-thirds  of 
the  cases;  and  severe  nervous  symptoms,  such  as  delirium  and  coma, 
not  infrequently  supervene.  In  favorable  cases,  desiccation  begins  on 
about  the  twelfth  day,  and  by  the  fifteenth  day  is  usually  far  advanced 
on  the  face.  Gradually  all  the  pocks  dry  up,  and,  as  a  rule,  by  the 
end  of  three  weeks  desquamation  is  complete.  With  the  beginning  of 
desiccation  the  secondary  fever  subsides,  that  is,  it  does  not  remain  high 
for  more  than  twenty-four  to  forty-eight  hours ;  it  gradually  falls  by  lysis 
and  reaches  normal  on  or  about  the  fifteenth  day,  and  though  irregular 
fluctuations  may  occur  for  some  days,  convalescence  is  now  established. 
The  amount  and  degree  of  pitting  depend,  as  a  rule,  upon  the  severity 
of  the  infection,  upon  whether  or  not  the  skin  papillse  have  been  destroyed. 
As  a  rule,  the  pits  are  pigmented  for  some  time,  and  gradually  whiten. 
The  hair  commonly  falls  out,  but  is  soon  restored. 

In  unfavorable  cases,  soon  after  pustulation  occurs,  a  typhoid  state 
with  marked  delirium  usually  develops;  the  pulse  becomes  rapid  and 
feeble,  coma,  subsultus  tendinum,  etc.,  supervene,  and  with  evidences 
of  profound  intoxication  the  patient  dies. 

The  pocks  on  the  mucous  membranes,  as  a  rule,  do  not  proceed  to 
suppuration,  but  rather  to  the  formation  of  small  ulcers.  By  their  presence 
in  the  nose  they  occasion  manifestations  of  coryza;  in  the  mouth,  fauces 
pharynx,  and  oesophagus,  sore  throat  and  dysphagia;  in  the  Eustachian 
tube,  purulent  median  otitis;  in  the  larynx,  oedema,  perichondritis,  and 
sometimes  laryngeal  obstruction;  in  the  trachea  and  bronchi,  tracheo- 
bronchitis; in  the  conjunctiva,  conjunctivitis,  sometimes  progressing  to 
keratitis  with  perforation,  panophthalmitis,  etc. 

Varieties. — Several  varieties  of  smallpox  are  described:  (1)  Discrete 
smallpox — in  which  the  pocks  are  relatively  few  in  number  and  discrete, 
and  the  general  symptoms  moderate  in  degree.  (2)  Confluent  smallpox 
— in  which  the  pocks  are  numerous  and  tend  to  coalesce,  wiience  the 
greatest  distortion  of  the  countenance  and  limbs  not  infrequently  occurs. 
Often  the  skin  of  the  entire  head  and  of  the  extremities  becomes  a  large, 
superficial  abscess.  The  general  symptoms  are  severe — high  fever, 
delirium,  the  typhoid  state,  etc.;  death  may  ensue,  or  convalescence  is 
prolonged.  (3)  Hemorrhagic  smallpox:  (a)  in  which  the  disease  at  the 
beginning  pursues  an  ordinary  course,  but  in  which  hemorrhages  occur 
into  the  vesicles  and  pustules  (variola  hemorrhagica  pustulosa).  Death 
usually  follows  on  from  the  seventh  to  the  ninth  day.  Gradations, 
however,  are  observed  between  this  type  of  the  disease  and  the  more  mild 
cases,  in  which  occasionally  small  hemorrhages  occur  into  the  pocks. 
(6)  Petechial,  black,  or  malignant  smallpox  (purpura  variolosa),  in  which 
the  blood  dyscrasia  is  extreme,  the  initial  rash  markedly  hyperemic 
(often  purplish)  and  petechial;  later  the  hemorrhages  increase  in  size 
and  involve  the  conjunctivae  and  the  mucous  membranes  (hematuria, 


VARIOLA  231 

hematemesis,  melena,  menorrhagia,  hemoptysis,  etc.),  the  pulse  becomes 
rapid,  the  respirations  very  much  accelerated,  and  death  often  occurs 
as  early  as  the  third  day — that  is,  before  the  true  rash  appears.  (4) 
Varioloid,  or  modified  smallpox,  which  occurs  in  persons  that  have  been 
vaccinated.  The  initial  manifestations  are  much  like  those  of  true 
smallpox  (variola  vera),  though  they  are  usually  milder.  The  pocks 
are  few  in  number,  usually  confined  to  the  face  and  hands,  and  may  not 
progress  beyond  the  vesicular  stage,  though  some  of  them  may  become 
pustular;  there  is  little  if  any  secondary  fever,  and  rarely  any  scarring. 
(5)  A  verrucose  form  has  been  described — one  in  which  the  pocks 
dry  up  by  the  fifth  or  sixth  day  to  a  horny  consistency — hornpox,  wartpox, 
crystalline  pox.  (6)  A  variola  sine  eruptione  has  also  been  described; 
it  is  said  to  occur  during  epidemics,  to  affect  young  persons  especially, 
and  the  initial  manifestations  (fever,  headache,  backache)  only  develop. 
It  must  be  exceedingly  rare,  if  it  occurs  at  all.  (7)  Abortive  cases,  with 
severe  initial  symptoms,  but  subsequently  a  rapid  favorable  course. 

Complications. — Complications,  considering  the  common  severity  of 
the  disease,  are  singularly  few,  though  certain  of  the  more  common 
lesions  may  become  aggravated  and  constitute  real  complications,  such 
as  laryngitis  (which  may  lead  to  oedema  and  necrosis),  conjunctivitis 
(and  keratitis),  and  secondary  infections,  especially  of  the  skin  (furun- 
cles, erysipelas,  gangrene,  etc.).  Bronchopneumonia  is  common  in  the 
fatal  cases.  Pleuritis  (often  suppurative),  otitis  media,  parotitis,  orchitis, 
ovaritis,  arthritis,  and  certain  disorders  of  the  nervous  system  attended 
l)y  paralysis  are  sometimes  observed. 

Diagnosis. — ^The  initial  symptoms,  abrupt  onset,  with  severe  chill, 
high  fever,  vomiting,  severe  lumbar  pains,  and  headache,  especially 
during  an  epidemic,  suggest  the  disease.  While  the  initial  rashes  may 
cause  confusion  in  some  cases,  measles  may  be  excluded  by  the  absence 
of  prodromes,  of  coryza,  of  conjunctivitis,  of  cough,  and  of  Koplik's 
spots,  and  scarlatina  may  be  excluded  by  the  absence  of  sore  throat, 
of  unduly  rapid  pulse,  of  the  hyperemic  punctate  rash  in  the  fauces, 
and  by  the  less  uniform  distribution  of  the  cutaneous  rash.  Difficulty 
is  often  experienced  in  distinguishing  between  smallpox  and  chickenpox, 
but  smallpox  is  suggested  by  a  longer  prodromal  period,  severe  initial 
symptoms,  long  preemptive  stage,  the  abundance  of  pocks  on  the  face, 
wrists,  and  hands  (as  contrasted  with  the  trunk),  by  the  hard  and  "shotty" 
character  of  the  pocks  which  appear  in  one  crop  (within  thirty-six 
hours),  and  are  uniform  in  size,  deep-seated,  umbilicated,  and  multi- 
locular,  and  do  not  show  different  stages  side  by  side  (as  in  varicella), 
by  the  occurrence  of  secondary  fever  and  of  leukocytosis,  and  by  the 
absence  of  a  recent  successful  vaccination.  Typhus  fever  may  be 
distinguished  by  the  special  etiological  factors,  by  the  macular  and 
later  petechial  character  of  the  rash,  which  is  usually  most  abundant 
on  the  chest  and  the  abdomen,  and  by  the  absence  of  remission  of  the 
fever  upon  the  appearance  of  the  rash.  In  pustular  syphilis  there  is  a 
history  of  syphilitic  infection  from  six  months  to  two  y^f^i's  previously; 


232  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

there  are  not  the  preemptive  manifestations  of  smallpox  nor  remission 
of  the  fever  upon  the  appearance  of  the  rash  (though  there  may  be  some 
neuromuscular  pains  and  slight  fever);  the  cutaneous  lesions  are  poly- 
morphous ;  the  pustular  syphiloderm  has  usually  been  preceded  by  macu- 
lar and  papular  syphiloderms ;  the  pustules  are  usually  discrete,  come 
out  in  crops,  are  more  abundant  upon  the  trunk  (relative  freedom  of 
the  face),  are  rarely  as  deep-seated  as  in  smallpox,  though  they  usually 
have  an  indurated  base;  and  there  are  frequently  other  evidences  of 
syphilis.  Impetigo  contagiosa  begins  as  vesiculo-pustules  (not  papules), 
and  enlarging  by  peripheral  extension,  the  lesions  sometimes  attain 
the  dimensions  of  a  ten-cent  piece. 

Prognosis. — The  mortality  varies  much  in  different  epidemics;  it  is 
commonly  from  25  to  40  per  cent,  in  unprotected  individuals,  but  in 
recent  years  the  disease  seems  to  have  become  milder,  or  rather  there  have 
been  many  epidemics  of  mild  smallpox.  Severe,  confluent,  and  hemor- 
rhagic forms,  as  well  as  milder  but  complicated  cases  (especially  in  the 
debilitated),  are  likely  to  terminate  fatally.  The  mortality  of  varioloid 
is  from  1  to  3  per  cent. 

Treatment. — The  patient  must  be  isolated  and  the  strictest  measures  of 
prophylaxis  rigidly  enforced  (page  29) .  During  the  fever  period  the  patient 
should  be  confined  to  bed,  and  should  have  an  abundance  of  fresh  air 
and  a  light  nutritious  diet — small  amounts  at  frequent  intervals.  Atten- 
tion to  securing  a  sufficient  diet  is  especially  necessary  during  the  later 
periods  of  the  disease,  v^hen  the  abundant  suppuration  saps  the  vitality 
of  the  patient.  Water  should  be  given  in  large  amounts — to  relieve  the 
thirst  and  to  promote  the  elimination  of  the  toxins  by  flushing  the 
kidneys.  The  addition  of  the  alkaline  diuretics  (potassium  citrate, 
acetate,  etc.)  to  the  water  subserves  a  useful  purpose. 

In  the  absence  of  a  specific,  treatment  is  largely  symptomatic  and 
supportive.  Morphine  is  of  much  service  in  relieving  the  early  pains, 
and  later  in  controlling  the  cutaneous  irritation  and  consequent  nervous 
unrest,  as  well  as,  sometimes,  the  delirium.  Vomiting,  if  continued, 
may  be  relieved  by  cocaine,  cracked  ice,  champagne,  or  dilute  hydrocyanic 
acid.  The  fever  often  calls  for  a  diaphoretic  febrifuge  mixture  (spirit  of 
nitrous  ether  and  solution  of  ammonium  acetate) ,  and  cold  sponging  (occa- 
sionally the  cold  bath),  which  is  of  excellent  service  not  only  in  controlling 
the  fever,  but  in  alleviating  the  evidences  of  toxemia  (delirium,  prostra- 
tion, etc.).  In  some  cases  continuous  warm  baths  (hours  or  days)  are 
valuable.  The  throat  pain  may  be  relieved  by  cracked  ice  or  orthoform 
lozenges  (1  grain,  0.06  gram  each).  Stimulants  (whiskey,  brandy,  strych- 
nine, etc.)  are  often  required  in  the  later  stages  of  the  disease. 

But  little  can  be  done  to  prevent  pitting;  puncturing  the  pocks,  and 
the  use  of  silver  nitrate,  carbolic  acid,  iodine,  etc.,  for  this  purpose  are 
almost  if  not  quite  useless.  The  use  of  hot  or  cold  compresses,  or  of 
carbolized  vaseline  or  oil  is  often  grateful  to  the  patient.  Welch  and 
Schamberg  recommend  painting  the  face  once  or  twice  daily  with  tincture 
of  iodine.     Crusts,  when  they  form,  should  be  kept  moist  by  vaseline  or 


VACCINIA  233 

oil,  which  not  only  reUeves  the  cutaneous  irritation,  but  also  prevents  the 
dispersion  of  the  infectious  flakes.  During  the  whole  course  of  the  dis- 
ease the  eyes  and  the  mouth  should  be  kept  clean  by  the  use  of  mild 
antiseptic  lotions.  The  patient  may  be  permitted  to  get  out  of  bed  as  soon 
as  the  temperature  is  normal.  Repeated  bathing  and  the  use  of  anti- 
septic soaps  should  be  encouraged  during  convalescence.  If  pocks  have 
occurred  in  the  scalp,  the  hair  should  be  cut  very  close. 

CEdema  of  the  glottis  may  necessitate  tracheotomy.  The  severer 
forms  of  smallpox  require  considerable  stimulation,  but  it  is  doubtful 
whether  ergot,  iron,  gallic  acid,  etc.,  that  have  been  administered  in  the 
hemorrhagic  forms  have  been  of  any  real  service.  Most  of  the  special 
forms  of  treatment  advocated  from  time  to  time,  including  the  red-light 
treatment,  have  not  proved  of  service  in  the  hands  of  impartial  observers 
of  large  experience. 

VACCINIA. 

{Coivpox;  Vaccination.) 

Vaccinia  is  an  acute,  specific,  infectious,  and  highly  contagious  disease 
of  bovine  animals  which,  when  inoculated  into  man  (vaccination), 
produces  fever,  constitutional  disturbance,  and  a  specific  eruption,  con- 
sisting of  papule,  vesicle,  pustule,  and  crust,  and  affords  protection  against 
smallpox. 

Etiology. — Since  Jenner  introduced  vaccination,  in  1796,  there  has  been 
discussion  as  to  its  nature — whether  cowpox  is  an  independent  disease 
or  smallpox  modified  by  transmission  through  the  cow.  The  weight 
of  evidence,  however,  tends  to  confirm  Jenner's  opinion  that  cowpox 
is  modified  smallpox,  that,  at  least,  both  are  descended  from  a  common 
ancestor,  since  (1)  smallpox  and  cowpox  afford  immunity,  the  one  to  the 
other,  and  (2)  human  smallpox  virus  when  inoculated  into  cows  has 
produced  cowpox  (though  cows  are  often  refractory),  and  the  lymph 
from  such  cowpox  vesicles  when  inoculated  into  man  has  produced  vac- 
cinia, and  occasionally  even  more  or  less  generalized  eruptions — which 
may  be  regarded  as  smallpox.  Some  support  to  this  view  is  found 
also  in  the  results  (still  awaiting  confirmation)  of  the  investigations  by 
Councilman,  Magrath,  and  Brinckerhoft'  regarding  the  supposed  para- 
sites of  smallpox  and  of  vaccinia.  The  many  examinations  of  vaccine 
lymph  have  not  disclosed  with  certainty  the  specific  vaccine  organism; 
divers  cocci  (including  contaminating  pyococci),  bacilli  (including 
occasionally  contaminating  tetanus  bacilli),  and  certain  supposed  animal 
parasites  have  been  detected  by  different  observers.  Whatever  its  exact 
nature,  the  virus  is  filtrable,  and  doubdess  belongs  to  the  class  of  ultra- 
microscopic  organisms. 

Method  of  Vaccination. — Cow  lymph  alone  should  be  used,  and  only 
that  obtained  from  trustworthy  sources.  The  use  of  human  virus  has 
deservedly  fallen  into  disrepute.  During  recent  years  the  use  of  glycerin- 
ated  cow  lymph  has  become  widespread,  but  many  competent  observers 


234  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

still  prefer  the  dried  "points,"  Assuredly  the  lymph  should  be  as  free 
as  possible  from  contaminating  microorganisms — which  has  not  always 
been  the  case. 

The  arm  (near  the  insertion  of  the  deltoid  muscle)  or  the  calf  of  the 
leg  (frequently  in  girls)  is  usually  selected  for  vaccination.  The  skin 
having  been  cleansed  with  water  and  soap  (no  antiseptics,  since  they 
destroy  the  vaccine),  an  area  one-eighth  to  one-quarter  inch  in  diameter 
should  be  scarified  with  a  sterile  scalpel  or  needle  so  as  to  remove  only 
the  epidermis,  whereupon  the  vaccine  should  be  rubbed  in.  One  should 
be  careful  not  to  draw  blood,  A  single  area  for  inoculation  is  suffi- 
cient, though  many  European  physicians  prefer  several,  as  many  as  five. 
After  the  vaccine  has  dried  it  should  be  covered  with  an  aseptic  dressing, 
and  the  wound  thereafter  treated  aseptically.  Most  of  the  cases  of  serious 
inflammation  of  the  arm  following  vaccination  are  attributable  to  second- 
ary infection  of  the  wound. 

Symptoms. — ^The  period  of  incubation  of  vaccinia  is  usually  about 
forty-eight  hours,  and  is  commonly  unattended  by  symptoms.  On  the 
third  day  a  papule  attended  by  swelling,  redness,  induration,  and  a 
feeling  of  tension  becomes  apparent  at  the  site  of  inoculation;  by  the  fifth 
or  sixth  day  this  has  developed  into  an  umbilicated,  multilocular  vesicle, 
the  contents  of  which  are  at  first  clear  but  soon  become  turbid.  Gradu- 
ally the  vesicle  increases  in  size,  and  by  the  eighth  day  has  reaced  its 
maximum — when  it  is  very  itchy  and  surrounded  by  a  wide  zone  of  in- 
flammatory induration  and  oedema.  By  the  eleventh  or  twelfth  day  the 
contents  of  the  pock  are  distinctly  purulent,  and  the  inflammatory  zone 
may  be  quite  extensive;  the  adjacent  lymphatics  are  swollen  and  tender 
and  inhibit  the  motion  of  the  limb;  and  rarely  almost  if  not  quite  the 
entire  limb  is  swollen,  but  this  is  a  manifestation  of  secondary  infection. 
Soon  after  the  twelfth  day  the  inflammatory  phenomena  begin  to  sub- 
side, and  by  the  fifteenth  day  a  dried  crust  has  formed,  which  usually 
drops  off  during  the  early  part  of  the  fourth  week,  leaving  a  pitted  scar. 

While  the  local  lesions  are  at  their  height  there  is  usually  some  eleva- 
tion of  the  bodily  temperature  (100°  to  102°  F.),  more  or  less  malaise, 
slight  headache,  and  occasionally  chilliness. 

Sometimes  the  evolution  of  the  pock  is  unusually  delayed.  In  other 
cases  what  may  be  mistaken  for  the  true  pock  develops  very  early,  but  it 
does  not  present  the  characteristic  appearances  (vesiculation  and  um- 
bilication) ;  it  soon  drys,  and  by  the  seventh  or  eighth  day  the  crust  drops 
off.  These  so-called  spurious  vaccinations  afford  no  protection  against 
smallpox.  In  revaccinations  the  appearances  of  the  pock  are  not 
infrequently  atypical. 

Complications. — Acland  has  arranged  the  possible  complications  as 
follows:  During  the  first  three  days — erythema,  urticaria,  vesicular  and 
bullous  eruptions,  invaccinated  erysipelas;  after  the  third  day  and  until 
the  pock  reaches  maturity — urticaria,  lichen  urticatus,  erythema  multi- 
forme, accidental  erysipelas;  about  the  end  of  the  first  week — general- 
ized vaccinia,  impetigo,  vaccinal  ulceration,  glandular  abscess,  septic 


VARICELLA  235 

infections,  gangrene;  after  the  involution  of  the  pocks — invaccinated 
diseases — syphiHs.  Complications,  as  a  rule,  are  uncommon,  the  most 
common  being  septic  infection  attributable  to  lack  of  attention  to  the 
wound.  Syphilis  has  rarely  been  transmitted,  and,  of  course,  never 
when  cow  lymph  has  been  used.  Tetanus  has  occasionally  been  trans- 
mitted, and  has  proved  fatal. 

The  time  for  vaccination  is  during  the  first  or  second  year  of  life, 
or  immediately  after  birth  if  an  epidemic  prevails.  Revaccination 
should  be  done  before  or  about  puberty,  and  every  five  or  seven  years 
thereafter,  or  oftener  if  an  epidemic  prevails. 

The  value  of  vaccination  cannot  be  questioned — since  where  vaccina- 
tion and  revaccination  are  most  thoroughly  carried  out  smallpox  is  least 
common  or  is  never  seen  (as  in  the  German  army,  whence  it  has  been 
banished),  and  where  vaccination  is  most  lax  smallpox  finds  its  readiest 
victims  and  exerts  its  greatest  ravages. 


VARICELLA. 

(Chicken-pox.) 

Chicken-pox  is  an  acute  specific,  infectious,  and  moderately  contagious 
disease,  characterized  by  mild  fever  and  a  papulo-vesicular  eruption. 

Etiology. — Chicken-pox  is  essentially  a  disease  of  childhood,  occurring 
usually  before  the  seventh  year,  and  attacking  the  sexes  indiscriminately. 
It  is  rather  uncommon  in  very  young  infants,  but  is  probably  more 
common  in  adults  than  is  usually  supposed.  The  disease  generally 
occurs  epidemically,  but  sporadic  cases  are  rather  frequently  encountered. 
One  attack  usually,  but  not  always,  confers  immunity. 

The  exciting  cause  of  the  disease  has  not  been  isolated,  although  it 
is  unquestionably  present  in  the  skin  lesions.  Infection  is  usually  trans- 
mitted by  direct  contact  or  proximity,  but  may  be  transmitted  by  a  third 
person  or  by  fomites.  Infection  is  believed  to  be  acquired  by  inhalation, 
and  is  much  favored  by  previous  ill  health  and  overcrowding,  such  as 
obtains  in  asylums  and  some  schools,  etc.  There  is  no  longer  any  question 
of  the  non-identity  of  smallpox  and  chicken-pox — an  attack  of  one  of 
these  diseases  does  not  confer  immunity  from  the  other. 

Pathology. — The  characteristic  lesion  is  the  papulo-vesicular  eruption. 
The  lesions  of  the  internal  organs  are  those  common  to  most  of  mild 
infections  and  toxemias. 

Symptoms. — The  period  of  incubation  is  commonly  fourteen  days,  al- 
though it  is  said  to  vary  from  ten  to  nineteen  days.  The  onset  is  usually 
mild  in  character  and  is  often  not  preceded  by  prodromes,  although 
slight  fever,  malaise,  and  slight  pain  in  the  back  and  legs  may  be  present 
for  a  day;  occasionally  there  are  chilly  sensations,  and  rarely  convulsions. 
Often  the  rash,  which  comes  out  within  the  first  twenty-four  Iiours,  is 
the  first  evidence  of  ill  health.  The  rash  appears  first  on  the  trunk 
(chest  and  liack),  but  soon  also  on  the  neck,  face,  and  forehead  (ne;ir 


236  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

or  in  the  hairy  scalp),  and  is  sometimes  encountered  on  the  oral,  pharyn- 
geal, and  laryngeal  mucous  membrane — even  in  some  cases  on  the  con- 
junctivae and  the  genital  mucosae.  The  rash  consists  of  small,  reddish 
papules  which  speedily  (within  several  hours)  develop  into  vesicles;  in 
some  cases  the  papular  stage  may  be  apparently  absent.  The  pocks,  as 
a  rule,  are  roundish  or  ovoid  in  outline,  vary  somewhat  in  size,  contain 
clear  fluid  (though  it  may  be  turbid),  are  rather  superficial,  sometimes 
(but  not  often)  umbilicated,  although  as  desiccation  progresses  they 
become  flattened  and  even  somewhat  depressed  in  the  centre;  though 
sometimes  situated  upon  a  slightly  hyperemic  base,  this  is  often  wanting, 
the  pocks  resembling  clear  blisters  such  as  might  be  caused  by  drops 
of  boiling  water,  and  a  peripheral  zone  of  infiltration  is  not  encountered. 
During  the  course  of  the  second  day  the  contents  of  the  pock  often  become 
seropurulent,  especially  in  ill-nourished  children  and  in  consequence  of 
secondary  infection.  The  individual  pocks  usually  reach  maturity  at 
about  the  end  of  two  days,  and  at  the  end  of  the  third  or  fourth  day 
desiccation  begins;  a  scab  soon  forms,  and  is  shed,  as  a  rule,  within  two 
weeks,  without  leaving  a  scar.  The  rash  is  usually  discrete,  rarely  con- 
fluent, and  in  consequence  of  its  coming  out  in  crops  from  the  first 
to  the  third  day,  all  stages  in  its  development  may  be  seen  side  by  side. 
Usually  not  more  than  a  dozen  pocks,  there  may  rarely  be  several 
hundred.  In  a  few  cases  a  scarlatinous  rash  precedes  the  development 
of  the  pocks.  The  temperature  which  is  highest  on  the  second  and  third 
days  (as  the  rash  comes  out),  rarely  exceeds  102°  F.,  though  in  severe 
infections  in  debilitated  children  it  may  reach  104°  F.  It  falls  by  lysis 
as  the  rash  fades.  Some  glandular  enlargement,  especially  of  the  neck, 
may  be  encountered. 

In  unusual  cases,  the  vesicles  may  become  very  large,  forming  bullae 
and  resembling  pemphigus  (varicella  bullosa);  in  other  cases  hemor- 
rhages into  the  cutaneous  lesions  and  the  mucous  membranes  occur 
(varicella  hemorrhagica);  and  occasionally  necrosis  and  gangrene  about 
the  pocks  develop  (varicella  gangrenosa). 

Complications. — Nephritis  and  adenitis  sometimes  occur.  Secondary 
infection  of  the  pocks  sometimes  leads  to  suppuration  and  subsequent 
scar  formation,  and  occasionally  to  rather  extensive  streptococcic  infec- 
tion (erysipelas).  Varicella  is  often  associated  with  other  infections 
(epidemically  as  well  as  individually),  especially  measles  and  scarlatina. 

Diagnosis. — Difficulty  is  sometimes  experienced  in  distinguishing 
between  varicella  and  mild  smallpox,  but  varicella  is  suggested  by  a 
short  prodromal  period,  the  abundance  of  pocks  on  the  trunk  (as  con- 
trasted with  the  face),  the  occurrence  side  by  side  of  pocks  in  difl'erent 
stages  of  development  (papule,  vesicle,  and  crust),  the  apparent  super- 
ficiality, bleb-like  and  unilocular  character  of  the  pocks,  and  a  previous 
and  rather  recent  successful  vaccination.  Impetigo,  pustular  eczema, 
etc.,  sometimes  must  be  considered  in  the  differential  diagnosis. 

Treatment. — ^The  treatment  consists  of  isolation  (for  two  or  three  weeks) 
and  general  hygienic  management  (page  29).     Carbolized  vaseline  or  hot 


TYPHUS  FEVER  237 

boric  acid  solution  should  be  applied  to  the  pocks  if  there  is  much  irri- 
tation. Medicines  are  rarely  recjuired,  but  stimulants  should  be  admin- 
istered to  the  weakly,  and  a  generous  diet  is  always  advisable,  especially 
during  convalescence. 


TYPHUS  FEVER. 

(Exanthematic  Typhus  Fever;  Spotted  Fever;  Jail  Fever;  Ship  Fever; 
Camp  Fever;  Famine  Fever.) 

Typhus  fever  is  an  acute,  specific,  infectious,  and  highly  contagious 
disease,  characterized  by  sudden  onset,  macular  eruption,  grave  nervous 
symptoms,  and  a  characteristic  fever  curve  ending  by  crisis  on  or  about 
the  fourteenth  day. 

Etiology. — ^Typhus  fever  seems  especially  prone  to  attack  those  of 
adult  life,  but  age,  sex,  race,  season,  and  climate  have  little  if  any 
etiological  significance.  Formerly  a  widespread  disorder  and  frequently 
occurring  epidemically  in  different  parts  of  the  world,  the  disease  is  now 
seldom  encountered,  although  sporadic  cases  occur  in  large  cities  from 
time  to  time.     One  attack  usually  confers  immunity. 

The  exciting  cause  of  the  disease  has  not  been  isolated,  although  it 
it  is  probably  present  in  the  exhalations  and  evacuations  of  the  patient, 
in  the  blood,  the  skin  lesions,  and  the  scales.  Recently  Krompecher, 
Goldzieher,  and  Argyan  have  described  what  they  believe  to  be  protozoa 
in  the  blood.  The  disease  is  extremely  contagious,  the  contagium  being 
transmitted  directly,  by  a  third  person,  and  especially  by  fomites,  such  as 
clothes,  bed  linen,  dishes,  toys,  etc.,  to  which  the  contagium  clings  with 
extreme  pertinacity.  Anderson  and  Goldberger,  and  Ricketts  and  Wilder 
studying  tabardillo,  the  typhus  fever  of  Mexico,  have  transmitted  the 
disease  to  monkeys;  they  have  found  that  the  virus  is  in  the  blood 
of  the  patient  during  the  febrile  stage,  and  that  it  is  not  filtrable; 
that  monkeys  that  recover  show  an  immunity  comparable  with  that  in 
man;  and  that  the  body  louse  (Pediculus  vestimenti)  may  transmit  the 
infection.  The  infection  probably  may  also  be  acquired  by  inhalation, 
since  physicians,  nurses,  and  attendants  upon  the  sick  during  epidemics 
are  very  likely  to  contract  the  disease.  The  likelihood  of  infection  is 
increased  by  general  insanitary  practices,  destitution,  and  overcrowding 
such  as  obtain  in  tenements,  asylums,  jails,  ships,  camps,  etc. 

Pathology. — There  are  no  characteristic  anatomical  lesions,  the  lesions 
present  being  those  common  to  most  severe  toxemias.  Thus,  the  spleen 
is  moderately  enlarged  and  soft;  the  liver,  kidneys,  heart,  voluntary 
muscles,  nerves,  etc.,  reveal  parenchymatous  and  granular  degeneration 
and  necrosis;  and  there  are  marked  hemolysis,  subcutaneous  petechial 
hemorrhages,  and  bronchial  catarrh. 

Symptoms. — The  period  of  incubation  varies  from  seven  to  twenty-one 
days,  l)eing  usually  twelve  days.  In  some  cases  there  are  prodromal 
symptoms  lasting  a  day  or  two,  and  consisting  of  general  malaise,  loss 


238 


INFECTIONS  OF   UNKNOWN  ETIOLOGY 


of  appetite,  headache,  vertigo,  and  sometimes  coryza.  The  onset  of 
the  disease  is  usually  sudden,  and  manifested  by  chill,  high  fever,  head- 
ache, pains  in  the  back  and  limbs,  prostration,  and  sometimes  vomiting. 
The  temperature  may  reach  104°  to  105°  F.,  by  the  end  of  twenty-four 
or  thirty-six  hours,  and  it  continues  high  with  slight  morning  remissions 
(Fig.  12).     The  chill  may  recur  for  a  day  or  two.     With  continuance 


Fig.   12 


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The  temperature  in  typhus  fever,  showing  the  decline  by  crisis.      (Dotj'.) 

of  the  high  fever,  marked  nervous  manifestations  referable  to  toxemia 
soon  appear,  such  as  severe  headache,  vertigo,  tinnitus  aurium,  spots 
before  the  eyes,  etc.  The  patient  becomes  dull  and  listless,  sometimes 
wildly  maniacal.  There  is  much  thirst,  the  bowels  are  confined,  and  the 
urine  is  concentrated  and  may  contain  a  small  amount  of  albumin. 

On  the  fourth  or  fifth  day,  by  which  time  the  temperature  has  reached 
its  maximum,  often  106°  F.,  the  characteristic  eruption  makes  its  appear- 
ance, first  on  the  anterior  fold  of  the  axillse,  and  the  wrists,  or  the  backs 
of  the  hands,  then  on  the  sides  of  the  abdomen  and  chest,  and  finally 
on  the  trunk,  including  the  back  and  the  extremities,  but  being  rare  on 
the  face.  It  is  made  up  of  two  elements — rose-colored  or  dusky  macules 
superimposed  upon  a  subcuticular  motding,  whence  it  much  resembles 
measles,  and  has  been  spoken  of  as  the  mulberry  rash  of  t}-phus  fever. 
It  comes  out  rapidly,  within  twenty-four  hours  usually,  and  not  in  crops 
as  does  the  rash  of  typhoid  fever.  At  first  the  macules,  which  fade 
almost  imperceptibly  into  the  surrounding  mottling,  disappear  upon 
pressure,  but  they  soon  become  darker  and  less  deleble,  and  later  (eight 
to  tenth  day)  become  hemorrhagic  (petechise).     The  rash  is  rarely  missed, 


TYPHUS  FEVER  239 

except  perhaps  in  the  mildest  cases,  in  which,  however,  it  is  largely 
petechial. 

During  the  course  of  the  second  week,  concurrent  with  the  change  in 
character  of  the  rash,  profound  toxemia  (the  typhoid  state)  develops. 
Delirium,  often  noisy  at  first,  but  later  usually  milder,  muttering,  and 
attended  by  sleeplessness,  stupor  (coma  vigil),  subsultus  tendinum,  and 
carphologia,  continue.  Prostration  is  extreme,  and  face  expressionless 
and  flushed,  the  pupils  contracted,  and  the  eyes  injected.  The  tempera- 
ture, though  somewhat  lower  than  during  the  first  week,  continues  high 
(102.5°  to  103.5°  F.),  the  pulse  is  weak  (120  to  130  per  minute),  small, 
and  often  irregular  and  dicrotic.  The  apex  beat  and  the  heart  sounds 
are  weak,  and  a  soft,  systolic  murmur  is  common.  There  may  be  a  slight 
leukocytosis.  The  tongue  becomes  dry  and  fissured,  and  later  sordes 
collect  on  the  lips,  gums,  teeth,  and  tongue.  The  breath  and  the  body 
generally  are  malodorous  (by  some  said  to  be  characteristic).  Bronchitis 
continues,  and  with  failure  of  the  heart,  hypostatic  congestion  of  the 
lungs  may  develop.  The  urine  is  usually  concentrated  and  contains 
a  little  albumin,  lessened  chlorides,  and  is  frequently  voided  involun- 
tarily, although  it  may  be  retained.  The  spleen  is  usually  enlarged  and 
palpable.  Bed  sores  not  infrequently  develop.  In  unfavorable  cases, 
death  ensues  from  exhaustion  due  to  toxemia  or  from  complications,  the 
temperature  often  rising  just  before  death  to  108°  to  109°  F. 

In  favorable  cases  at  the  end  of  the  second  week,  usually  on  the 
fourteenth  day,  and  sometimes  preceded  by  a  precritical  rise,  the  tem- 
perature falls  by  crisis,  within  twelve  to  twenty-four  hours,  to  normal 
or  below,  the  patient  sweats  profusely,  toxemia  lessens,  the  general 
symptoms  improve,  and  convalescence  ensues. 

Varieties. — Mild  and  severe  are  sufficiently  descriptive  of  the  majority 
of  cases.  In  certain  abortive  cases,  the  crisis  occurs  early  and  the 
eruption  and  delirium  are  not  marked.  In  certain  malignant  or  fulmin- 
ating cases  (typhus  siderans)  death  ensues  early  under  manifestations 
of  profound  toxemia,  marked  delirium,  high  fever,  cardiac  collapse, 
and  degeneration  of  the  viscera.  In  some  cases  the  disease  is  protracted, 
the  fever  and  other  manifestations  extending  into  the  third  week.  An 
afebrile  typhus  fever  has  been  described.     Relapse  is  very  rare. 

Complications  and  Sequels. — Bronchitis,  hypostatic  congestion  of  the 
lungs,  and  bronchopneumonia  are  common.  Gangrene  of  the  liuig  some- 
times develops.  Throml)osis  and  embolism  with  consequent  infarction 
of  the  viscera  and  gangrene  of  the  extremities  occur.  Extensive 
gangrenous  bed  sores,  suppuration  of  the  glands  and  of  other  tissues,  due 
to  secondary  infections,  furunculosis,  parotitis,  meningitis,  hemolysis,  also 
have  been  observed.  Hemiplegia  or  monoplegia,  the  result  of  throm- 
bosis or  embolism,  and  paralysis  due  to  neuritis,  sometimes  follow. 
Rarely  various  forms  of  insanity  persist  for  some  time. 

Diagnosis. — In  cases  of  moderate  severity,  the  diagnosis  is  apparent 
from  the  presence  of  an  epidemic,  exposure  to  infection,  characteristic 
onset,  high   fever,  and   characteristic  rash.      The  recognition  of   mild 


240  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

cases,  in  the  absence  of  an  epidemic,  requires  a  knowledge  of  the  entire 
cHnical  course.  Typhus,  as  contrasted  with  typhoid  fever,  is  distin- 
guished by  a  sudden  onset  with  chill,  high  initial  and  more  continued 
temperature,  early  prostration,  severe  nervous  symptoms  (delirium, 
stupor),  a  characteristic  petechial  rash  (with  diffuse  mottling),  more 
likely  injection  of  the  sclerotics,  and  the  termination  by  crisis  on  or 
about  the  fourteenth  day,  and  by  the  absence  of  abdominal  symptoms, 
the  presence  of  the  Gruber-Widal  reaction,  typhoid  bacilli  in  the  blood, 
feces,  urine,  and  rose  spots.  Cerebrospinal  meningitis,  measles,  small- 
pox, uremia,  purpura,  acute  infective  endocarditis,  and  malaria  have 
more  or  less  resemblance  in  certain  minor  or  major  points  to  typhus 
fever,  but  regard  for  the  clinical  manifestations  of  each  disease  should 
soon  settle  the  diagnosis. 

Prognosis. — ^The  mortality  rate  in  epidemics  varies  from  10  to  20 
per  cent.  The  extent  of  the  rash  is  said  to  bear  a  direct  relation  to 
the  severity  of  the  infection.  Unfavorable  signs  are  hyperpyrexia, 
extreme  toxemia,  and  the  different  complications.  The  young  usually 
recover. 

Treatment. — ^The  treatment  in  general  does  not  differ  from  that  of 
typhoid  fever.  The  strictest  isolation,  thorough  disinfection,  and  free 
ventilation  (treatment  in  the  open  air),  are  imperative  (page  29).  The 
general  management  comprises  the  use  of  hydrotherapy  and  stimulants — 
hydrotherapy  by  sponging  or  bathing,  large  amounts  of  water  to  the 
patient  to  drink  (much  overlooked  because  of  the  stupor),  and  enteroclysis 
and  h}'podermoclysis  to  promote  the  elimination  of  toxins.  Stimulants 
comprise  the  sponging  and  bathing  just  mentioned,  alcohol  (especially 
in  subjects  over  twenty  years  of  age),  and  strychnine,  ammonium 
carbonate,  camphor,  etc.  Coal  tar  derivatives  should  be  avoided 
on  account  of  the  cardiac  weakness.  The  food  must  be  nutritious, 
easily  digestible,  given  at  stated  intervals,  bearing  in  mind  that  if  we 
can  support  the  patient  for  a  stated  time  he  is  likely  to  recover  from 
the  self-limited  disease.  The  complications  are  to  be  treated  on 
general  principles. 

SCARLET  FEVER. 

{Scarlatimi :  Scarlet  Rash.) 

Scarlet  fever  is  an  acute,  specific,  infectious,  and  highly  contagious 
disease,  characterized  by  high  fever,  rapid  pulse,  sore  throat,  an  ery- 
thematous rash,  and  a  marked  tendency  to  nephritis. 

Etiology. — Scarlet  fever  is  essentially  a  disease  of  childhood,  attacking 
the  sexes  equally,  and  being  especially  prevalent  before  the  tenth  year 
(90  per  cent,  of  all  cases).  It  is  rare  in  young  infants,  but  more  common 
in  non-immune  adults.  The  disease  is  endemic  in  most  large  cities 
and  frequenty  prevails  epidemically,  especially  during  the  fall  and 
winter.  One  attack  usually  confers  immunity,  although  recurrences  are 
observed.     Some  persons  are  naturally  immune  to  the  disease. 


SCARLET  FEVER  241 

The  exciting  cause  of  the  disease  has  not  been  isolated  witii  certainty. 
IVIany  observers  view  the  disease  as  a  modified  streptococcic  infection ; 
the  streptococcus  may  be  isolated  from  most  of  the  lesions,  and  assuredly 
plays  an  important  part  in  the  affection.  Mallory  has  described  a  pro- 
tozoan-like organism  between  the  epithelial  cells  of  the  epidermis,  and 
Duval  has  found  the  organism  in  blister-serum;  but  the  proof  is  not 
yet  conclusive  that  this  is  the  specific  infectious  agent.  The  blood, 
nasopharyngeal  and  oral  discharges,  epidermic  scales,  and  urine  are 
infectious.  The  disease  is  highly  contagious  and  spreads  with  rapidity, 
though  not  as  rapidly  or  widely  as  measles.  Infection  in  the  great  ma- 
jority of  cases  is  transmitted  by  direct  contact  or  proximity  to  a  patient, 
or  a  "carrier;"  or  by  means  of  infected  food,  such  as  milk  (responsible 
for  a  number  of  epidemics);  occasionally  by  a  third  person,  or  by 
fomites.  Infection  is  usually  acquired  through  inhalation,  sometimes 
through  swallowing,  and  wounds.  Patients  with  surgical  wounds  and 
puerperal  women  appear  to  be  very  susceptible  to  the  infection,  though 
most  of  the  cases  of  supposed  scarlatina  described  in  such  subjects  are 
instances  of  streptococcic  or  staphylococcic  infection. 

Pathology. — Scarlatina  is  devoid  of  characteristic  lesions.  The 
lesions  in  the  nasopharynx  are  those  of  inflammation  and  ulceration; 
those  in  the  skin,  of  hyperemia,  which  disappears  after  death.  The 
lesions  in  the  internal  organs  are  those  common  to  most  toxemias,  with 
sometimes  special  characteristics  due  to  the  frequent  association  of 
the  streptococcus.  The  kidneys  frequently  show  a  rather  characteristic 
lesion — a  glomerulonephritis,  though  diffuse  and  hemorrhagic  nephritis 
also  occurs.  Catarrh  of  the  gastro-intestinal  mucous  membrane  is  com- 
mon; the  lymph  nodes,  especially  those  of  the  neck,  not  infrequently 
suppurate;  and  fibrinopurulent  inflammation  of  the  serous  membranes 
is  often  encountered  in  fatal  cases. 

Symptoms. — The  period  of  incubation  is  from  one  to  seven  days, 
usually  from  two  to  four  days.  The  invasion  is  sudden — prodromal 
symptoms  being  entirely  in  abeyance  or  consisting  merely  of  slight  in- 
disposition. The  initial  symptoms,  which  are  quite  characteristic  and  of 
themselves  suggest  the  disease,  consist  of  nausea,  vomiting,  high  fever, 
104°  to  105°  F.  (Fig.  13),  sore  throat  with  pain  on  swallowing,  swelling  and 
tenderness  of  the  glands  at  the  angles  of  the  jaw,  and  an  unusually  rapid 
pulse  (140  to  180  per  minute).  Occasionally  there  is  an  initial  chill; 
more  often  chilliness.  Convulsions  are  common  in  young  children. 
The  throat  is  found  to  be  acutely  inflamed — the  fauces,  soft  palate,  and 
pharynx  revealing  a  dift'use  hyperemic  redness  and  a  fine,  pimctiform 
rash  (even  before  the  skin  rash  appears). 

On  the  second  day,  often  even  within  the  first  twenty-four  hours,  the 
characteristic  rash  appears — first  on  the  neck  and  chest  and  then  (within 
twenty-four  hours)  rapidly  spreading  over  the  entire  body.  This  con- 
sists of  a  multitude  of  minute  red  points,  for  the  most  part  corresponding 
with  the  points  of  emergence  of  the  hairs,  set  in  the  dift'usely  hyperemic 
and  slightly  swollen  skin.  The  hyperemic  areas  are  usually  confluent 
16 


242 


INFECTIONS  OF   UNKNOWN  ETIOLOGY 


and  impart  to  the  patient's  skin  an  appearance  suggesting  a  boiled  lobster. 
The  eruption  is  distinctly  punctate  in  character — a  character  the  more 
apparent  the  less  the  diffuse  hyperemia;  hence  during  the  later  stages 
of  the  disease.  It  disappears  temporarily  on  pressure,  and  is  usually 
most  marked  at  the  natural  folds  of  the  body — the  groins,  the  bends  of 
the  elbow,  the  axillfe,  and  often  on  the  lower  part  of  the  abdomen  and 
on  the  inner  aspects  of  the  thighs.  As  contrasted  with  measles  the  face 
is  often  relatively  unaffected. 


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The  temperature  in'scarlet  fever,  showing  the  decline  about  the  fourth  or  fifth  day,  and  a  sub-^ 
sequent  risejand  irregularity,  due  to  nephritis  and  swollen  glands.     (Musser.) 

On  the  third  day  of  the  eruption,  that  is,  at  the  end  of  about  forty- 
eight  hours,  the  disease  is  usually  at  its  height.  The  fever  remains 
high  (104°  to  105°  F.)  with  slight  morning  remissions,  the  pulse  frequent 
(140  to  160  per  minute),  and  the  entire  integument  presents  a  diffuse, 
bright  scarlet  hue  (that  serves  to  distinguish  scarlatina  from  other 
exanthemas).  The  concomitants  of  fever  and  the  expressions  of 
toxemia  are  usually  well  marked :  the  patient  is  delirious  at  night  and  at 
least  stuporous  during  the  day,  and  the  urine  is  reduced  in  amount, 
concentrated,  of  high  specific  gravity,  and  may  contain  a  little  albumin. 
The  tongue,  at  first  red  at  the  tip  and  edges  and  covered  on  the  dorsum 
with  a  grayish-white  fur,  through  which  the  swollen  papillae  project 
(strawberry  tongue),  soon  loses  the  fur  and  frequently  also  the  super- 
ficial epithelium,  and  presents  a  swollen,  red,  and  irregular  surface 
(raspberry  tongue).  The  fauces  exhibit  different  grades  of  inflamma- 
tion: in  the  one  case  slight  hyperemia  with  a  punctate  rash;  in  another 
case,  a  more  severe  inflammation  especially  of  the  tonsils,  possibly  a 
follicular  tonsillitis;  and  in  another  case,  pseudomembranous  inflamma- 


SCARLET  FEVER  243 

tion  with  more  or  less  extensive  induration  and  suppuration  of  the 
adjacent  tissues.  The  glands  at  the  angle  of  the  jaw,  swollen  in  all  cases, 
frequently  become  exquisitely  tender  and  may  suppurate.  The  appetite 
is  lost.  The  spleen  may  be  palpable.  Leukocytosis  is  common  and 
may  be  marked. 

Having  lasted  four  or  five  days  (in  mild  cases,  two  or  three  days),  the 
rash  begins  to  fade,  the  throat  manifestations  abate,  and  the  fever  falls 
by  lysis — reaching  the  normal,  in  moderately  severe  cases,  by  the  eighth 
or  ninth  day — in  mild  cases  earlier,  in  severe  cases  and  in  the  event  of 
complications,  later.  The  subsidence  of  the  rash  is  followed  by  a  branny 
or  flaky  desquamation,  which  begins  (as  did  the  rash)  on  the  neck  and 
chest,  and  is  usually  proportionate  to  the  severity  of  the  rash.  In  severe 
cases  veritable  casts  of  the  hands  and  feet  may  be  shed;  sometimes  even 
the  hair  and  nails  are  lost.  Desquamation  is  usually  complete  at  the 
end  of  fifteen  or  twenty-days,  but  may  be  prolonged  until  the  seventh 
or  eighth  week. 

Varieties. — Depending  upon  the  severity  of  the  infection,  the  following 
varieties  of  scarlatina  may  be  recognized: 

1.  Mild  scarlatina,  in  which  the  general  and  local  symptoms  are  mild, 
and  in  which  the  rash  is  slight  and  lasts  but  a  day  or  two.  In  some  cases 
it  may  be  absent — scarlatina  sine  eruptione.  In  some  cases  the  nature 
of  a  mild  sore  throat  is  unsuspected  until  the  skin  desquamates,  or  until 
nephritis  develops,  or  until  an  epidemic  attributable  to  it  ensues. 

2.  Severe  scarlatina,  in  which  the  general  and  local  symptoms  are 
severe:  sudden  onset,  high  fever  (108°  F.),  scanty  albuminous  urine, 
marked  prostration,  severe  nervous  manifestations,  headache,  rapid 
feeble  pulse,  heart  weakness,  delirium,  convulsions,  coma,  etc. — the  so- 
called  atatic  form.  This  form,  the  expression  of  severe  toxemia,  is 
frequently  fatal  within  a  day  or  two — in  some  cases  even  before  the 
appearance  of  the  rash  (during  the  period  of  invasion). 

3.  Malignant  scarlatina,  of  which  we  may  distinguish:  (a)  The 
hemorrhagic  form — in  which  hemorrhages  occur  into  the  mucous  mem- 
branes and  the  skin.  Often  the  hemorrhages  are  petechial,  but  fre- 
quently ecchymoses,  involving  large  areas,  develop;  and  epistaxis,  hemop- 
tysis, hematuria,  etc.,  may  occur.  Intoxication  is  severe  and  death 
usually  results  on  the  second  or  third  day.  (6)  The  anginose  form — in 
which  the  throat  symptoms  assume  the  predominance.  Ulcerative 
and  pseudomembranous  inflammation  of  the  tonsils  and  fauces,  with 
marked  fetor,  induration  and  suppuration  of  the  adjacent  cellular  and 
lympliatic  tissues  ensue.  The  lesions  may  spread  to  the  nose  and  the 
larynx,  leading  to  death  from  asphyxia;  or  the  cellular  inflammation 
may  become  widespread,  and  lead  to  Ludwig's  angina,  or  perforation  of 
the  carotid  artery,  etc.  Otitis  media  is  common.  Bacteremia  is  the 
rule,  and  death  speedily  follows  in  most  cases.  T'he  throat  lesions,  fre- 
quently diphtheroid,  may  sometimes  reveal  the  Klebs-Loeffier  bacillus. 

The  rash  sometimes  exhibits  peculiarities.  Instead  of  becoming 
diffuse,  the  hyperemic  areas  may  remain  discrete — ^scarlatina  maculosa; 


244  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

sometimes  papular  elevations  occur — scarlatina  papulosa;  sometimes 
sudaminal  vesicles  appear — scarlatina  miliaris;  the  vesicles  may  become 
purulent — scarlatina  pustulosa;  or  large  blebs  may  form — scarlatina 
pemphigoidea. 

Complications  and  Sequels. — The  most  important  complications  and 
sequels  are  nephritis  and  inflammation  of  the  serous  membranes.  In 
addition  to  the  albumin  present  in  most  cases  and  attributable  to  the 
toxemia,  a  true  nephritis  may  occur.  It  may  develop  during  the  course 
of  severe  cases,  but  is  quite  common  after  mild  cases,  especially  during 
convalescence  (third  or  fourth  week) — postscarlatinal  nephritis.  The 
onset  is  usually  manifested  by  dropsy,  but  sometimes  by  lessening  in 
the  amount  of  urine  or  by  uremia.  The  oedema  often  goes  on  to  ana- 
sarca and  effusions  within  the  serous  cavities  and  the  meninges.  These 
may  lead  to  death,  but  usually  recovery  ensues  after  several  weeks, 
although  convalescence  may  be  protracted  for  several  months.  An 
oedema  without  nephritis,  and  attributed  to  impoverishment  of  the 
blood,  has  been  described.  A  septic  nephritis,  as  part  of  a  general 
pyemia,  sometimes  occurs.  Chronic  nephritis  rarely  develops  out  of  the 
acute  lesions,  but  the  kidneys  may  remain  susceptible  for  a  long  time, 
and  in  later  life  exposure  to  appropriate  etiological  factors  may  result  in 
the  ready  production  of  a  serious  and  even  fatal  nephritis. 

Of  the  inflammations  of  the  serous  membranes,  pleuritis  and 
pericarditis  are  common,  and  usually  fibrinopurulent  in  character. 
Simple  and  malignant  endocarditis,  as  well  as  myocarditis,  may  occur. 
Meningitis  may  develop  and  remain  for  a  time  unsuspected,  especially 
in  the  event  of  convulsions.  Pains  in  the  joints  are  not  uncommon — 
scarlatinal  synovitis  (miscalled  rheumatism).  Usually,  an  expression 
of  the  toxemia,  the  pain  subsides  with  the  toxemia;  occasionally  it  persists 
longer,  and  the  lesions  may  go  on  to  suppuration  (usually  mono-articular). 
An  associated  chorea  has  been  observed.  Suppurative  otitis  media,  the 
result  of  extension  of  inflammation  along  the  Eustachian  tube  is  common, 
and  answerable  for  much  of  the  deafness  of  later  life.  If  neglected  it 
may  lead  immediately  to  mastoid  disease,  sinus  thrombosis,  cerebral 
abscess,  etc.  An  otorrhoea  or  rhinorrhoea  persisting  after  apparent 
convalescence,  even  if  non-purulent  ("chronic  carriers"),  is  answerable 
for  the  propagation  of  the  disease  and  even  for  some  epidemics.  Sup- 
purative adenitis,  especially  of  the  neck,  is  rather  common.  Sudden 
death  from  acute  cardiac  failure  sometimes  occurs  during  convalescence. 

Concurrent  infections  are  not  infrequent — especially  diphtheria, 
chicken-pox,  measles,  pertussis,  erysipelas,  typhoid  fever,  etc. 

Diagnosis. — The  diagnosis  is  usually  easy.  The  short  period  of  incuba- 
tion, the  characteristic  initial  symptoms,  especially  the  early  sore  throat, 
the  vomiting,  the  rapid  pulse,  the  punctate  hyperemia  of  the  mucous 
membrane  of  the  mouth  and  fauces,  followed  by  the  characteristic  skin 
eruption,  serve  to  exclude  other  diseases.  From  measles  scarlatina 
may  be  excluded  by  the  sore  throat  (as  contrasted  with  general  catarrhal 
symptoms),  shorter  preemptive  period,  the  punctiform  rash  in  the  throat. 


SCARLET  FEVER  245 

the  absence  of  the  Filatow-Koplik's  spots,  the  more  unifonn  erythematous 
rash  (as  contrasted  with  the  blotchy  or  mottled  rash  of  measles),  the 
relative  freedom  of  the  face,  the  raspberry  tongue,  the  undue  accelera- 
tion of  the  pulse,  and  the  presence  of  leukocytosis.  In  rotheln,  the  onset 
is  less  abrupt,  there  is  rarely  initial  vomiting,  the  fever  is  less  high,  the 
pulse  is  less  rapid,  the  rash  is  not  punctiform,  there  is  no  raspberry  tongue, 
the  general  symptoms  are  less  marked,  and  there  is  little  tendency  for 
the  development  of  nephritis.  In  scarlatina  the  throat  lesions  sometimes 
become  "diphtheroid,"  and  may  not  be  distinguishable  from  those  of 
true  diphtheria,  except  by  bacteriological  examination.  Diagnostic 
difficulties  are  sometimes  enhanced  by  an  erythematous  rash  that 
occasionally  occurs  in  diphtheria.  However,  this  is  uncommon,  and 
is  darker  and  of  shorter  duration  than  the  true  scarlatinous  rash,  and 
is  usually  confined  to  the  trunk.  The  two  diseases  not  infrequently 
co-exist.  In  acute  tonsillitis  there  is  rarely  an  erythematous  rash,  but 
this  is  not  punctiform,  there  is  no  raspberry  tongue,  no  undue  accelera- 
tion of  the  pulse,  and  no  epidemic.  Acute  exfoliative  dermatitis  is  often 
difficult  of  differentiation,  but  is  suggested  by  absence  of  throat  symp- 
toms and  of  the  characteristic  tongue,  and  by  the  rather  marked  tendency 
to  recurrence,  the  earlier  commencement  of  desquamation  (even  before 
the  eruption  has  faded),  the  frequent  involvement  of  the  hair  and  the 
nails,  and  the  comparative  rarity  of  involvement  of  the  kidneys.  Drug 
rashes  sometimes  follow  the  administration  of  belladonna,  quinine, 
potassium  iodide,  antitoxic  serums,  etc.,  and  ptomaine  rashes  may 
occur  after  the  use  of  tainted  oysters,  fish,  etc.,  but  these  rashes  are 
usually  slight  and  transient  (though  they  may  be  diffuse  and  marked), 
they  are  not  pimctiform,  and  there  are  none  of  the  characteristic  symp- 
toms of  scarlatina. 

Prognosis. — The  mortality  varies  much — from  about  5  per  cent  in  the 
mildest  epidemics  to  30  per  cent,  in  the  more  severe.  The  death  rate  is 
higher  the  younger  the  child,  and  in  general  the  poorer  the  social  condi- 
tions. Unfavorable  symptoms  in  individual  cases  are  high  fever,  marked 
toxemia  (delirium,  etc.),  hemorrhages,  severe  throat  lesions,  laryngeal 
obstruction,  and  nephritis. 

Treatment. — The  patient  must  be  isolated  and  the  usual  prophylactic 
measures  enforced  (page  29).  Specific  therapy  is  still  a  hope  of  the 
future.  Some  good  results  have  followed  the  use  of  a  polyvalent  anti- 
streptococcic serum.  More  recently  streptococcic  vaccines  have  been  em- 
ployed for  prophylactic  and  curative  purposes — with  encouraging  result. 
In  the  absence  of  specific  treatment,  the  special  function  of  the  physician  is 
to  guide  tiie  child  through  the  attack,  and  to  prevent  the  development  of 
complications.  Mild  cases,  as  a  rule,  pursue  a  favorable  course  under  the 
beneficent  influence  of  rest  in  bed,  flannel  garments  (to  lessen  the  likeli- 
hood of  chill),  an  abundance  of  fresh  air,  a  milk  diet,  considerable  water 
(to  promote  tiie  elimination  of  toxins),  and  regulation  of  the  bowels. 
In  all  cases  it  is  wise  to  insure  a  daily  evacuation  of  the  bowels,  to 
administer  a   mild    diuretic   and   diaphoretic    febrifuge  mixture  (such. 


246  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

for  instance,  as  is  given  on  page  250),  to  give  the  child  a  warm  bath 
twice  daily  and  to  follow  this  by  oil  inunctions.  In  the  event  of  high 
fever  and  delirium,  an  ice  bag  should  be  applied  to  the  head,  and  the 
bathings  should  be  more  frequent  (every  three  hours).  The  bathing 
is  much  preferable  to  the  use  of  antipyretic  drugs.  An  alcohol  rub  at 
night  often  promotes  a  restful  sleep.  Stimulants  (brandy,  whiskey, 
strychnine,  ammonium  preparations,  etc.)  are  called  for  in  the  event 
of  marked  toxemia  (prostration,  marked  delirium,  subsultus  tendinum, 
the  typhoid  state,  coma,  etc.).  The  bromides  are  often  serviceable 
in  the  wakefulness  that  sometimes  attends  the  nervous  irritability. 
J.  C.  Wilson  recommends  the  routine  use  of  chloral,  in  dosage  sufficient 
to  produce  light  somnolence,  believing  that  it  promotes  diuresis  and 
lessens  the  likelihood  of  nephritis,  favorably  modifies  the  nervous  mani- 
festations, and  allays  the  itching.  Robert  Milne  recommends  thorough 
rubbing  of  the  body,  from  the  crown  of  the  head  to  the  soles  of  the  feet, 
morning  and  evening,  for  the  first  four  days,  and  then  once  daily  until 
the  tenth  day,  with  10  per  cent,  eucalyptus  oil;  and  swabbing  the  throat, 
every  two  hours,  for  the  first  twenty-four  hours,  with  10  per  cent,  car- 
bolic-acid oil — stating  that  this  treatment  modifies  the  severity  of  the 
attack,  prevents  nasal,  oral,  and  renal  complications,  and  abolishes  the 
infectivity  of  the  disease. 

The  throat  manifestations,  as  a  rule,  do  not  call  for  special  treatment, 
but  cleansing  preparations  should  always  be  used — to  reduce  if  possible 
the  bacterial  content  of  the  throat,  but  more  especially  to  remove  all 
secretion  that  may  tend  to  obstruct  the  inlet  to  the  Eustachian  tube 
and  thus  favor  the  development  of  middle-ear  disease.  Normal  salt 
solution,  Dobell's  solution,  hydrogen  peroxide  (15  per  cent),  potassium 
chlorate  (2  per  cent.),  or  potassium  permanganate  (2  per  cent.),  may  be 
used  for  this  purpose.  Many  physicians  are  partial  to  the  use  of  iron 
which  may  be  employed  as  follows :  Tincture  of  iron  chloride  (^  ounce, 
15  c.c),  glycerin  (^  ounce,  15  c.c),  and  water  (1  ounce,  30  c.c).  10  to 
15  minims  of  carbolic  acid  may  be  added  to  the  mixture.  In  severer 
cases  Loffler's  solution  is  serviceable:  Menthol,  10  c.c;  toluol,  36  c.c; 
tincture  of  iron  chloride,  4  c.c;  and  absolute  alcohol,  60  c.c.  This  may 
be  applied  by  means  of  a  cotton  swab.  Should  cultures  from  the  throat 
reveal  the  diphtheria  bacillus  antidiphtheritic  serum  should  be  used 
without  delay. 

During  desquamation  the  child  should  be  bathed  daily  with  warm 
water  and  an  antiseptic  soap  and  then  annointed  with  vaseline  or  oil. 
Especial  attention  should  be  paid  to  the  ears,  and  in  the  event  of  pain 
appropriate  measures,  including  early  puncture  of  the  drum  membrane, 
should  be  instituted  so  as  to  obviate,  if  possible,  deafness  in  later  life. 
Iron  and  the  bitter  tonics  are  useful  during  convalescence.  The  child 
should  be  confined  to  the  bed  for  at  least  ten  days  after  the  temperature  is 
normal.  During  the  entire  convalescence  one  should  always  be  guided 
by  the  knowledge  that  nephritis  may  develop  (after  exposure)  three  or 
more  weeks  after  the  temperature  has  reached  the  normal,  and  that  the 


MEASLES  247 

child  is  perhaps  infectious  as  long  as  there  is  any  desquamation  and  cer- 
tainly as  long  as  a  naso-pharyngeal  or  aural  discharge  persists.  The 
complications  are  to  be  treated  on  general  principles. 


MEASLES. 

(MorbilH;  Rubeola.) 

Measles  is  an  acute,  specific,  infectious,  and  highly  contagious  disease 
characterized  by  catarrhal  inflammation  of  the  conjunctivae  and  the 
respiratory  mucous  membrane,  fever,  and  a  peculiar  maculopapular 
rash. 

Etiology. — Measles  is  essentially  a  disease  of  childhood,  attacking  the 
sexes  equally,  and  being  especially  prevalent  between  the  second  and  the 
eighth  year.  It  is  unusual  under  six  months  of  age,  but  it  is  more  common 
in  non-immune  adults  than  certain  other  infective  diseases,  such  as 
scarlatina.  Recurrences  are  not  uncommon,  but  one  attack  usually 
confers  immunity.  In  many  large  cities  the  disease  is  endemic,  and  it 
frequently  prevails  epidemically,  especially  during  the  fall  and  winter. 

The  exciting  cause  of  the  disease  has  not  been  isolated,  although  it 
seems  to  be  present  in  the  emanations  from  the  patient,  especially  the 
breath,  the  nasopharyngeal  secretions,  and  the  desquamations.  The 
disease  is  highly  contagious  and  spreads  with  extreme  rapidity.  Infec- 
tion may  be  transmitted  directly,  or  by  a  third  person,  or  by  fomites. 
It  is  acquired  through  inhalation,  and  is  much  favored  by  overcrowding, 
such  as  obtains  in  close,  unsanitary  dwellings,  school-rooms,  etc. 

Pathology. — Measles  is  devoid  of  characteristic  lesions.  Catarrh  of  the 
conjunctivae  and  the  respiratory  mucous  membrane  and  hyperemia  of 
the  skin  with  slight  if  any  cellular  exudation  occur.  In  severe  and  fatal 
cases  bronchopneumonia,  capillary  bronchitis,  atelectasis,  pleuritis,  and 
swelling  of  the  bronchial  lymph  nodes  and  of  the  mucous  membrane  of 
the  gastro-intestinal  tract  may  be  encountered. 

Symptoms. — The  period  of  incubation  is  from  seven  to  fourteen  or 
eighteen  days,  the  average  being  about  ten  days.  The  invasion,  usually, 
is  rather  abrupt,  with  chilliness  (or  convulsions  or  vomiting  in  infants) 
moderate  fever,  101°  to  102°  V.  (Fig.  14),  well-marked  coryza,  and 
catarrhal  inflammation  of  the  conjunctivae  and  the  respiratory  mucous 
membrane.  The  child  appears  to  suffer  from  a  cold  in  the  head.  It  has 
a  profuse  nasal  discharge,  its  eyes  are  injected,  it  complains  of  headache, 
photophobia,  lacrymation,  and  sneezes  frecjuently.  Within  twenty-four 
hours,  as  a  result  of  extension  of  the  catarrhal  inflammation  to  the 
pharynx  and  bronchi,  a  cough  develops.  The  fever  and  catarrhal 
manifestations  continue  and  lead  to  anorexia,  increase  of  the  cough  with 
bronchial  secretion,  wheezing,  and  dyspnoea.  There  is  usually  a  slight 
remission  of  fever  on  the  second  and  third  days. 

On  the  fourth  flay  when  the  general  symptoms  are  at  their  height, 
and  the  fever  often  103°  to  104°  F.,  the  characteristic  eruption  appears, 


248 


INFECTIONS  OF   UNKNOWN  ETIOLOGY 


first  on  the  forehead  or  cheeks,  and  spreads,  within  a  very  short  time, 
over  the  entire  body.  The  eruption  consists  of  minute  purphsh-red 
papules,  which  are  slightly  elevated,  and  tend  to  coalesce  to  form  cres- 
centic  figures  with  intervening  areas  of  clear  skin,  giving  rise  to  a 
blotched  or  mottled  appearance.  Usually  confluent,  the  eruption  may 
remain  discrete,  especially  on  the  trunk  and  limbs.  In  severe  cases  it 
is  quite  dusky  in  appearance  and  the  affected  skin  is  much  swollen. 
Being  hyperemic,  it  usually  disappears  on  pressure,  but  hemorrhages  may 
occur.  In  most  cases  there  is  usually  swelling  of  the  lymph  nodes, 
especially  those  of  the  neck. 


Fig.   14 


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The  temperature  curve  in  measles,  complicated  by  pneumonia,  in  a  boy,  aged  five  years 

(Tuley.) 


Preceding  the  rash  by  twenty-four,  sometimes  forty-eight,  hours  or 
more,  the  Filatow-Koplik  spots,  a  characteristic  feature  of  the  disease, 
may  be  observed  on  the  buccal  and  the  labial  mucous  membrane. 
These  consist  of  small,  irregular  spots  of  bright  red  color,  in  the  centre 
of  which,  in  strong  daylight,  a  minute  bluish  speck  may  be  seen. 

By  the  fifth  day,  in  the  majority  of  cases,  the  fever,  the  general  symp- 
toms, and  the  eruption  have  reached  their  height.  By  the  sixth  or  seventh 
day,  after  having  lasted  two  or  three  days,  the  rash  begins  to  fade  as  it 
developed,  from  the  face  first,  and  it  is  succeeded  by  a  branny  desquam-. 
ation.  The  nasal  discharge  lessens,  the  cough  becomes  looser,  and  there 
may  be  free  expectoration.  By  the  eighth  day,  usually,  the  temperature, 
having  fallen  by  rapid  lysis,  is  normal  and  convalescence  is  established. 


MI'JASLES  249 

Varieties. — in  unusual  or  atypical  cases,  the  rash  may  occur  unusually 
early,  within  thirty-six  hours,  or  it  may  be  unduly  delayed  (sixth  day). 
In  other  cases  of  house  epidemics  the  child  may  manifest  the  initial 
coryza  and  no  eruption  at  all  may  appear.  Hemorrhagic  measles  is  a 
severe  infection,  attended  by  petechial  eruption,  sometimes  hemorrhages 
from  the  mucous  membranes,  and  marked  prostration  from  toxemia. 
It  is  often  fatal,  and  occurs  usually  in  institutions  or  barracks  where 
the  sanitary  arrangements  are  bad. 

Complications  and  Sequels. — Capillary  bronchitis  or  bronchopneumonia, 
which  is  responsible  for  most  of  the  fatalities,  with  atelectasis,  may 
result  from  extension  of  the  ordinary  bronchitis.  The  less  common 
complications  are  lobar  pneumonia,  pleuritis,  severe  catarrhal  pseudo- 
membranous inflammation  of  the  mouth  and  larynx,  oedema  of  the  glottis, 
catarrhal  inflammation  and  suppuration  of  the  middle  ear,  gastro- 
enteritis, gangrene  of  the  mouth,  vulva,  etc.  Tuberculosis  of  the  lungs 
and  of  the  bronchial  and  mediastinal  lymph  nodes  is  an  important  and 
not  infrequent  sequel.  Arthritis  and  paralysis  due  to  myelitis  and 
multiple  neuritis  (polyneuritis)  have  been  observed. 

Diagnosis. — The  diagnosis  is  usually  easy.  The  presence  of  an  epi- 
demic, initial  coryza,  fever,  and  catarrh  of  the  respiratory  mucous 
membrane,  suggest  the  disease,  even  before  the  appearance  of  the  path- 
ognomonic Filatow-Koplik  spots  and  the  characteristic  eruption.  From 
scarlatina  measles  may  be  distinguished  by  the  longer  preeruptive  stage, 
the  general  catarrhal  symptoms  (instead  of  mere  sore  throat),  the 
Filatow-Koplik  spots,  the  blotched  or  mottled  appearance  of  the  rash 
with  special  involvement  of  the  face  (as  distinguished  from  the  more 
uniform  erythema  of  scarlatina  with  relative  freedom  of  the  face),  the 
absence  of  leukocytosis  (except  in  the  event  of  complications),  the 
absence  of  undue  acceleration  of  the  pulse,  absence  of  the  characteristic 
scarlatinal  tongue^  and  the  fall  of  temperature  after  the  rash  is  well  out. 

It  may  he  difficult  or  impossible  in  some  cases  to  differentiate  measles 
from  rotheln,  but  rotheln  is  suggested  by  less  fever,  shorter  preeruptive 
stage  (one  or  two  days),  less  catarrhal  symptoms,  more  sore  throat, 
general  uniform  distribution  of  the  rash,  absence  of  crescentic  arrange- 
ment, and  very  slight  desfjuamation.  The  presence  of  fever  and  catarrhal 
symptoms  serve  to  differentiate  measles  from  urticaria  and  multiform 
erythema,  as  well  as  from  different  drug  eruptions,  in  which  the  history 
also  may  be  of  service.  The  initial  eruption  of  smallpox  may  be  mis- 
taken for  measles,  V)ut  the  differential  diagnosis  does  not  long  remain  in 
abeyance.  Four  days  of  fever  and  catarrh  usually  exclude  variola, 
varicella,  rotheln,  and  scarlatina. 

Prognosis. — The  prognosis  is  favorable  in  simple  cases.  Complica- 
tions, such  as  bronchopneumonia,  hemorrhagic  rash,  etc.,  render  the 
prognosis  grave. 

Treatment. — Hygienic  regulations  (page  29),  rest  in  bed,  and  light 
nutritious  diet  are  most  important.  Otherwise  the  treatment  is  purely 
symptomatic.      The    fever    is   rarely  high    enough    to  demand    special 


250  Infections  of  unknown  etiology 

attention,  but  the  general  comfort  of  the  child  may  be  enhanced  by  daily 
tepid  sponging  or  a  tepid  bath,  especially  if  the  temperature  is  about 
103°  F.  Should  the  rash  not  appear,  a  hot  bath  and  warm  drinks  will 
please  the  elderly  nurse  and  do  no  harm:  they  are  believed  to  hasten 
the  development  of  rash.  The  distressing  cough  and  the  general  con- 
dition of  the  child  may  be  relieved  by  a  mild,  sedative  and  diaphoretic 
fever  mixture,  such  as  the  following: 

I^ — Spirit  of  nitrous  ether 3  drams  12  00 

Camphorated  tincture  of  opium 2  drams  8  00 

Wine  of  ipecac 1  dram  4  00 

Solution  of  ammonium  acetate,  sufficient  to  make  .       .      3  ounces  100  00 — M. 

S. — To  a  child,  two  years  old,  one  teaspoonful  (5  e.c.)  every  three  hours. 

During  desquamation  the  skin  should  be  anointed  daily  with  vaseline, 
olive  oil,  or  cacao  butter,  and  the  daily  bath  continued.  Great  care 
must  be  exercised  during  convalescence,  especially  if  the  child  is  weakly. 
Nutritious  diet,  milk,  tonics,  such  as  iron,  quinine,  and  strychnine, 
hj-pophosphites,  and  cod-liver  oil  subserve  a  useful  purpose. 


ROTHELN. 

(Rubella;  German  Measles;  Rubella  Notha;  Epidemic  Roseola.) 

Rotheln  is  an  acute,  specific,  infectious,  and  highly  contagious  disease 
characterized  by  slight  fever,  coryza,  and  a  maculopapular  rash. 

Etiology. — Rotheln  occurs  during  childhood  and  in  adult  life,  but  it 
is  more  common  during  childhood,  and  attacks  the  sexes  equally. 
Sporadic  cases  are  common,  but  the  disease  often  appears  epidemically. 
One  attack  usually  confers  immunity,  but  recurrences  have  been  observed. 

The  exciting  cause  of  the  disease  has  not  been  isolated,  though  it 
seems  to  be  present  in  the  emanations  from  the  patient,  especially  the 
nasal  and  oral  discharges  and  the  skin  lesions.  The  disease  is  highly 
contagious  and  spreads  with  extreme  rapidity.  Infection  may  be  trans- 
mitted by  direct  contact,  by  a  third  person,  and  by  fomites.  Infection 
is  acquired  by  inhalation.  The  patient  is  infectious  from  the  period  of 
incubation  until  convalescence. 

Pathology. — ^There  are  no  characteristic  anatomical  lesions. 

Symptoms. — The  period  of  incubation  is  usually  from  ten  to  twelve 
days,  but  it  has  been  reported  to  vary  between  three  days  and  three  weeks. 
The  invasion  is  usually  mild,  and  may  be  devoid  of  prodromal  symp- 
toms, although  chilliness,  mild  fever  (rarely  more  than  100°  F.),  malaise, 
headache,  backache,  coryza,  sore  throat,  and  dry  cough  may  be  observed 
for  a  day  or  two.  Usually  on  the  second  day,  that  is,  at  the  end  of  the 
first  twenty-four  hours  (sometimes  earlier),  the  characteristic  rash  ap- 
pears— first  on  the  oral  and  faucial  mucous  memlirane  and  the  face, 
then  on  the  chest,  and  within  twenty-four  hours  spreads  over  the  entire 
body.     In  some  cases,  however,  it  remains  curiously  restricted  to  certain 


ROTHELM  ^51 

parts  of  the  body,  and  may  be  observed  only  on  the  roof  of  the  mouth 
and  the  fauces.  The  eruption  consists  of  rosy-red,  sHghtly  elevated 
papules,  that  are  usually  discrete,  though  they  may  become  confluent. 
They  show  little  tendency  to  form  crescentic  patches,  and  the  intervening 
skin  is  often  hyperemic.  With  or  just  before  the  appearance  of  the  rash 
the  temperature  may  become  a  little  more  elevated,  and  it  remains 
usually  between  100°  and  102°  F.  while  the  rash  is  out;  the  pulse  is 
proportionately  rapid;  coryza,  conjunctivitis,  sore  throat,  and  evidences 
of  bronchitis  become  more  marked ;  and  the  cervical  lymph  nodes  (rarely 
other  lymph  nodes)  are  enlarged.  The  rash  lasts  usually  two  to  five 
days,  gradually  fades,  and  is  succeeded  by  a  very  slight  branny  desquama- 
tion and  a  brownish  discoloration  of  the  skin,  which  disappears  after 
a  day  or  two.  With  the  fading  of  the  rash  the  general  symptoms  lessen, 
and  convalescence  is  usually  established  at  the  end  of  a  week. 

Complications. — Severe  bronchitis  and  bronchopneumonia  sometimes 
occur. 

Diagnosis. — Considerable  confusion  in  diagnosis  often  occurs,  inasmuch 
as  rotheln  exhibits  the  sore  throat  of  scarlatina  and  the  rash  of  measles. 
From  measles,  however,  rotheln  may  be  distinguished  by  the  less  fever, 
shorter  preemptive  stage,  less  catarrhal  symptoms,  more  sore  throat, 
general  uniform  distribution  of  the  rash,  absence  of  crescentic  arrange- 
ment, and  very  slight  desquamation.  From  scarlatina  rotheln  may  be 
distinguished  by  the  less  abrupt  onset,  less  high  fever,  less  rapid  pulse, 
absence  of  vomiting,  absence  of  the  strawberry  tongue,  absence  of  a 
punctiform  rash,  and  the  non-occurrence  of  nephritis.  Dukes'  so-called 
"fourth  disease"  is  a  disorder  of  which  the  incubation  period  is  that  of 
German  measles;  prodromes  are  usually  absent;  the  onset  is  abrupt, 
with  moderate  fever,  sore  throat,  and  a  rash  that  may  cover  the  body 
within  a  few  hours,  although  the  face  may  remain  free;  the  rash  is 
brighter  red  than  that  of  scarlatina,  and  may  be  followed  by  slight 
desquamation  (more  than  in  rotheln),  rarely  by  marked  desquamation; 
there  are  no  sequels;  and  the  disease  does  not  protect  against  rotheln 
or  scarlet  fever.  Whether  or  not  it  is  an  independent  disease  has  not 
been  determined.  Infectious  erythema  is  a  disorder  described  by  Esch- 
erich,  and  characterized  by  a  rose-red,  maculopapular  (morbilliform) 
rash  developing  especially  on  the  face  and  the  flexor  surfaces  of  the 
extremities;  it  occurs  epidemically  in  children  between  the  ages  of  four 
and  twelve  years;  there  may  be  no  subjective  symptoms;  the  rash 
usually  fades  in  five  to  six  or  ten  days,  and  is  not  followed  by  des- 
quamation. 

Prognosis. — Recovery  is  the  rule. 

Treatment. — The  treatment  is  similar  to  that  of  measles. 


252  IXFECTIOXS   OF    UXKXOWX   ETIOLOGY 

GLANDULAR  FEVER. 

{Dru-senfieber,  Pfeiffer.) 

Glandular  fever  is  an  acute,  infectious,  and  moderately  contagious  dis- 
ease, characterized  by  fever  and  swelling  and  tenderness  of  the  lymph 
nodes. 

Etiology. — Glandular  fever  is  essentially  a  disease  of  childliood, 
though  a  few  cases  have  been  observed  in  adults.  It  often  prevails 
epidemically,  especially  in  the  late  fall,  the  winter,  and  the  spring,  but 
sporadic  cases  are  sometimes  observed.  A  specific  exciting  cause  of  the 
disease  has  not  been  isolated.  Streptococci,  staphylococci,  influenza 
bacilli,  and  pneumococci  have  been  found  in  the  oral  secretions  in 
dilTerent  cases,  and  suggest  the  opinion  that  the  disease  is  probably  not 
always  due  to  the  same  cause.  The  disease  is  contagious,  but  how 
the  contagium  is  transmitted  has  not  been  determined  with  certainty. 
Infection  is  believed  to  be  acquired  by  inhalation,  the  causative  bacteria 
acquiring  a  nidus  in  the  mouth  and  the  upper  respiratory  tract,  whence 
they  readily  gain  access  to  the  regional  iMXiph  nodes. 

Pathology. — The  conspictiotis  feature  of  the  disease  is  inflammatory 
.swelling  of  the  lymph  nodes,  especially  the  cervical,  biu  sometimes  also 
the  axillary,  inguinal,  and  mesenteric. 

Symptoms. — The  period  of  incubation  is  not  definitely  known,  biU 
it  is  probably  several  days.  The  onset  is  usually  abrupt,  with  chill  or 
chilliness,  fever  (101°  to  103°  F.),  headache,  restlessness,  sometimes 
nausea  and  vomiting,  and  pain  in  the  neck,  especially  on  motion.  Some- 
times there  is  complaint  of  sore  throat,  and  slight  swelling  and  redness  of 
the  tonsils  may  be  discovered.  Usually  on  the  second  day  the  enlarged 
lymph  nodes  become  apparent — swollen,  painftd,  varying  in  size  from  that 
of  a  pea  to  a  walnut,  and  not  infrequently  associated  with  periglandular 
oedema.  Cough  and  oppression  in  the  chest  sometimes  suggest  involve- 
ment of  the  bronchial  lymph  nodes.  The  mesenteric  nodes  are  some- 
times palpable,  and  explain  the  rather  common  abdominal  pain  and  ten- 
derness. The  bowels  are  tisually  constipated,  and  pains  in  the  joints  are 
not  infrequent.  The  fever  continties,  as  a  rule,  about  a  week  and  falls 
by  lysis;  the  lymph-node  enlargement  lasts  from  two  to  three  weeks,  and 
gradually  subsides.  Suppuration  is  rare.  Cutaneous  erythemas,  otitis 
media,  bronchopneumonia,  and  nephritis  are  the  more  common  com- 
plications, and  are  answerable  for  the  few  fatalities. 

Diagnosis. — The  diagnosis  is  tisually  easy,  but  occasionally,  especially 
in  the  event  of  the  cutaneous  rash,  one  must  be  careful  to  exclude  scar- 
latina. 

Treatment. — Rest  in  bed  during  the  period  of  fever  at  least,  a  Ucjuid 
diet,  an  antiseptic  mouth  wash,  a  preliminary  course  of  calomel,  and  a 
mild  diuretic  fever  mixttire  (such  as  that  mentioned  on  page  250)  are  all 
that  are  required— since  we  ar?  unable  directly  to  influence  the  duration 
of  the  disease;  Init  one  should  endeavor  to  preveiu  complications. 


RHEUMATIC  FEVER  253 

RHEUMATIC  FEVER. 

{Acute  and  Subacute  Rheumatism;  Articular  Rheumatism.) 

Rheumatic  fever  is  an  acute  and  subacute  (possibly  specific)  infectious 
and  non-contagious  disease,  characterized  by  fever,  multiple  arthritis, 
sweating,  and  a  tendency  to  inflammation  of  the  serous  membranes  and 
the  fibrous  tissues  of  the  body. 

Etiology. — Rheumatic  fever  occurs  especially  in  adults  between  the 
ages  of  fifteen  and  thirty-five  years,  but  no  age  is  exempt,  and  the  disease 
has  been  observed  in  very  young  children.  In  children,  however, 
the  arthritic  manifestations  are  often  quite  subsidiary  to  the  cardiac. 
The  disease  is  especially  common  in  those  exposed  to  the  influences  of 
wet,  cold,  and  sudden  changes  in  temperature — hence  males  rather  than 
females,  and  among  men,  laborers,  coachmen,  drivers,  sailors,  etc., 
and  among  women,  serving-maids,  washerwomen,  etc.  Between  the 
ages  of  ten  and  fifteen  years,  however,  girls  are  more  commonly  affected, 
while  prior  to  the  tenth  year  the  sexes  suffer  equally.  The  disease  is 
endemic  in  temperate  climates,  and  prevails  especially  during  February, 
March,  and  April,  but  also  during  the  colder  months.  Occasionally 
it  exhibits  epidemic  characteristics.  One  attack,  rather  than  conferring 
immunity,  predisposes  to  subsequent  attacks. 

The  exciting  cause  of  the  disease  has  not  been  isolated,  although 
etiological  importance  has  been  attributed  to  a  number  of  different 
microorganisms,  and  the  anatomical  and  clinical  characteristics  of  the 
disease  permit  of  no  doubt  of  its  being  an  infection.  Possibly  the  same 
etiological  factor  is  not  operative  in  all  cases,  and  we  may  yet  be  able 
to  differentiate  a  true  rheumatic  fever  from  other  pseudorheumatic, 
pyemic,  or  toxic  disorders  with  arthritic  manifestations.  Although  the 
disorder  has  been  attributed  to  streptococci,  staphylococci,  etc.,  the  most 
likely  causative  factor  is  a  diplococcus  studied  by  Poynton  and  Paine, 
who  isolated  it  from  the  joint  lesions,  the  rheumatic  nodules,  the  blood, 
etc.,  and  were  able  to  produce  arthritis,  valvulitis,  etc.,  in  rabbits.  How 
infection  is  acquired  has  not  been  definitely  determined  for  all  cases,  but 
there  is  an  increasing  disposition  to  regard  the  tonsils  as  the  portals  of 
entry  for  the  infection  in  many,  if  not  all,  cases:  the  clinical  relation 
is  undoubted. 

Pathology. — The  inflammatory  manifestations  in  the  joints,  serous 
membranes,  and  fibrous  tissues  exhibit  scarcely  anything  characteristic, 
with  the  possible  exception  of  the  rheumatic  nodule  (found  in  tendon 
sheaths  and  over  bony  prominences),  which  consists  of  a  central  area 
of  necrosis,  surrounded  by  swollen  and  (^edematous  connective  tissue 
and  cellular  exudation.  The  articular  fluid  is  turl)id,  albuminous,  and 
usually  contains  a  few  fibrin  flakes  and  leukocytes. 

Symptoms. — The  period  of  incubation  is  not  definitely  known.  Pro- 
dromes, such  as  malaise,  irregular,  fugitive  pains,  and  sore  throat  (ton- 
sillitis) may  be  present  for  a  few  hours  or  a  day  or  two;  but,  as  a  rule,  the 


254  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

disease  sets  in  abruptly  with  chilliness  (occasionally  a  definite  chill),  fever, 
and  inflammatory  manifestations  in  one  or  several  joints.  The  affected 
joints  are  usually  the  larger  joints — the  knee,  ankle,  shoulder,  elbow, 
and  wrist;  less  commonly  the  hip,  fingers,  toes,  and  intervertebral  joints. 
They  are  swollen,  red,  hot,  painful,  and  tender;  motion  is  much  restricted 
and  when  made  aggravates  the  pain.  A  characteristic  of  the  joint  lesions 
is  their  fugaciousness,  the  fact  that  the  inflammatory  phenomena  some- 
times develop  and  subside  with  marked  rapidity  (but  sometimes  more 
slowly),  and  that  they  flit  from  one  joint  to  another.  In  different  cases, 
therefore,  at  one  time,  one  or  several  joints  may  be  involved  in  varying 
degrees.  In  some  cases,  later  in  the  course  of  the  disease,  the  lesions 
show  a  disposition  to  linger  in  certain  joints.  It  is  rare,  however,  for 
a  single  joint  only  to  be  involved.  Intra-articular  effusion  is  usually 
slight  or  moderate,  the  marked  swelling  of  the  joint  being  due  largely  to 
serous  infiltration  of  the  periarticular  tissues — the  tendon  and  muscular 
sheaths,  bursse,  etc.  Rheumatic  nodules  (misnamed  fibrous  nodules)  are 
present  in  some  cases,  and  are  of  much  diagnostic  importance.  They  are 
more  common  in  children  than  in  adults,  and  consist  of  small  swellings 
(1  to  4  mm.  in  diameter)  attached  to  bony  prominences  (the  periosteum) 
or  tendon  sheaths  just  beneath  the  skin — the  hands,  wrists,  elbows, 
vertebrae,  etc.  They  are  sometimes  more  apparent  to  sight  than  to 
touch,  are  usually  not  tender,  and  sometimes  appear  and  disappear  with 
marked  rapidity,  although  they  may  last  for  a  long  time  (when  they 
really  become  fibrous  nodules). 

The  general  manifestations  of  rheumatic  fever  are  usually  subsidiary 
to  the  articular.  The  fever,  as  a  rule,  varies  from  102°  to  104°  F., 
though  hyperpyrexia  (106°  to  108°  F.)  is  occasionally  observed  in  severe 
cases.  The  fever  pursues  an  irregular  course  and  ends  by  lysis.  The 
pulse  is  rapid  (above  100)  and  soft;  other  symptoms  of  toxemia  are 
present,  such  as  loss  of  appetite,  thirst,  coated  tongue,  constipation, 
enlargement  of  the  spleen,  and  concentrated  urine  (which  is  usually 
highly  acid  and  may  be  albuminous).  Profuse  acid  sweats  of  a  peculiar 
odor  are  the  rule  and  often  correspond  with  remissions  in  the  tempera- 
ture; and  sudamina  and  milaria  are  common.  Leukocytosis  is  present; 
a  secondary  anemia  usually  develops  rapidly. 

Complications. — Complications  are  many,  though  doubtless  many 
lesions  heretofore  regarded  as  complications  are  really  part  and  parcel 
of  the  rheumatic  fever  (manifestations  of  the  rheumatic  poison) ;  but  some 
are  the  result  of  secondary  infection.  Hyperpyrexia  (108°,  even  110°  F.) 
is  occasionally  observed,  especially  in  primary  attacks.  It  is  a  serious 
symptom,  usually  associated  with  severe  nervous  manifestations,  such  as 
delirium,  rapid  pulse,  marked  prostration,  and  frequently  soon  leads  to 
death.  The  term  "cerebral  rheumatism"  has  been  given  to  some 
cases  in  which  toxic  (nervous)  symptoms  are  severe,  usually  from  the 
beginning.  To  the  high  fever,  delirium,  and  rapid  pulse,  evidences  of 
motor  irrital^ility  (tonic  spasms,  sometimes  general  convulsions)  may  be 
added;  these  are  often  followed  by  coma  and  death,     The  brain  at 


RHEUMATIC  FEVER  255 

necropsy  usually  reveals  no  lesions;  in  some  cases  meningitis  (purulent 
and  other)  has  been  found;  but  these  cases  were  probably  not  true 
rheumatic  fever,  the  joint  lesions  being  pyemic  and  improperly  inter- 
preted clinically.  Delirium  and  coma  may  occur  without  hyperpyrexia — 
being  in  some  cases  uremic.  Chorea  may  occur  in  association  with  or  as 
a  sequel  to  rheumatic  fever.  Cardiac  complications  are  the  most  com- 
mon, and  in  many  respects  the  most  serious.  Myocarditis  (toxic)  is 
common  in  the  early  stages  and  often  leads  to  dilatation.  Endocarditis 
occurs  in  many  cases  (50  to  75  per  cent.),  and  its  likelihood  increases 
with  the  youth  of  the  patient  and  the  number  of  attacks.  The  lesions 
most  frequently  involve  the  mitral  valve,  and  may  be  benign  (usually) 
or  malignant  (unusually).  Often  the  lesions  are  mild  and  overlooked, 
and  are  not  detected  until  later  in  life,  when  sclerotic  changes  in  the  valve 
segments  have  occurred.  Many  of  the  murmurs  that  develop  during 
rheumatic  fever,  however,  are  not  attributable  to  endocarditis,  but  to 
dilatation  of  the  heart  or  the  very  common  anemia,  and  they  disappear 
with  convalescence.  Pericarditis  is  not  uncommon,  and  is  found  in 
most  fatal  cases.  It  may  be  fibrinous,  serofibrinous,  or  purulent.  In 
many  cases  the  lesions  constitute  a  pancarditis.  Serous  pleuritis  and 
even  serous  peritonitis  may  also  occur,  and  two  or  more  serous  mem- 
branes may  be  involved  simultaneously — a  multiple  serositis.  Con- 
gestion of  the  lung  and  pneumonitis  a?e  observed  in  some  cases  and 
may  prove  fatal.  Tonsillitis  and  pharyngitis  are  sometimes  marked; 
nephritis  is  rare.  Different  skin  lesions  have  been  observed — sudamina, 
miliaria  (already  mentioned),  urticaria,  multiform  erythema,  scarlatini- 
form  rash,  purpura,  etc. ;  so-called  purpura  (peliosis)  rheumatica  is  really 
not  a  rheumatic  affection.  The  muscles  are  often  swollen  and  painful, 
and  sometimes  become  atrophic  (arthritic  atrophy). 

Rheumatic  fever  in  children  usually  sets  in  abruptly  with  high  fever, 
and  sometimes  convulsions.  It  involves  the  joints,  as  a  rule,  less  than 
the  heart — myocarditis  (with  dilatation),  endocarditis,  pericarditis; 
anemia  and  exhaustion  develop  apace,  and  if  the  child  does  not  soon  die, 
the  fatal  termination  from  valvular  disease,  etc.,  is  usually  merely  a 
question  of  time.  Aberrant  rheumatism  is  quite  common  in  children — 
growing  pains,  stiff  neck,  recurring  tonsillitis,  etc. 

Diagnosis. — The  diagnosis  is  usually  quite  apparent  from  the  fever, 
polyarthritis  (and  its  peculiarities),  acid  sweats,  and  the  rarity  of  in- 
volvement of  the  temporomaxillary,  sternoclavicular,  sacro-iliac,  intra- 
vertebral,  and  pubic  joints.  Gonorrhoeal  arthritis  maybe  distinguished 
by  a  history  of  gonorrhoea;  involvement  of  one  joint  often  (especially 
the  knee  or  wrist),  although  several  joints  may  be  involved;  severity  of 
the  local  lesions — extreme  pain  and  marked  swelling  due  chiefly  to  peri- 
articular oedema;  persistence  of  the  articular  lesions — often  leading  to 
more  or  less  permanent  disability  of  the  joint;  relative  absence  of  general 
symptoms — little  fever,  etc.  Acute  osteomyelitis,  involving  especially  the 
lower  end  of  the  femur  or  the  upper  end  of  the  tibia,  may  be  distinguished 
by  the  involvement  of  the  epiphysis  and  shaft  of  the  bone  (rather  than  the 


256  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

articulating  surfaces),  the  great  intensity  of  the  local  signs,  and  the 
grave  constitutional  symptoms  (pyococcic).  Acute  arthritis,  such  as  may 
occur  in  infants,  in  scarlatina,  in  cerebrospinal  meningitis,  in  puerperal 
infection,  etc.,  is  usually  septic  in  character  (pyococcic),  may  go  on  to 
suppuration,  and  is  attended  by  the  usual  symptoms  of  septicemia — 
chills,  fever,  sweating,  etc.,  and  a  focus  of  infection  may  often  be  demon- 
strable. If  not  pyococcic,  the  so-called  acute  rheumatic  joints  of  chil- 
dren are  likely  to  be  syphilitic  or  scorbutic.  Gout  may  be  distinguished 
by  its  occurrence  in  males  (especially  beyond  the  fiftieth  year),  its  char- 
acteristic onset,  predilection  for  the  great  toe  (though  other  joints  are 
often  involved),  uratic  deposits  in  the  body,  and  an  analysis  of  the  urine. 

Prognosis. — Rheumatic  fever  is  very  variable  in  its  course,  though  it 
usually  terminates  in  recovery  without  permanent  damage  to  the  joints 
in  from  two  to  six  weeks.  In  some  cases,  however,  recovery  is  less 
rapid,  and  exacerbations  of  fever  and  articular  lesions  recur  from  time  to 
time — ^subacute  rheumatic  fever.  The  prognosis  is  worse  in  children  than 
in  adults,  and  in  both  is  influenced  by  the  occurrence  of  complications — 
some  of  which,  such  as  hyperpyrexia  and  purulent  pericarditis,  are 
immediately  serious,  whereas  others,  such  as  endocarditis,  are  of  more 
remote  concern.     One  attack  predisposes  to  others. 

Treatment. — ^The  patient  should  be  confined  to  bed,  even  in  the  mild 
cases,  and  should  wear  a  flannel  night  gown  and  sleep  between  blankets. 
The  diet  should  consist  largely  of  milk,  but  broths  and  soups  may  be 
allowed,  and  water  should  be  given  in  large  quantities.  Salicylic  acid 
and  its  derivatives  exert  a  more  or  less  specific  action  and  should  be  given 
in  full  doses  at  the  outset  in  all  cases  with  the  idea  of  obtaining  an 
immediate  effect.  In  a  case  of  average  severity  in  an  adult  sodium 
or  ammonium  salicylate,  aspirin,  salicin,  salicylic  acid,  or  other 
well-known  salicyl  compounds,  should  be  administered  in  20  grain 
(1.3  gram)  doses,  every  two  hours,  until  the  symptoms  abate  or 
manifestations  of  salicyl  intoxication  supervene.  By  the  third  day 
usuallv  the  dose  may  be  reduced  to  15  grains  (1  gram)  every  four  or 
five  hours.  If  symptoms  of  marked  intoxication  (tinnitus  aurium,  gastric 
irritability,  delirium  in  some  cases),  supervene,  the  drug  may  be  with- 
drawn for  twelve  to  eighteen  hours.  Oil  of  wintergreen  in  20  minim 
(1.25  c.c.)  doses  may  be  substituted  for  the  other  salicyl  compounds. 
Should  the  attack  not  respond  to  the  salicylates,  the  so-called  alkaline 
treatment  may  be  employed,  or  both  may  be  used  together — a  form  of 
treatment  especially  serviceable  in  children.  To  an  adult  30  grains 
(2  grams)  of  potassium  bicarbonate  may  be  given  every  two  or  three 
hours  for  the  first  few  days  or  until  the  urine  is  alkaline;  or  potassium 
acetate  or  citrate  or  sodium  bicarbonate  may  be  used.  The  salicyl 
treatment  seems  to  relieve  the  joint  symptoms,  to  shorten  the  course  of 
the  disease,  to  render  relapse  less  likely,  and  to  protect  the  heart,  although 
endocarditis  appears  to  be  less  common  under  the  alkaline  treatment. 
With  a  view  to  protect  the  heart,  Caton  urges  the  use  of  small  blisters 


PERTUSSIS  257 

applied  successively  along  the  course  of  the  third,  fourth,  fifth,  and 
sixth  left  intercostal  nerves. 

Attention  to  the  local  articular  symptoms  is  of  the  utmost  importance ; 
but  of  all  forms  of  treatment  suggested,  none  is  so  valuable  as  absolute 
rest.  Under  the  beneficent  influence  of  rest  enjoined  by  a  splint  the 
local  pain  and  tenderness  often  subside  almost  immediately.  In  addi- 
tion the  joint  may  be  wrapped  in  cotton  wool,  or  in  cloths  saturated  with 
lead  water  and  laudanum,  or  a  saturated  solution  of  magnesium  sul- 
phate; or  an  ointment  of  methyl  salicylate  (20  per  cent.)  may  be  applied. 
Occasionally  the  pain  is  so  severe  as  to  call  for  the  use  of  morphine, 
especially  at  night.  In  this  event  a  Dover's  powder  is  often  serviceable. 
The  coal  tar  products  are  scarcely  ever  necessary.  Hyperpyrexia  calls 
for  the  cold  bath  or  the  cold  pack.  Since  anemia  usually  develops 
rapidly,  iron  is  practically  always  indicated  during  convalescence,  when 
quinine  and  strychnine  will  be  found  useful  adjuvants. 


PERTUSSIS. 

(Whooping  Cough.) 

Pertussis  is  a  subacute,  specific,  infectious,  and  moderately  contagious 
disease,  characterized  by  catarrhal  inflammation  of  the  respiratory 
mucous  membrane  and  paroxysms  of  convulsive  coughing  that  terminate 
in  a  protracted  inspiration — the  "whoop." 

Etiology. — Pertussis  is  essentially  a  disease  of  childhood,  being  espe- 
cially prevalent  between  the  second  and  the  seventh  year.  It  is  unusual 
under  six  months  of  age.  It  probably  attacks  the  sexes  equally,  although 
girls  are  said  to  be  more  susceptible  than  boys.  It  sometimes  occurs 
in  non-immune  adults,  and  even  in  elderly  persons,  in  whom  it  usually 
runs  a  severe  and  frequently  fatal  course.  In  some  cities  the  disease  is 
endemic;  in  most  sections  of  the  country  sporadic  cases  occur  from  time 
to  time;  but  the  disease  usually  prevails  epidemically  in  the  winter  and 
spring.  It  frequently  follows  or  precedes  epidemics  of  measles,  rarely  epi- 
demics of  scarlatina.  One  attack  usually  establishes  immunity,  although 
recurrences  are  observed.  Some  persons  possess  a  natural  immunity. 

The  exciting  cause  of  the  disease  is  probably  a  bacillus,  somewhat 
resembling  the  influenza  bacillus,  found  by  Koplik,  and  by  Czaplewski 
and  Hensel,  in  the  mucous  discharges.  The  disease  is  only  moderately 
contagious,  and  especially  during  the  catarrhal  stage.  Infection  is 
usually  transmitted  directly,  but  it  may  be  transmitted  by  a  third  person 
and  perhaps  by  fomites.  It  is  acquired  through  inhalation,  and  is  some- 
what favored  by  overcrowding,  such  as  obtains  in  close,  insanitary 
dwellings,  school  rooms,  etc.,  and  by  previous  ill  health,  especially  catarrh 
of  the  air  passages;  but  ])rolonged  personal  contac-t  with  an  infected 
person  seems  necessary  for  infection. 

Pathology. — Pertussis  is  devoid  of  characteristic  lesions.  The  lesions 
found  after  death  are  those  of  the  complications,  such  as  broncho- 
17 


258  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

pneumonia,  capillary  bronchitis,  atelectasis,  emphysema,  etc.,  but  they 
present  nothing  characteristic. 

Symptoms. — The  period  of  incubation  is  from  seven  to  ten  days. 
Clinically  the  disease  may  be  divided  into  two  stages — the  catarrhal  and 
the  paroxysmal.  The  invasion  is  rather  slow,  the  disease  beginning 
as  an  ordinary  catarrh  of  the  air  passages,  with  injection  of  the  conjunc- 
tivae, coryza,  cough,  a  few  rales,  and  moderate  fever  (102°  F.).  Grad- 
ually the  paroxysmal  stage  is  developed.  At  the  end  of  ten  or  fourteen 
days,  the  fever  having  almost  if  not  entirely  subsided,  the  cough,  instead 
of  improving  (as  in  ordinary  catarrh),  gradually  becomes  extremely 
severe  and  paroxysmal  in  character,  in  some  cases  especially  at  night. 
A  typical  paroxysm  consists  of  a  series  of  short  coughs,  increasing  in 
severity  and  interrupted  only  occasionally  by  a  prolonged  inspiration — 
the  characteristic  whoop.  The  child  begins  to  cough,  the  expiratory 
efforts  succeed  one  another  with  great  rapidity  until  the  lungs  are  almost 
emptied  of  air  (sometimes  they  last  even  longer,  consisting  then  of 
purposeless  and  almost  noiseless  vibrations  of  the  chest  wall),  until 
finally  with  apparently  a  great  effort  a  prolonged  high-pitched  crowing 
inspiration — the  "whoop" — follows  through  the  partially  closed  glottis. 
During  the  attack  the  child  becomes  more  or  less  asphyxiated — the  face 
becomes  swollen  and  livid,  the  cervical  veins  swell,  the  conjunctivae 
become  injected,  the  eyes  protrude  and  become  bathed  in  profuse 
lacrymation,  and  subconjunctival  and  subdermal  facial  ecchymoses, 
and  even  hemorrhages  from  the  nose,  mouth,  and  sometimes  the 
lungs,  may  occur.  Usually  the  attack  is  terminated  by  the  expectora- 
tion of  a  small  amount  of  characteristic,  tenacious,  glairy  mucus;  fre- 
quently the  attack  terminates  in  vomiting,  which  serves  to  eject  a  con- 
siderable amount  of  tenacious  mucus.  The  paroxysms  may  occur  singly 
or  several  may  follow  in  rapid  succession,  and  they  may  be  repeated 
several  times  or  as  often  as  forty  or  fifty  times  during  the  twenty-four 
hours.  During  the  inter\^als,  in  the  absence  of  complications,  such  as 
bronchopneumonia,  the  child  may  appear  relatively  well  and  may  play. 
Spells  of  coughing  devoid  of  the  terror  and  not  followed  by  the  tv^ical 
whooping  spells  may  also  occur.  In  adults  the  paroxysms  are  usually 
less  severe  and  less  typical  than  in  children.  A  lymphocytic  leukocy- 
tosis is  present  in  about  85  per  cent,  of  the  cases,  especially  during 
the  early  (catarrhal)  stage.  The  physical  signs  are  those  of  bronchitis, 
and  are  not  distinctive. 

Having  lasted  three  or  four  weeks,  as  a  rule,  the  paroxysms  gradually 
lessen  in  severity  and  frequency,  expectoration  becomes  freer,  muco- 
purulent in  character,  and  gradually  lessens  (the  stage  of  decline).  The 
paroxysms,  however,  may  last  for  weeks,  even  months,  and  emotion  and 
excitement  have  been  known  to  provoke  an  attack  long  after  the  disease 
has  been  apparently  cured. 

Complications  and  Sequels. — The  most  frequent  and  most  important 
complication  is  bronchopneumonia,  or  capillary  bronchitis,  which  is 
responsible  for  most  of  the  fatalities.     Emphysema  sometimes  arises  in 


PERTUSSIS  259 

consequence  of  the  severe  coughing.  Usually  it  subsides,  but  it  may  form 
the  basis  of  an  emphysema  that  may  give  rise  to  symptoms  in  later  life. 
Hemorrhage  into  the  brain,  occasioning  convulsions,  paralysis,  even 
death,  has  occurred.  Anemia  and  marked  emaciation  sometimes  result 
from  defective  nourishment  occasioned  by  the  repeated  vomiting. 
Ulceration  of  the  frenum  of  the  tongue  sometimes  results  from  forcible 
projection  of  the  tongue  against  the  teeth.  Severe  heart  strain  and  its 
consequences,  tuberculosis,  swelling  of  the  bronchial  lymph  nodes  (suffi- 
cient to  occasion  substernal  and  vertebral  dulness),  nephritis,  temporary 
glycosuria,  noma,  etc.,  have  been  observed  as  sequels. 

Diagnosis. — The  diagnosis  in  the  early  or  catarrhal  stage  is  impossible. 
As  soon  as  the  whoop  appears  the  diagnosis  is  clear.  In  the  absence  of 
an  epidemic,  however,  the  disease  may  be  suspected  in  the  event  of  severe 
coughing  (without  the  whoop)  and  vomiting,  puffiness  of  the  con- 
junctiva, or  swelling  and  duskiness  of  the  face. 

Prognosis. — In  consequence  of  the  common  association  of  complica- 
tions, pertussis  is  a  very  fatal  disease — the  mortality  in  some  epidemics 
being  as  high  as  12  per  cent.  It  is  especially  fatal  in  children  under 
two  years  of  age,  and  in  the  w^eakly. 

Treatment. — The  patient  should  be  isolated  and  the  ordinary  measures 
of  prophylaxis  carried  out  (page  29) .  During  the  catarrhal  stage  rest  in  bed 
is  essential,  and  the  room  should  be  well  ventilated  by  day  and  by  night. 
If  two  rooms  are  available,  the  child  may  be  taken  from  one  to  the  other, 
and  each  fumigated  daily  with  a  view  to  prevent  re-infection.  The  diet 
should  consist  largely  of  milk,  but  after  the  catarrhal  stage  has  passed 
other  articles  of  a  readily  assimilable  nature  may  be  permitted — bearing 
in  mind  the  frequent  vomiting  induced  by  the  paroxysms  of  coughing. 
Sometimes  it  is  wise  to  give  a  small  amount  of  food  immediately  after  the 
cessation  of  a  paroxysm  that  has  brought  on  vomiting.  During  the 
catarrhal  stage  a  simple  febrifuge  or  sedative  expectorant  mixture,  such 
as  is  serviceable  in  an  ordinary  acute  bronchitis,  may  prove  of  value. 
For  treatment  during  the  paroxysmal  stage  many  remedies  have  been 
suggested  from  time  to  time,  but  none  is  really  satisfactory.  Quinine 
has  long  been  used,  and  is  probably  as  satisfactory  as  any  drug — I  grain 
(0.01  gram)  for  each  month  of  age,  or  1.5  grain  (0.09  gram)  for  each  year 
of  age  under  five  years,  three  times  daily.  Jacobi  has  obtained  the  best 
results  from  the  use  of  belladonna  when  given  to  the  physiological  limit. 
Many  writers  extol  the  virtues  of  antipyrin,  1  grain  (0.06  gram)  three  times 
daily  to  a  child  of  one  year.  Its  ill  effects  may  be  somewhat  neutralized 
by  the  concurrent  use  of  whiskey;  and  it  may  be  combined  with  the 
bromides  or  with  belladonna;  or  belladonna  may  be  combined  with  the 
bromides.  Bromoform,  asaffx^tida,  and  many  other  remedies  have 
enjoyed  a  more  or  less  ephemeral  reputation.  Local  treatment  is  some- 
times efficacious — sprays  or  swabs  to  the  throat  of  hydrogen  peroxide, 
resorcin  (1  per  cent.),  and  other  antiseptics;  or  compound  tincture  of 
benzoin,  creosote,  carbolic  acid,  or  oil  of  eucalyptus,  by  inhalation  (croup 
kettle).     Spirit  of  chloroform,  or  chloral,  or  rarely  opium  (paregoric, 


260  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

Dover's  powder,  heroin,  or  morphine)  may  be  resorted  to  in  severe  cases 
at  night  to  insure  rest.  An  elastic  binder,  as  originally  recommended  by 
Kilmer,  is  of  service  in  obviating  vomiting,  as  well  as  in  supporting  the 
abdominal  wall  during  severe  paroxysms  of  coughing. 


INFECTIOUS  PAROTITIS. 

(Epidemic  Parotitis;  Mumips.) 

Infectious  parotitis  is  an  acute,  infectious,  and  moderately  contagious 
disease,  characterized  by  inflammation  of  the  parotid  gland,  and  exhibit- 
ing a  predilection  to  involve  the  testicles,  the  breasts,  and  the  ovaries. 

Etiology. — Infectious  parotitis  is  most  common  in  children,  but  it 
occurs  also  in  adults;  it  is  rare  in  infants  and  the  aged.  It  is  more  com- 
mon in  males  than  in  females.  It  usually  prevails  epidemically,  espe- 
cially in  the  late  fall,  the  winter,  and  the  early  spring,  but  sporadic  cases 
are  not  uncommon.  The  exciting  cause  of  the  disease  has  not  been 
isolated.  The  disease  is  contagious,  and  though  the  contagium  may  be 
transmitted  by  fomites,  rather  close  personal  contact  seems  necessary 
for  infection  in  most  cases.  The  breath  and  the  saliva  are  believed 
to  be  infectious — for  about  three  weeks.  Infection  is  probably  acquired 
by  inhalation  and  is  transmitted  along  Stenson's  duct. 

Pathology. — The  lesions  consist  of  swelling  of  the  mucosa  of  Stenson's 
duct,  and  hyperemia  and  oedema  (sometimes  minor  inflammatory  altera- 
tions) of  the  parotid  gland  and  the  periglandular  tissues. 

Symptoms. — The  period  of  incubation  varies  from  one  to  three  weeks, 
and,  as  a  rule,  is  unattended  by  prodromal  symptoms.  The  onset  is 
usually  with  moderate  fever  (101°  to  102°,  occasionally  103°  to  104°  F.), 
pain  at  the  angle  of  the  jaw,  headache,  and  general  malaise.  Swelling 
of  the  parotid  begins  soon,  and  at  the  end  of  thirty-six  or  forty-eight 
hours  is  usually  quite  marked — occasioning  swelling  in  front  of  and 
below  the  ear  and  elevating  the  ear.  Sometimes  the  swelling  and 
oedema  extend  far  onto  the  cheek,  into  the  infraparotid  region,  and  the 
floor  of  the  mouth.  The  region  is  painful  (though  rarely  as  painful  as  one 
might  judge  from  the  extreme  swelling)  and  tender;  opening  the  mouth, 
chewing,  and  swallowing  cause  distress;  and  usually  there  is  ptyalism 
(though  occasionally  the  mouth  is  very  dry).  In  most  cases  the  lesions 
are  unilateral  at  first  (most  frequently  left-sided),  but  in  a  day  or  two 
both  glands  are  usually  involved.  Occasionally  the  other  salivary 
glands  are  swollen;  the  spleen  is  usually  enlarged  and  may  be 
palpable.  In  a  few  cases  there  is  quite  high  fever  and  marked  prostra- 
tion. The  fever  subsides  by  lysis,  and  by  tlie  seventh  to  tenth  day 
the  patient  is  usually  convalescent.  Suppuration  is  quite  rare,  and  a 
second  attack  is  uncommon  (though  not  unknown). 

Complications. — Orchitis  is  common  after  puberty,  and  may  be 
single  or  bilateral.  It  usually  develops  as  the  parotid  swelling  subsides; 
rarely  it  precedes   the  parotitis.     Atrophy  not  infrequently  ensues  in 


YELLOW  FEVER  261 

severe  cases.  Vulvovaginitis  is  not  uncommon  in  young  girls;  the 
breasts  may  become  enlarged  and  painful;  and  rarely  the  ovaries  are 
swollen  and  tender.  Rarer  complications  comprise  otitis  media,  menin- 
gitis, and  divers  nervous  disorders  (paralyses,  etc.). 

Diagnosis. — The  diagnosis  is  usually  easy.  One  should  exclude 
disorders  of  the  throat  that  might  cause  enlarged  lymphatics,  as  well  as 
dental  caries  with  suppuration,  etc. 

Prognosis. — The  prognosis  is  good;  suppuration  is  rare,  and  a  second 
attack  uncommon. 

Treatment.^Rest  in  bed  is  advisable.  The  bowels  should  be  well 
opened  with  a  saline  cathartic.  A  simple  diuretic  fever  mixture  (aconite, 
potassium,  citrate,  etc.)  is  serviceable  in  many  cases.  An  antiseptic  mouth 
wash,  hot  fomentations,  an  ice-bag,  or  ichthyol  ointment  may  be  applied 
to  the  parotid  swelling.  In  the  event  of  high  fever  and  delirium,  the 
usual  hydropathic  and  other  treatment  for  such  toxemic  states  is  called 
for.  Should  orchitis  develop,  the  patient  must  be  put  absolutely  at 
rest,  the  testicles  elevated,  and  lead  water  and  laudanum,  or  some  similar 
preparation,  applied. 

YELLOW  FEVER. 

Yellow  fever  is  an  acute,  specific,  infectious  disease,  characterized 
by  fever,  jaundice,  albuminuria,  and  a  disposition  to  hemorrhage, 
especially  from  the  gastric  mucous  membrane. 

Etiology. — Yellow  fever  is  endemic  in  the  West  Indies  and  Central 
American  sea  ports;  Havana  was  for  more  than  a  century  a  well-recog- 
nized focus  of  endemic  infection,  whence  the  disease  was  periodically 
widely  disseminated.  The  spread  of  the  disease  is  favored  by  general 
insanitary  conditions,  low  lands,  and  the  summer  months — all  of  which 
are  now  known  to  bear  an  intimate  relation  to  the  mosquito.  One 
attack  confers  immunity.  The  apparent  immunity  of  natives  in  yellow 
fever  zones  is  due  largely  to  their  having  survived  an  attack  of  the 
disease  during  childhood. 

Though  Carlos  Finlay,  in  1881,  stated  that  the  mosquito  is  active  in 
propagating  yellow  fever,  the  exact  etiological  factors  remained  un- 
known until  the  United  States  Army  Commission,  composed  originally 
of  Drs.  Walter  Reed,  James  Carroll,  Jesse  W.  Lazear,  and  Aristides 
Agramonte,  proved  the  correctness  of  Finlay's  contention,  and  added 
much  additional  information — one  of  the  members,  Lazear,  lost  his 
life  in  the  investigation;  Reed  and  Carroll  escaped  a  similar  fate, 
but  undermined  their  vitality,  and  later  succumbed.  The  conclusions 
of  the  Commission  are  as  follows:  (1)  The  mosquito,  Stegomyia  fasci- 
ata,  serves  as  the  intermediate  host  for  the  parasite  of  yellow  fever. 
(2)  Yellow  fever  is  transmitted  to  the  non-immune  individual  by  means 
of  the  bite  of  the  mosquito  that  has  previously  fed  on  the  blood  of  those 
sick  with  this  disease.  (3)  An  interval  of  about  twelve  days  or  more 
after  contamination  appears  to  be  necessary  before  the  mosquito  is 


262  INFECTIONS  OP   UNKNOWN  ETIOLOGY 

capable  of  conveying  the  infection.  (4)  The  bite  of  the  mosquito  at  an 
earher  period  after  contamination  does  not  appear  to  confer  any  immunity 
against  a  subsequent  attack.  (5)  Yellow  fever  can  also  be  experi- 
mentally produced  by  the  subcutaneous  injection  of  blood  taken  from  the 
general  circulation  during  the  first  and  second  days  of  this  disease. 
(6)  An  attack  of  yellow  fever,  produced  by  the  bite  of  the  mosquito, 
confers  immunity  against  a  subsequent  attack  of  the  non-experimental 
form  of  this  disease.  (7)  The  period  of  incubation  in  thirteen  cases 
of  experimental  yellow  fever  has  varied  from  forty-one  hours  to  five 
days  and  seventeen  hours.  (8)  Yellow  fever  is  not  conveyed  by  fomites, 
and  hence  disinfection  of  clothing,  bedding,  or  merchandise,  supposedly 
contaminated  by  contact  with  those  sick  with  this  disease,  is  unnecessary. 
(9)  A  house  may  be  said  to  be  infected  with  yellow  fever  only  when  there 
are  present  within  its  walls  contaminated  mosquitoes  capable  of  con- 
veying the  parasite  of  this  disease.  (10)  The  spread  of  yellow  fever 
can  be  most  effectually  controlled  by  measures  directed  to  the  destruc- 
tion of  mosquitoes,  and  the  protection  of  the  sick  against  the  bites  of 
these  insects.  (11)  Wliile  the  mode  of  propagation  of  yellow  fever  has 
now  been  definitely  determined,  the  specific  cause  of  this  disease  remains 
to  be  discovered. 

Stegomyiia  fasciata  bites  in  the  day  time  (which  is  quite  characteristic) ; 
it  is  a  very  black  mosquito  with  silver  bands  on  its  body  and  legs,  a  lyre- 
shaped  silver  mark  on  the  back  being  characteristic.  Although  the 
specific  microorganism  of  yellow  fever  has  not  yet  been  discovered,  it 
passes  through  a  fine  porcelain  filter,  and  doubtless  therefore  belongs  to 
the  ultramicroscopic  organisms. 

Pathology. — Jaundice  is  constant.  The  blood  is  disorganized,  and 
hemoglobinemia  may  be  present.  Hemorrhages  from  the  mucous  mem- 
branes, especially  the  stomach,  are  quite  characteristic;  less  frequently 
there  are  cutaneous  and  serous  membrane  hemorrhages.  The  liver,  at 
first,  is  congested;  later  it  is  pale,  and  reveals  fatty  degeneration  and 
focal  necroses.  The  kidneys  and  the  heart  show  parenchymatous  de- 
generation.    The  lymph  nodes  are  usually  enlarged. 

Symptoms. — ^The  period  of  incubation  is  usually  two  to  three  days 
(forty-one  hours  to  five  days  and  seventeen  hours,  according  to  the  United 
States  Army  Commission),  and  is  usually  unattended  by  prodromes, 
except  perhaps  slight  headache  and  malaise.  The  onset  of  the  disease 
is  usually  abrupt,  with  chill  or  chilliness,  fever  (103°  to  104°  F.), 
headache,  severe  pains  in  the  eyes,  the  back,  and  the  legs,  epigastric 
distress,  nausea,  vomiting,  coated  tongue,  and  constipation.  On  the 
first  day  often  a  peculiar  facies  (one  of  the  characteristic  symptoms  of 
the  disease,  according  to  Guiteras)  develops — congested  face,  injected 
eyes,  slight  swelling  of  the  eyelids  and  lips,  and  a  noticeable  element  of 
jaundice  ("undoubtedly  the  most  characteristic  feature  of  the  facies," 
Guiteras).  By  the  evening  of  the  first  day  the  temperature  may  reach 
106°  F.  or  more,  but  in  the  majority  of  cases  it  is  scarcely  more  than  104° 
F.;  it  remains  at  this  level  with  slight  fluctuations  for  two  or  three  days 


YELLOW  FEVER  263 

and  then  gradually  falls.  In  very  mild  cases  the  lysis  may  occur  even  on 
the  second  day.  At  the  onset  the  pulse  rate  is  somewhat  increased,  but 
it  is  rarely  more  than  100  or  110;  on  the  second  day  it  begins  to  fall, 
even  with  a  rising  temperature  (a  second  characteristic  symptom  of  the 
disease,  Guiteras),  and  it  may  be  not  more  than  75,  with  a  temperature 
of  104°  F.  or  more.  The  pulse  becomes  still  slower  during  convales- 
cence— 60,  40,  even  less.  Albuminuria  is  a  third  characteristic  symp- 
tom, according  to  Guiteras;  it  varies  much  in  intensity,  but  is  usually 
more  marked  in  the  evening  urine.  In  severe  cases  it  may  be  present 
on  the  evening  of  the  first  day,  and  it  is  practically  always  present  by 
the  evening  of  the  second  day,  being  one  of  the  few  diseases  in  which 
albuminuria  is  present  very  early.  It  may  be  slight  and  transient,  but  is 
sometimes  extreme  and  associated  with  tube  casts  and  other  manifesta- 
tions of  nephritis,  and  is  usually  disproportionate  to  the  severity  of  the 
other  symptoms.  Complete  suppression  of  urine  may  supervene  and  the 
patient  may  die  of  uremia  even  within  thirty-six  hours. 

With  the  fall  of  the  temperature,  on  the  third  day  of  the  disease, 
the  period  of  remission  (so-called  period  of  calm)  develops;  but  this  is 
often  missed.  In  favorable  cases  the  patient  may  now  go  on  to  complete 
recovery.  Usually,  however,  he  exhibits  evidences  of  infection,  such  as 
jaundice,  epigastric  distress,  albuminuria,  mental  dulness,  and  prostra- 
tion, and  at  the  end  of  twenty-four  or  thirty-six  hours  of  comparative 
comfort  (in  severe  cases,  without  such  period)  the  period  of  secondary 
fever  or  collapse  supervenes.  The  fever  returns  and  becomes  remittent; 
jaundice  and  albuminuria  increase,  and  the  urine  may  become  almost 
if  not  quite  suppressed;  epigastric  distress  becomes  worse;  nausea  and 
vomiting  return,  the  vomitus  consisting  at  first  of  the  stomach  contents, 
but  soon  of  altered  blood  (black  vomit);  hemorrhages  from  the  other 
mucous  membranes  and  into  the  skin  may  develop ;  prostration  becomes 
extreme,  and  the  patient  passes  into  a  typhoid  state  (Hippocratic  facies, 
coma,  delirium,  subsultus  tendinum,  etc.),  and  commonly  dies.  Re- 
covery, however,  may  ensue  even  in  the  severest  infections.  In  some 
cases  the  temperature  does  not  become  elevated,  but  may  become  even 
subnormal,  "black  vomit"  occurs,  the  patient  collapses,  and  dies  (algid 
form).  Mental  alertness  is  a  noteworthy  feature  of  many  cases,  even 
in  the  presence  of  "  black  vomit,"  but  delirium  may  occur  at  any  time, 
even  at  the  onset;  when  it  occurs  later,  however,  it  is  due  quite  as  often 
to  uremia  as  to  the  yellow  fever  intoxication.  The  bowels  are  usually 
constipated,  and  the  stools  are  bile-stained  (normal),  but  later  they  may 
contain  blood. 

Varieties. — Mild,  severe,  and  fulminant  cases  may  be  distinguished. 
The  mild  cases  often  escape  recognition,  since  the  patient  complains  only 
of  slight  indisposition  for  a  day  or  two,  and  does  not  take  to  bed.  In 
certain  (fulminant)  cases  the  patient  is  overwhelmed  with  the  intoxica- 
tion; vomiting,  collapse,  coma,  perhaps  convulsions,  develop,  and  the 
the  patient  dies  within  a  day  or  two.  Convalescence  is  often  protracted, 
and  attended  with  anemia,  enteritis,  abscesses,  parotitis,  etc. 


264  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

Diagnosis. — The  recognition  of  the  disease  is  comparatively  easy 
during  the  prevalence  of  an  epidemic,  but  some  epidemics  have  been  so 
mild  that  much  acrimonious  discussion  regarding  their  true  nature, 
whether  the  disease  is  dengue  or  yellow  fever,  has  arisen,  especially  in 
the  South.  In  case  of  doubt,  the  three  characteristic  features  of  the 
disease  mentioned  by  Guiteras  should  be  of  much  importance.  Guiteras 
also  believes  that  a  high  hemoglobin  value  (90  to  100  or  more)  in  the 
first  four  or  five  days  of  the  disease  is  of  diagnostic  value — serving  to 
exclude  malaria,  t}^hoid  fever,  and  influenza,  in  which  the  hemoglobin 
is  said  to  become  low  early  in  the  disease.  In  dengue  jaundice  is  not 
so  common  as  in  yellow  fever,  nor  does  it  occur  so  early,  and  hemor- 
rhages are  less  frequent.  Pernicious  malaria  fever  may  be  excluded  by 
the  absence  of  malarial  parasites  from  the  blood,  absence  of  enlarged 
spleen,  and  the  presence  of  the  characteristic  symptoms  of  yellow  fever. 

Prognosis. — The  mortality  varies  in  different  epidemics  between 
15  and  85  per  cent.,  and  is  in  direct  ratio  to  the  severity  of  the  infection 
and  the  resistance  of  the  individual. 

Treatment. — The  patient  should  be  quarantined  (page  29),  and,  in 
accordance  with  what  we  now  know  of  the  etiology  of  the  disease,  especial 
attention  should  be  directed  to  screening  the  patient's  bed,  room,  or 
house  (so  as  to  prevent  the  access  of  mosquitoes),  and  to  destroying  all 
mosquitoes  and  their  breeding  places  or  places  suitable  for  breeding. 
Special  attention  must  be  directed  to  the  occurrence  of  mild  cases, 
especially  among  children  and  young  adults;  these  often  act  as  sources 
of  infection. 

Since  we  have  no  specific,  the  treatment  of  the  developed  disease  is 
largely  supportive  and  symptomatic.  The  patient  must  rest  in  bed 
until  he  is  entirely  convalescent,  and  should  have  a  plentiful  supply  of 
fresh  air,  sunshine,  and  light,  nutritious  food.  Hot  fomentations  to  the 
back  and  epigastrium,  and  an  ice-bag  to  the  head  may  relieve  the  pains; 
morphine  and  the  coal-tar  products  should  be  given  only  in  the  very 
early  stages  of  the  disease,  if  at  all,  and  very  cautiously.  Fever  calls  for 
hydropathic  measures — which  not  only  reduce  the  temperature,  but  act 
as  a  general  nervous  stimulant.  Vomiting  is  often  intractable,  but  may 
be  controlled  by  cracked  ice,  sips  of  very  hot  water,  cocaine,  or  dilute 
hvdrocvanic  acid.  Large  amounts  of  water  should  be  given  by  the  mouth 
(if  retained),  and  saline  solutions  by  the  bowels  or  h^-podermicly.  Alka- 
lies, such  as  sodium  bicarbonate,  may  be  added  to  the  drinking  water, 
to  reduce  the  acidity  of  the  gastric  juice  (as  well  as  the  m-ine);  or  one 
may  use,  as  advised  by  Sternberg  years  ago,  sodium  bicarbonate,  4  grains 
(0.25  gram),  mercuric  bichloride,  yt5  grain  (0.0005  gram),  and  water, 
2  teaspoonfuls  (10  c.c.)  every  hour  in  a  severe  case.  Other  intestinal 
antiseptics  may  be  tried,  such  as  salol,  naphthalene,  etc.  Quinine,  as 
well  as  iron,  has  been  highly  recommended,  especially  to  control  the 
hemorrhages,  over  which,  however,  we  can  exert  very  little  influence. 
Stimulants  are  usually  called  for,  sooner  or  later — strychnine,  alcohol, 
etc.     Uremia  is  to  be  treated  on  general  principles. 


DENGUE  265 

DENGUE. 

{Break-hone  Fever;  Dandy  Fever.) 

Dengue  is  an  acute,  specific,  infectioiLs,  and  highly  contagious  disease, 
characterized  by  high  fever,  severe  neuromuscular  and  arthritic  pains, 
and  an  initial  erythematous  and  a  subsequent  polymorphous  rash. 

Etiology. — Dengue  prevails  endemically,  even  pandemically,  in  warm 
climates,  such  as  India,  Cairo  (and  the  surrounding  country),  Java, 
the  West  Indies,  our  own  Southern  States,  etc.,  and  during  the  summer 
montlis  sometimes  spreads  to  the  subtropical  and  temperate  zones. 
The  disease  is  highly  infectious,  and  once  developed  attacks  almost 
the  entire  population  almost  simultaneously — no  age,  sex,  nor  race 
escaping.     One  attack  does  not  confer  immunity. 

The  exciting  cause  of  the  disease  has  not  been  isolated  with  certainty; 
it  is  probably  ultramicroscopic.  Graham,  in  Beirut,  Syria,  found  what 
he  believes  to  be  a  hematozoon  in  the  blood,  and  believes  the  mosquito, 
Culex  fastigans,  to  be  the  active  factor  in  propagating  it.  Ashburn  and 
Craig  also  inculpate  the  mosquito. 

Pathology. — Since  the  disease  is  rarely  fatal,  careful  and  extended 
pathological  studies  have  not  been  carried  out. 

Symptoms. — The  period  of  incubation  is  from  one  to  five  days,  and  is 
unattended  by  prodromal  symptoms.  The  onset  is  sudden,  with  chill 
or  chilliness,  fever  (104°  to  107°  F.),  and  severe,  even  excruciating,  pains 
in  the  head,  eyeballs,  back,  and  the  extremities  (the  muscles  and  joints) — 
whence  the  term  break-bone  fever.  The  large  or  small  joints,  and  few 
or  many,  may  be  affected  simultaneously  or  successively,  and  in  addition 
to  being  painful,  they  may  be  also  red  and  swollen.  Furthermore,  the 
pulse  is  rapid,  the  appetite  lost,  the  urine  concentrated,  and  the  patient 
may  be  slightly  delirious;  the  face  is  bloated,  the  eyes  injected,  and  the 
skin  and  the  visible  mucous  membranes  may  exhibit  a  diffuse  erythema- 
tous rash,  and  the  skin  may  be  unduly  sensitive.  On  the  third  or  the 
fourth  day  the  fever  falls  usually  by  crisis  attended  by  sweating,  some- 
times by  lysis,  and,  aside  from  some  muscular  soreness  and  stiffness,  the 
patient  feels  comparatively  well.  At  the  end  of  two  or  three  days  of 
apyrexia,  the  fever  and  the  neuromuscular  pains  return,  but  they  are 
usually  less  severe  and  last  not  more  than  twenty-four  to  forty-eight 
hours;  they  are  often  accompanied  by  a  polymorphous  rash — measly, 
scarlatiniform,  papular,  sometimes  urticarial  and  even  vesicular — which 
develops  first  upon  the  hands,  and  then  spreads  to  the  arms,  face,' trunk, 
and  legs.  This  gradually  fades  and  is  followed  by  a  fine,  branny,  often 
almost  imperceptible,  desquamation.  The  lymph  nodes  are  often  en- 
larged, and  may  remain  palpable  well  into  convalescence  or  beyond. 
Hemorrhages  from  the  mucous  membranes  have  occasionally  been 
observed. 

The  disease  lasts  usually  from  seven  to  ten  days,  but  convalescence 


266  INFECTIONS  OF  UNKNOWN  ETIOLOGY 

is  sometimes  protracted  by  prostration,  anemia,  insomnia,  even  menin- 
gitis, or  a  relapse. 

Diagnosis. — ^The  epidemic  prevalence  of  the  disease,  the  almost  simul- 
taneous implication  of  a  very  large  portion  of  the  population,  the  charac- 
teristic fever  curve,  and  the  cutaneous  rashes  serve  to  distinguish  the 
disease,  although  some  difficulty  may  be  experienced  in  differentiating 
rheumatism  in  early  cases,  and  influenza,  measles,  and  scarlatina  may 
have  to  be  taken  into  consideration  in  other  cases.  Greatest  difficulty 
has  been  experienced  in  differentiating  yellow  fever,  but  yellow  fever  is 
suggested  by  the  characteristic  jaundiced  facies,  the  slowing  of  the  pulse 
with  increasing  temperature,  the  early  albuminuria,  and  by  the  fact  that 
slight  jaundice,  though  it  may  be  observed  occasionally  in  dengue,  does 
not  occur  as  early  as  in  yellow  fever,  and  hemorrhages  are  much  less 
common. 

Prognosis. — The  prognosis  is  good.  Death  rarely  results,  and  then 
only  in  the  debilitated,  and  in  the  event  of  coma  or  hemorrhages. 

Treatment. — ^The  treatment  is  purely  symptomatic.  The  severe  pains 
usually  necessitate  the  use  of  morphine,  although  quinine,  salol,  and  other 
salicylates  have  proved  of  some  service.  Tincture  of  gelsemium  has  been 
highly  recommended  by  McLaughlin.  Chloral  and  the  bromides  are 
useful  for  the  insomnia  and  general  restlessness.  High  fever  calls  for 
the  use  of  hydrotherapy.  Tonics  are  required  during  convalescence, 
and  potassium  iodide  is  said  to  be  valuable  for  the  persistent  arthritic 
pains. 

HYDROPHOBIA. 

(Rabies;  Lyssa.) 

Hydrophobia  is  an  acute,  specific,  infectious  disease  communicable 
to  man  by  the  bite  of  an  animal  infected  with  rabies. 

Etiology. — Rabies  is  a  disease  of  dogs  especially,  but  occurs  also  in 
wolves,  foxes,  cats,  rarely  in  cows  and  horses,  and  may  be  communicated 
to  pigs,  rabbits,  etc.  The  disease  occurs  in  all  parts  of  the  world, 
and  is  probably  more  common  in  spring  than  in  summer  (contrary  to 
the  vulgar  opinion).  The  etiological  factor  has  not  yet  been  isolated,  but 
it  exists  in  the  saliva,  in  the  brain,  spinal  cord,  and  nerves,  and  probably 
in  other  secretions,  and  the  blood;  it  seems  not  to  be  present  in  the 
viscera.  It  is  filtrable  and  doubtless  belongs  to  the  class  of  ultra- 
microscopic  organisms.  Infection  is  transmitted  to  men  usually  through 
the  bite  of  a  rabid  dog,  but  not  more  than  10  per  cent,  of  those  bitten 
become  infected.  Children  are  more  commonly  affected,  because  they 
are  more  frequently  bitten.  Punctured  wounds  of  the  exposed  surfaces, 
hands,  face,  neck,  etc.,  are  especially  dangerous,  clothes  largely  pre- 
venting wounds  of  other  parts  of  the  body  from  becoming  infected. 

Pathology. — The  lesions  consist  of  congestion  of  the  medulla  and  the 
spinal  cord,  sometimes  associated  with  minute  hemorrhages,  and  are  in 
no  way  specific — occurring  in  other  convulsive  states.     Accumulations  of 


HYDROPHOBIA  267 

leukocytes  about  the  bloodvessels  and  nerve  cells,  especially  the  m.otor 
cells  of  the  medulla  (Babes'  rabic  tubercle),  are  usually  present. 
Van  Gehuchten  and  Nelis  have  described  proliferation  of  the  endo- 
thelial cells  of  the  capsules  of  the  intervertebral,  pneumogastric,  and 
sympathetic  ganglia,  with  destruction  of  the  proper  nerve  cells.  Negri 
has  described  protozoan-like  bodies  in  the  nerve  cells,  especially  those  in 
the  horn  of  Ammon,  in  rabid  animals.  These  lesions  may  be  reproduced 
experimentally  and  are  resorted  to  for  diagnostic  purposes. 

Symptoms  in  the  Dog. — Two  forms  of  rabies  are  recognized:  (1) 
Maniacal  rabies,  in  which  there  is  usually  a  preliminary  stage  of  depres- 
sion, followed  by  a  stage  of  excitement  or  mania,  in  which  the  dog  eats 
little,  runs  about  with  saliva  drooling,  and  shows  a  disposition  to  bite 
persons,  and  real  and  imaginary  objects ;  followed  by  a  third  or  paralytic 
stage,  in  which  weakness  and  emaciation  proceed  rapidly.  Death  ensues 
usually  within  eight  days.  (2)  Dumb  rabies,  in  which  the  second  or 
excited  stage  is  absent,  and  in  which  paralysis  and  death  occur  earlier. 
It  is  quite  important  to  recognize  this  form,  as,  though  more  readily 
overlooked,  it  is  quite  as  infectious  as  the  maniacal  form,  and  is  the 
only  form  that  occurs  in  rodents. 

Symptoms  in  Man. — In  'man  the  period  of  incubation  varies  between 
two  weeks  and  eighteen  months;  in  most  cases  it  is  about  eight  weeks; 
and  in  children  it  is  less  than  in  adults.  As  a  rule,  the  wound  heals 
without  noteworthy  manifestations.  The  onset  of  the  disease  is  insidious. 
Toward  the  end  of  the  period  of  incubation  the  site  of  the  wound  may 
itch  or  pain  a  little,  and  the  adjacent  lymph  nodes  may  be  somewhat 
enlarged  and  tender,  but  often  there  are  no  local  manifestations.  The 
premonitory  symptoms,  which  last  one  or  two  days,  are  depressive — 
melancholia,  undue  anxiety,  loss  of  appetite;  later,  perhaps  headache, 
irritability  of  temper,  and  intolerance  for  noises,  and  sleeplessness. 
The  temperature  may  be  slightly  elevated  and  the  pulse  somewhat 
increased  in  frequency.  Gradually  spasm  of  the  muscles  of  deglutition 
and  of  respiration,  and  a  disposition  to  refuse  water  (hydrophobia)  is 
developed.  The  stage  of  excitement  then  comes  on  apace.  The  spasm 
of  the  muscles  of  deglutition  and  of  respiration  become  more  marked; 
they  become  convulsive  in  character,  and  may  even  spread  to  the  trunk 
and  the  extremities.  They  may  be  excited  by  the  slightest  touch,  sound, 
visual  impression,  or  auditory  suggestion;  and  the  paroxysms  induced 
by  the  sight  of  water  or  the  attempt  to  swallow  are  merely  one  expression 
of  the  universal  hyperesthesia,  of  which  the  greatly  exaggerated  reflexes 
are  another.  The  paroxsyms,  however  induced,  may  last  for  a  few 
minutes  or  a  half  hour;  they  are  associated  with  inability  to  swallow, 
sensations  of  extreme  dyspncpa  (even  in  the  absence  of  obstruction  to 
the  air  passages),  and  with  the  greatest  mental  anxiety,  distress,  and 
terror.  Thirst  is  sometimes  present,  and  the  temperature  is  increased 
during  the  paroxysms.  The  inability  to  swallow  the  saliva  (which  is 
not  infrequently  increased),  a  slight  spasmodic  cough  (designed  to 
expel  the  saliva),  and  certain  guttural  sounds  produced  by  spasmodic 


268  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

movements  of  the  larynx,  occasion  the  "frothing  at  the  mouth"  and 
the  "barks  like  a  dog"  associated  in  the  public  mind  with  the  disease. 
Between  the  paroxysms  the  patient  is  mentally  alert,  and  only  too 
vividly  apprehends  his  danger.  Should  the  patient  not  die  from  asphyxia 
or  exhaustion,  in  from  two  to  four  days  the  final,  or  paralytic,  stage  sets 
in;  the  spasmodic  attacks  lessen  and  finally  cease,  the  heart  becomes 
weak,  exhaustion  and  coma  supervene,  and  in  from  twelve  to  twenty- 
four  hours  the  patient  dies. 

Diagnosis. — Under  no  circumstances  should  the  suspected  animal  be 
killed,  except  by  a  physician  with  a  view  to  secure  the  nervous  tissues, 
examine  them,  and  inoculate  them  into  rabbits — which  should  always  be 
done  in  animals  suspected  of  rabies.  In  the  event  of  rabies  the  inocu- 
lated rabbit  dies  of  the  paralytic  form  of  the  disease  in  from  fifteen  to 
twenty  days;  whereupon  the  lesions  described  by  Van  Gehuchten  and 
Nelis  may  be  found  in  the  plexiform  ganglion  of  the  pneumogastric  nerve, 
and  the  Negri  bodies  may  be  found  in  the  horn  of  Ammon.  Hydro- 
phobia rather  than  tetanus  is  suggested  by  the  history  of  a  bite,  the  special 
involvement  of  the  muscles  of  deglutition  and  of  respiration,  the  psychic 
symptoms,  and  the  absence  of  lockjaw,  of  opisthotonos,  and  of  persistent 
tetanic  spasm.  Pseudohydrophobia  or  lyssaphobia  is  a  neurosis  that 
sometimes  develops  in  hysterical  and  neurotic  subjects,  not  infrequently 
as  early  as  twenty-four  hours  after  a  bite  by  a  rabid  or  a  supposedly 
rabid  dog,  and  often  simulates  true  hydrophobia;  usually,  however, 
the  patient  has  exhibited  considerable  dread  lest  hydrophobia  develop, 
and  the  hysterical  element  is  always  in  the  foreground;  the  premonitory 
symptoms  are  missed,  there  is  no  true  respiratory  spasm,  obvious  imita- 
tions of  a  dog  (such  as  bites,  growls,  etc.)  are  conspicuous,  the  disorder 
lasts  longer  than  true  hydrophobia,  and  is  quite  amenable  to  certain 
severe  and  well-recognized  measures  used  to  control  hysterical  attacks. 

Prognosis. — No  patient  has  been  known  to  recover  from  an  indubitable 
attack  of  hydrophobia. 

Treatment. — If  possible  the  wound  should  be  excised;  at  least  it  should 
be  well  laid  open  and  cauterized  with  nitric  acid,  carbolic  acid,  or  caustic 
potash,  and  subsequently  treated  antiseptically  as  an  open  wound  (not 
allowed  to  heal)  for  several  weeks.  Pasteur's  preventive  inoculations 
should  be  instituted  as  soon  as  possible.  Pasteur  found  that  the  virulence 
of  the  rabic  virus  could  be  markedly  increased  by  passing  it  through  a 
series  of  rabbits  (subdural  injections  of  emulsions  of  the  dog's  spinal 
cord),  so  that  ultimately  the  period  of  incubation  is  reduced  to  about  six 
days,  and  the  duration  of  the  disease  to  between  two  and  five  days.  The 
spinal  cords  of  these  rabbits  contains  his  virus  fixe,  which,  however, 
gradually  loses  its  virulence  upon  being  dried  in  the  air,  and  gradually 
becomes  inert.  Beginning  then,  with  the  inoculations  of  least  active 
virus  and  progressing  to  those  of  high  activity,  immunity  in  man  is 
established  (within  about  two  weeks)  before  the  period  of  incubation 
of  the  disease  occasioned  by  the  dog's  bite  has  elapsed.  By  this  mode 
of  treatment,  the  mortality  of  an  otherwise  absolutely  fatal  disease  has 


ROCKY   MOUNTAIN  SPOTTED  FEVER  269 

been  reduced  almost  to  a  minimum.  Aside  from  the  foregoing,  treatment 
is  merely  palliative.  When  the  disease  has  developed,  the  patient  should 
be  confined  to  a  darkened  room,  free  from  noises ;  he  should  be  nourished 
bv  the  rectum,  and  his  distress  mitigated  by  chloroform,  chloral,  mor- 
phine, and  the  bromides.  One  may  try  the  Buisson  treatment,  con- 
sisting of  vapor  baths  and  jaborandi,  to  induce  profuse  sweating;  but 
the  treatment  has  not  commended  itself  to  the  thinking  profession.  An 
efficacious  antirabic  serum  has  not  yet  been  produced,  nor  are  Pasteur's 
preventive  inoculations  of  the  slightest  service  after  the  disease  has 
developed. 

ROCKY  MOUNTAIN  SPOTTED  FEVER. 

(Tick  Fever.) 

Rocky  Mountain  spotted  fever  is  an  acute,  infectious  disease,  occur- 
ring in  Western  Montana,  chiefly  in  the  Bitter  Root  Valley,  as  well  as 
in  Idaho,  Wyoming,  and  Nevada,  and  characterized  by  chills,  fever, 
neuromuscular  pains,  and  a  peculiar  maculopapular  or  petechial  eruption. 

Etiology. — ^Rocky  Mountain  spotted  fever  is  transmitted  by  the  bite  of 
a  tick,  Dermacentor  venustus  (andersoni)  in  Montana,  and  by  Dermacen- 
tor  modestus  in  Idaho;  and  is  transmissible  to  the  monkey  and  the  guinea- 
pig.  The  nature  of  the  infectious  agent  is  not  known.  Wilson  and 
Chowning  described  a  small  parasite  (resembling  hyaline  malarial  bodies) 
which  they  found  in  the  erythrocytes  as  well  as  free  in  the  blood  plasma, 
and  which  they  have  named  Pyroplasma  hominis  (whence  the  name  for 
the  fever,  Pyroplasmosis  hominis).  Stiles  and  Craig,  however,  doubt 
the  identity  of  these  supposed  parasites,  Craig  stating  that  the  appear- 
ances are  due  to  changes  in  the  hemoglobin.  Ricketts  has  described  a 
bacillus  found  in  the  tick  and  their  fresh  eggs. 

Symptoms. — The  period  of  incubation  is  said  to  be  from  three  to 
twelve  days.  The  onset  is  rather  sudden,  with  chills,  headache,  nausea, 
neuromuscular  pains,  and  fever.  Epistaxis  is  common,  the  bowels  are 
usually  constipated,  and  there  are  manifestations  of  catarrhal  inflam- 
mation of  the  conjunctiva  and  the  upper  respiratory  tract.  The  pulse 
is  usually  disproportionately  rapid — 120  to  140.  On  the  second  to  the 
seventh  day  of  the  disease  a  rather  r^rofuse  maculopapular  (occasionally 
petechial )  rash  appears.  It  is  usufJly  most  marked  on  the  wrists,  arms, 
legs,  forehead,  and  later  on  the  trunk.  Albuminuria  is  present  in  all 
cases.  The  fever  reaches  its  height  (103°  to  105°  F. )  on  about  the 
twelfth  day,  and  then  falls  by  lysis  to  reach  the  normal  in  four  or  five 
days  or  a  week.  Concurrent  with  the  fall  in  temperature  the  rash  fades, 
and  is  sometimes  followed  by  desquamation.  Gangrene  of  the  fingers, 
toes,  and  scrotum  has  been  observed. 

Diagnosis. — The  disease  is  readily  recognized  in  the  section  where 
it  ai)ounds,  a  history  of  a  tick  bite  being  important.  From  purpura  the 
affection  is  distinguished  by  the  absence  of  joint  symptoms  and  of  sore 
throat,  and  the  early  appearance  of  the  rash,  especially  on  the  wrist 


270  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

(as  contrasted  with  its  later  appearance,  especially  on  the  trunk  in  pur- 
pura). 

Prognosis. — The  mortality  is  very  high  in  some  regions — from  70  to  90 
per  cent.,  death  occurring  usually  on  about  the  tenth  day;  in  Idaho  it  is 
low — 2  to  5  per  cent. 

Treatment. — Quinine  seems  to  exert  a  more  or  less  specific  action,  and 
should  be  given  in  large  doses  (15  grains,  1  gram,  hypodermicly, 
every  six  hours,  Anderson)  throughout  the  course  of  the  disease.  Other- 
wise, the  disease  should  be  treated  as  typhoid  fever.  Stimulants  are 
usually  called  for. 

EPIDEMIC  POLIOMYELITIS. 

(Acute  Poliomyelitis;  Infantile  Paralysis.) 

Epidemic  poliomyelitis  is  an  acute,  infectious,  and  mildly  contagious 
disease,  characterized  by  hemorrhagic  inflammation  and  softening  of  the 
brain  and  spinal  cord,  often  widespread,  but  sometimes  limited  to  the 
anterior  horns  of  the  spinal  cord;  clinically  it  is  characterized  by  fever 
and  flaccid  paralysis  of  one  or  more  limbs. 

Etiology. — Poliomyelitis  may  occur  sporadically  or  epidemically.  Spo- 
radic cases  occur  widely  distributed  from  time  to  time,  but  especially 
during  the  summer;  they  are  almost  exclusively  confined  in  children 
from  two  to  four  years  of  age,  although  they  do  occur  in  older  children. 
The  epidemics  have  been  most  frequent  in  this  country  and  in  Norway. 
They  have  been  more  common  in  rural  districts,  but  have  occurred  also 
in  cities,  such  as  New  York,  Christiania,  Stockholm,  etc. ;  they  have  pre- 
vailed especially  during  the  autumn;  and  while  many  children  have  been 
affected,  the  disease  has  been  quite  common  in  young  adults. 

The  exciting  cause  of  the  disease  has  not  been  isolated.  Flexner  and 
Lewis,  using  an  emulsion  of  the  spinal  cord  from  a  fatal  case  in  a  child, 
have  been  enabled  to  transmit  the  infection  to  monkeys,  and  using  the 
spinal  cords  of  infected  monkeys  to  transmit  the  infection  to  several 
generations  of  monkeys.  Infections  have  been  made  successfully  by 
intracerebral  inoculation,  and  by  inoculation  into  a  large  nerve  (sciatic), 
into  the  circulation,  into  the  peritoneum,  and  beneath  the  skin.  The 
virus  is  filtrable  (like  that  of  rabies  and  vaccinia),  and  is  believed  to 
belong  to  the  class  of  ultramicroscopic  organisms.  How  the  infection 
is  acquired  is  not  definitely  known,  although  it  is  supposed  to  be  by 
inhalation,  the  naso-pharynx  being  the  primary  site  of  infection. 

Pathology. — ^The  lesions  consist  of  inflammation,  softening,  and  hemor- 
rhage, in  mild  cases,  more  or  less  limited  to  the  anterior  horns  of  the 
spinal  cord,  and  leading  to  marked  degeneration  of  the  motor  ganglion 
cells ;  the  lesions,  even  in  mild  cases,  however,  may  be  more  widespread 
and  may  be  associated  with  lymphocytic  infiltration  of  the  pia-arachnoid. 
Analogous  lesions  may  occur  in  the  medulla,  pons,  and  gray  matter  of 
the  cerebrum.  In  severe  cases  the  lesions  are  those  of  diffuse  myelitis 
and   encephalitis,  with   more  or  less   meningitis.     Flexner  and  Lewis 


EPIDEMIC   POLIOMYELITIS  271 

have  found  the  virus  in  the  central  nervous  system,  the  cerebrospinal 
fluid,  and  mesenteric  lymph  nodes.  After  the  disease  has  run  its  course, 
the  affected  portion  of  the  cord  is  found  lessened  in  size;  the  anterior 
horns  are  greatly  atrophied  and  contain  few  if  any  ganglion  cells;  the 
corresponding  motor  nerve  roots  are  atrophied;  and  the  muscles  supplied 
thereby  are  atrophic,  sclerotic,  and  perhaps  fatty.  The  lower  motor 
neuron,  therefore,  bears  the  brunt  of  the  infection. 

Symptoms. — ^The  period  of  incubation  is  not  known.  There  may  be 
slight  prodromal  symptoms,  but,  as  a  rule,  the  onset  is  abrupt,  with  fever 
(101°  to  103°  F.),  headache,  malaise,  perhaps  vomiting,  and  rarely  con- 
vulsions. In  some  cases  pains  are  complained  of  in  the  arms,  legs,  or 
back;  but,  as  a  rule,  attention  is  first  directed  to  the  limbs  by  paralyses. 
This  develops  rapidly,  usually  within  twenty-four  hours;  not  infrequently 
the  child,  perhaps  a  little  feverish  on  retiring  for  the  night,  is  found 
paralyzed  in  the  morning.  The  paralysis  is,  as  a  rule,  at  its  maximum 
at  the  beginning,  that  is,  usually  it  does  not  progress;  it  is  irregular  and 
asymmetrical  in  its  distribution;  it  may  involve  a  part  of  one  limb,  the 
entire  limb,  two  or  more,  or  all  four  limbs.  In  the  legs  the  tibialis  an- 
ticus  and  the  extensors  are  most  commonly  involved;  in  the  arm,  there 
is  an  upper-arm  type  (deltoid,  biceps,  brachialis  anticus,  and  supinator 
longus),  and  a  lower-arm  type  (extensors  or  flexors  of  the  wrist  and  fingers) 
— all  of  which  is  due  to  the  group  representation  of  muscles  in  the  spinal 
cord.  The  muscles  of  the  face  (cranial  nerves),  the  sphincters,  and  sen- 
sation are  rarely  affected.  The  reflexes  are  absent.  The  muscles  sup- 
plied by  the  affected  neurons  soon  undergo  atrophy,  become  soft  and 
flabby,  and  at  the  end  of  a  week  usually  reveal  the  reactions  of  degener- 
ation. As  a  rule,  after  several  weeks,  some  improvement  takes  place; 
in  case  there  was  only  slight  involvement  of  a  limb,  almost  complete 
recovery  may  ensue;  but  complete  initial  paralysis  always  results  in  more 
or  less  permanent  disability.  The  limb  remains  smaller  and  shorter  than 
its  fellow,  that  is,  growth  is  retarded;  the  muscles  remain  soft  and  flabby, 
and  the  skin  cold  and  livid;  and  contractures  and  deformities  may  ensue, 
[n  the  case  the  leg  is  involved,  apparatus  are  often  required  to  enable 
the  patient  to  get  about. 

Diagnosis. — ^The  diagnosis  is  readily  made,  fever  and  the  rapid  onset  of 
flaccid  paralysis  in  one  or  more  limbs,  soon  followed  by  the  reactions  of 
degeneration,  being  unequivocal;  these  exclude  the  cerebral  paralyses. 
The  pseudoparalysis  of  infantile  scurvy  (acute  rickets,  scurvy-rickets) 
may  be  excluded  by  the  usually  complete  loss  of  power  and  rapid  atrophy; 
in  infantile  scurvy,  movement  is  possible  although  it  is  painful,  and  there 
are  the  characteristic  changes  in  the  bones,  cutaneous  hyperesthesia,  etc. 

Prognosis. — The  outlook  is  not  hopeful;  that  is,  complete  restoration 
of  structure  and  function  is  unlikely.  The  condition  is  usually  at  its  worst 
ni  the  first  day  or  two;  after  a  stationary  period  more  or  less  improvement 
follows,  })ut  shortening,  contractures,  and  deformities  are  common. 

Treatment. — If  seen  during  the  period  of  fever,  the  child  slu)uld  be  put 
to  bed  and  given  a   diuretic  andfdiaphoretic  fever   mixture  (spirit  of 


272  INFECTIOXS  OF   UXKXOWX   ETIOLOGY 

nitrous  ether,  solution  of  ammonium  acetate,  or  of  potassium  citrate,  etc.). 
The  bowels  should  be  freely  opened;  and  the  affected  limb  or  limbs  may 
be  wrapped  in  cotton  wool.  Starr  recommends  the  use  of  hexamethy- 
lenamin,  1  grain  (0.06  gram)  every  six  hours,  to  a  child  three  years  of 
age;  the  drug  is  eliminated  in  the  cerebrospinal  tract  and  perhaps  exerts 
some  antiseptic  action  on  the  infectious  microorganisms.  Ergot,  bella- 
donna, quinine,  the  salicylates,  and  potassium  iodide  have  also  been 
recommended.  Attention  must  be  paid  to  the  general  nutrition  of  the 
child — good  food  and  fresh  air.  As  soon  as  the  sensitiveness  has  subsided, 
rubbing,  kneading,  and  warm  baths  to  the  affected  limbs  should  be  insti- 
tuted; electricity  is  of  less  value,  but  may  be  employed.  Strychnine  is 
a  serviceable  remedy  in  this  stage,  and  may  be  combined  with  other 
tonics.  Deformities  should  be  prevented  by  exercises  and  the  use  of 
orthopedic  apparatus;  developed  deformities  should  be  corrected,  by 
operation  if  necessary. 


•  ACUTE  INFECTIOUS  JAUNDICE. 

{Weil's  Disease.) 

From  the  large  group  of  cases  of  infectious  or  toxic  jaundice,  a 
special  form,  known  as  Weil's  disease,  is  usually  separated,  but  the  pro- 
priety of  this  is  doubtful.  Described  by  ^Yeil,  in  1886,  it  is  character- 
ized by  fever,  jaundice,  enlargement  of  the  liver  and  the  spleen,  and 
nephritis.  It  prevails  especially  during  the  summer  months,  is  most 
common  in  males  between  the  ages  of  twenty  and  forty  years,  and  seems 
to  have  a  special  predilection  for  butchers,  soldiers,  etc.  It  has  been 
ascribed  to  Bacillus  proteus  fluorescens,  which  has  been  found  in  de- 
caying meat,  sausages,  drinking  water,  etc.  Some  French  cases  are 
ascribed  to  Bacillus  coli  infections;  others  may  be  proteus  infections. 
Doubtless  all  cases  are  not  alike.  Infection  is  believed  to  be  acquired 
by  eating  infected  meat  or  cheese,  or  drinking  tainted  water. 

Pathology. — ^The  tissues  are  bile-stained;  the  liver  is  normal  in  size  or 
enlarged,  the  kidneys  are  swollen,  and  both  organs  exhibit  fatty  degener- 
ation of  the  epithelium,  and  the  liver  focal  necroses;  the  spleen  is 
enlarged;  and  hemorrhages  into  the  skin  and  the  mucous  and  the 
serous  membranes  may  be  encountered. 

Symptoms. — ^The  onset  is  sudden,  with  chilliness,  fever  (103°  to  104°F.), 
headache,  malaise,  rapid  pulse,  and  severe  neuromuscular  pains,  espe- 
cially in  the  back  and  the  calves  of  the  legs,  but  not  infrequently  also  in 
the  arms  and  even  the  cheeks.  Jaundice  develops  on  the  second  day; 
it  is  usually  slight  or  moderate  in  degree,  but  may  become  severe;  it  lasts 
ten  days  or  more,  and  gradually  lessens.  The  liver  is  usually  swollen 
and  tender,  the  spleen  is  enlarged;  the  stools  may  be  light  colored,  but 
commonly  contain  some  bile;  and  the  urine  contains  albumin  and  casts. 
Delirium  and  the  typhoid  state  may  supeiwene.  With  the  onset  of  the 
jaundice  the  pulse  becomes   slower.     Gastro-intestinal   symptoms   are 


FOOT-AND-MOUTH  DISEASE  273 

unusual.  The  fever,  which  is  characterized  by  marked  remissions,  lasts 
a  week  or  ten  days,  and  gradually  subsides.  Recovery  usually  ensues, 
but  convalescence  may  be  slow  and  relapses  are  not  infrequent  (40  per 
cent,  of  the  cases,  Quincke). 

Diagnosis. — In  the  diagnosis,  other  forms  of  infectious  or  toxic  jaundice, 
catarrhal  jaundice,  and  bilious  remittent  fever  must  be  considered.  . 

Treatment. — ^The  treatment  is  altogether  symptomatic,  and  consists 
of  rest  in  bed,  a  milk  diet,  cleansing  of  the  intestine  by  calomel,  the  use 
of  intestinal  antiseptics,  and  the  meeting  of  such  other  symptomatic 
indications  as  they  may  arise. 


FOOT-AND-MOUTH  DISEASE. 

{Epidemic  Stomatitis;  Aphthous  Fever;  Epizootic  Aphtha.) 

Foot-and-mouth  disease,  or  epidemic  stomatitis,  is  an  acute,  specific, 
infectious,  and  highly  contagious  disease  of  lower  animals,  transmissible 
to  man,  and  characterized  by  a  vesicular  eruption  on  the  oral  mucous 
membrane  and  sometimes  on  the  skin. 

Etiology. — Epidemic  stomatitis  is  common  among  cattle,  sheep,  and 
pigs,  and  is  transmissible  to  the  domestic  animals,  and  rarely  to  man, 
through  the  medium  of  infected  milk,  butter,  or  cheese;  rarely  infection 
occurs  directly  through  a  wound  (hands,  arm,  foot).  In  cows  the  udders 
are  not  infrequently  involved,  whence  the  ready  transference  of  the  dis- 
ease through  the  medium  of  the  milk.  The  specific  etiological  factor 
has  not  yet  been  isolated.  Loffler,  who  has  been  able  to  vaccinate 
animals  against  the  disease,  believes  that  the  specific  cause  is  an  ultra- 
microscopic  organism,  since  it  passes  through  porcelain  filters  the  pores 
of  which  do  not  permit  the  passage  of  the  smallest  bacteria  known. 

Symptoms. — The  period  of  incubation  is  from  three  to  seven  days. 
The  onset  of  the  disease  is  announced  by  moderate  fever,  slight  chilliness, 
a  sensation  of  heat  in  the  mouth  and  throat,  pain  and  difficulty  in  swal- 
lowing, and  soon  the  eruption  of  vesicles  on  the  lips,  oral,  buccal,  and 
pharyngeal  mucous  membrane,  occasionally  also  on  the  skin,  especially 
the  hands  (about  the  nails),  the  feet  (between  the  toes),  and  rarely  else- 
where. At  the  end  of  several  days  the  vesicles  rupture,  and  leave  small 
ulcers  that  usually  heal  in  a  week  or  ten  days.  Rarely  the  exanthem 
is  widespread,  and  has  even  been  known  to  be  hemorrhagic.  Severe 
gastro-intestinal  symptoms  and  endocarditis  may  occur  as  complications. 
The  duration  of  the  disease  is  two  to  four  weelvs. 

Diagnosis. — The  diagnosis  is  easy;  only  the  careless  would  mistake  it 
for  varicella. 

Treatment. — The  treatment  is  that  of  stomatitis.     If  it  be  necessary 
to  use  the  milk  during  the  prevalence  of  an  epidemic  among  the  cows,  it 
should  at  least  be  boiled, 
18 


274  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

MILIARY  FEVER. 

{Sweating  Sickness.)  ■ 

Miliary  fever  is  an  acute  infectious  and  moderately  contagious  disease 
characterized  by  fever,  profuse  sweats,  and  a  papulovesicular  rash. 

Etiology. — The  disease  attacks  children  and  adults  apparently  indis- 
criminately. It  usually  prevails  epidemically — in  Europe;  as  far  as  is 
known,  no  epidemic  has  occurred  in  this  country.  The  exciting  cause 
of  the  disease  is  not  known.  How  the  contagium  is  spread  is  not  defi- 
nitely known,  but  the  large  number  of  persons  affected  at  the  one  time 
lends  support  to  the  view  of  aerial  convection. 

Symptoms. — The  period  of  incubation  is  not  definitely  known,  but  it 
is  probably  not  more  than  a  day  or  two — during  which  there  may  be 
minor  prodromal  manifestations.  As  a  rule,  the  onset  is  rather  sudden, 
with  fever  and  profuse  sweating.  The  fever  is  usually  not  more  than 
103°  F.,  but  hyperpyrexia  has  been  observed.  In  addition,  the  patient 
complains  of  headache,  respiratory  oppression  (suggesting  suffocation), 
anorexia,  and  constipation.  On  the  second  or  third  day  the  character- 
istic rash  appears — on  the  skin  (often  first  on  the  face)  and  the  oral  mucous 
membrane;  it  consists  of  minute,  reddish  papules,  most  of  which  soon 
develop  a  tiny  vesicle  at  their  apex — much  resembling  sudamina.  Suda- 
mina,  that  is,  vesicles  not  on  an  inflammatory  base,  may  also  be  observed. 
Soon  after  vesiculation,  dessication,  followed  by  desquamation,  sets  in. 
Sweating  is  constant,  but  exacerbations  occur.  In  cases  with  high  fever, 
other  evidences  of  toxemia  are  present  (delirium,  prostration,  etc.), 
and  emaciation  usually  progresses  rapidly.  In  favorable  cases  the  fever 
falls  by  lysis,  and  by  the  tenth  day  the  patient  is  convalescent.  In  un- 
favorable cases  the  patient  dies  with  manifestations  of  increasing 
intoxication — delirium,  coma,  convulsions,  hemorrhages,  etc.  In  certain 
so-called  fulminant  cases  death  has  occurred  within  the  first  few  hours. 

Diagnosis. — ^In  an  epidemic  the  disease  is  unmistakable. 

Prognosis. — ^The  mortality  varies  up  to  25  per  cent,  in  different  epi- 
demics.    Relapses  are  common. 

Treatment. — ^The  treatment  should  consist  of  rest  in  bed,  soft  diet  with 
a  considerable  amount  of  fluids  (to  replace  the  water  lost  by  the  sweats), 
hydrotherapy  for  its  stimulating  effect  and  to  control  the  fever  and 
toxemia,  and  stimulants  (alcohol,  strychnine,  etc.);  atropine  may  be 
indicated  for  the  sweats. 


MILK  SICKNESS. 

(Trembles.) 

Milk  sickness  is  an  acute  infectious  disease  of  cattle  ("trembles"),  com- 
municable to  man,  and  characterized  by  gastro-intestinal  irritation  and 
nervous  phenomena  attributable  to  toxemia. 


BERIBERI  275 

Etiology, — ^l^'embles  prevails  among  cattle,  in  the  South  and  West, 
especially  in  newly  settled  regions,  and  is  communicable  to  man  and  the 
young  of  horses  and  sheep.  The  specific  infectious  agent  has  not  been 
isolated  with  certainty,  although  Jordan  and  Harris  describe  a  so-called 
Bacillus  lactimorbi.  The  infection  is  transmitted  to  man  by  means  of 
milk,  butter,  and  cheese;  and  these,  as  well  as  the  flesh  of  infected  cows, 
even  after  having  been  boiled,  are  poisonous  to  dogs. 

Symptoms. — In  cows,  mild  cases  may  be  symptomless,  unless  the  ani- 
mal is  hard-driven,  although  the  milk  may  be  infectious;  in  severe  cases 
the  cow  refuses  food,  the  eyes  become  injected,  the  animal  staggers  and 
trembles  all  over,  and  may  soon  die,  often  in  convulsions.  In  man  the 
symptoms  are  gastro-intestinal,  such  as  a  swollen,  coated,  and  tremulous 
tongue,  fetid  breath,  thirst,  epigastric  distress  and  pain,  nausea,  vomit- 
ing and  constipation;  and  toxic,  such  as  fever,  restlessness,  coma  and 
convulsions,  or  a  typhoid  state.  Death  may  occur  in  two  or  three  days 
in  acute  fulminant  cases.  In  other  cases  the  disease  may  last  from  ten 
days  to  about  three  weeks,  and  be  followed  by  a  tedious  convalescence. 

Treatment. — The  treatment  is  purely  symptomatic. 

BERIBERI. 

(Kakke;  Endemic  Multiple  Neuritis.) 

Beriberi  is  a  specific,  probably  infectious  or  toxic,  disease  of  tropical 
and  subtropical  countries  characterized  by  multiple  neuritis  and  different 
consequent  motor  and  sensory  paralyses,  muscular  atrophy,  and  ana- 
sarca. 

Etiology. — Beriberi  is  endemic  in  the  Malay  Archipelago,  China,  Japan, 
India,  certain  parts  of  South  America  (notably  Brazil),  the  West  Indies, 
the  Dutch  East  Indies,  the  Philippines,  and  other  South  Pacific  Islands. 
It  is  also  occasionally  met  in  different  parts  of  the  world,  but  largely 
as  an  imported  infection.  In  this  country  it  has  prevailed  especially 
among  the  Cape  Cod  fishermen,  in  asylums  in  Alabama  and  Arkansas, 
and  in  Louisiana.  Bad  hygienic  surroundings,  especially  overcrowding, 
seem  important  etiologically,  whence  the  frequent  occurrence  of  the 
disease  in  barracks,  jails,  ships,  etc.;  but  marked  heat  and  humidity 
seem  also  to  be  of  significance,  whence  its  frequent  occurrence  during 
the  rainy  season.  The  yellow  races  are  particularly  susceptible.  ]Males 
are  more  frequently  afl^ected  than  females,  largely  because  of  extraneous 
circumstances.  The  disease  is  most  common  during  adolescence  and 
early  adult  life — the  fifteenth  to  the  fortieth  year. 

The  exciting  cause  of  the  disease  has  not  been  determined.  There  is 
consi(leraV)le,  though  not  conclusive,  evidence  that  it  is  due  to  micro- 
organismal  infection,  as  maintained  by  Baelz,  Scheube,  and  Wright,  the 
last  mentioned  of  whom  believes  that  the  infecting  organism  gains 
entrance  to  the  body  through  the  mouth  and  elaborates  its  toxin  in  the 
stomach  and  duodenum.  Okata  and  Kokubo  have  described  a  coccus 
which  thev  have  isolated  from  the  urine  and  which  thev  believe  is  the 


276  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

specific  cause.  The  Japanese  generally  attribute  the  disease  to  bad 
food,  especially  rice  and  fish,  which  either  itself  directly  causes  the  dis- 
ease (whence  a  nutritional  disorder  due  largely  to  deficient  nitrogen 
supply  or  assimilation)  or  acts  as  the  carrier  of  the  infection  or  toxin. 
Ross  attributes  it  to  arsenical  poisoning,  since  arsenic  is  a  common 
adulterant  of  tobacco  in  the  East,  and  he  has  found  arsenic  in  the  hair 
of  a  number  of  patients. 

Pathology. — The  characteristic  lesions  consist  of  degeneration  of 
the  peripheral  nerves,  involving  the  axons  and  medullary  sheaths.  In 
severe  cases,  similar  lesions  are  found  in  the  pneumogastric  and  the 
phrenic  nerves.  There  is  also  congestion  of  the  pylorus  of  the  stomach 
and  of  the  duodenum  (considered  specific  by  Wright),  hyperemic  and 
cloudy  swelling  of  the  liver  and  the  kidneys,  enlargement  of  the  spleen, 
and  parenchymatous  and  fatty  degeneration  of  the  cardiac  and  the  volun- 
tary muscles;  and  in  some  cases  oedema  of  the  subcutaneous  tissues  and 
serous  cavities. 

Symptoms. — The  period  of  incubation  is  not  known,  but  it  has  been 
said  by  Wright  to  be  between  ten  and  fifteen  days.  Clinically,  Scheube 
distinguishes  four  types  of  the  disease — largely  variations  in  degree : 

The  rudimentary  form  begins  usually  with  pain  and  weakness  in 
the  extremities,  associated  with  paresthesia  and  anesthesia  of  the  leg, 
frequently  quite  circumscribed  and  irregular  in  distribution.  Slight 
oedema  also  may  develop,  the  muscles  may  become  tender,  and  palpita- 
tion of  the  heart,  dyspnoea,  and  abdominal  uneasiness  may  be  observed. 
The  symptoms  last  for  a  few  days  to  several  months,  and  generally 
disappear.     Recurrences,  however,  are  often  encountered. 

The  paralytic  or  atrophic  form  presents,  as  a  rule,  symptoms  similar 
to  the  foregoing,  but  the  pains  in  the  limbs  are  more  pronounced,  and 
the  muscles  of  the  legs  soon  become  paralyzed  and  atrophic.  The  par- 
alyses and  atrophy  may  extend  to  the  muscles  of  the  trunk,  less  frequently 
to  the  arms,  head,  and  neck.  The  paralyses  are  usually  flaccid,  reactions 
of  degeneration  are  present,  and  the  tendon  reflexes  are  absent.  The 
areas  of  anesthesia  and  of  paresthesia  are  often  irregularly  distributed. 
The  cardiac  symptoms  are  not  pronounced,  and  the  oedema  is  usually 
slight  (whence  the  term,  dry  beriberi).  Recovery,  when  it  ensues,  is 
very  slow. 

The  dropsical  form  begins  as  the  preceding  forms,  but  oedema  soon 
appears,  and  the  patient,  as  a  rule,  speedily  becomes  anasarcous — effusions 
into  the  subcutaneous  tissues  and  the  serous  cavities.  Palpitation  of  the 
heart,  rapid  heart  action,  dyspnoea,  and  cyanosis  of  the  extremities  are 
quite  marked.  Paralyses  and  muscular  atrophy  are  not  as  pronounced 
as  in  the  other  cases,  but  even  notable  atrophy  is  not  infrequently  ob- 
scured by  the  existing  oedema.  The  urine  is  diminished  in  amount, 
but,  as  a  rule,  contains  no  albumin.  The  condition  persists  for  weeks 
and  even  months,  and  if  recovery  eventually  ensues  there  is  sometimes 
a  very  rapid  disappearance  of  the  oedema,  with  great  increase  in  the 
amount  of  urine. 


EPIDEMIC  DROPSY  277 

The  acute  pernicious  or  cardiac  form  begins  as  the  preceding  forms, 
but  cardiac  weakness  is  soon  manifest,  and  complete  cardiac  failure  may 
supervene  within  twenty-four  hours.  Usually,  however,  it  lasts  several 
weeks. 

Diagnosis. — The  disease  where  it  is  endemic  presents  no  diagnostic 
difficulties,  especially  when  several  cases  exist  in  the  same  vicinity.  In 
sporadic  cases,  evidences  of  peripheral  neuritis,  with  anasarca,  and  an 
irritable  and  weak  heart,  in  a  patient  just  arrived  from  the  tropics  is 
extremely  significant.  Arsenical  and  alcoholic  neuritis  should  be  ex- 
cluded. 

Prognosis. — The  mortality  varies  from  2  per  cent,  in  mild  cases  to  40 
per  cent,  in  severe  cases.  Patients  seemingly  progressing  favorably  not 
infrequently  die  of  acute  cardiac  failure. 

Treatment. — The  patient  should  be  removed  from  the  endemic  locality, 
be  placed  amidst  the  best  hygienic  surroundings,  and  given  a  diet  rich 
in  nitrogen  and  phosphorus.  The  treatment  otherwise  is  largely  symp- 
tomatic. Stimulants  are  valuable  for  cardiac  weakness.  Acute  cardiac 
failure  should  be  met  with  bleeding  and  free  purgation.  During  conva- 
lescence the  neuritis  is  to  be  treated  as  any  other  neuritis.  Baelz  has 
recommended  the  salicylates  in  the  early  stages  of  the  disease. 


EPIDEMIC  DROPSY. 

Epidemic  dropsy  is  a  subacute,  infectious,  and  contagious  disease 
characterized  by  fever,  vomiting,  diarrhoea,  and  the  sudden  appearance 
of  anasarca. 

Etiology. — Epidemic  dropsy  is  peculiar  to  India,  where  it  prevails 
especially  during  the  cold  weather,  and  attacks  adolescents  and  adults 
of  both  sexes.  It  is  rare  in  infants.  The  exciting  cause  of  the  disease 
has  not  been  isolated,  though  there  is  some  evidence  that  the  contagium  is 
more  or  less  readily  communicable  from  the  sick  to  the  well. 

Symptoms. — The  onset  of  the  disease  is  often  marked  by  fever,  varying 
from  99°  to  102°  F.,  which  often  precedes  but  sometimes  accompanies 
the  development  of  dropsy — the  most  characteristic  feature  of  the 
disease.  Vomiting  and  diarrhoea  are  common,  and  sometimes  mark 
the  development  of  the  disease.  The  dropsy  begins,  as  a  rule,  in  the 
legs,  and  soon  involves  the  entire  body;  it  may  be  preceded  by 
burning,  pricking,  and  itching  of  the  skin.  Marked  anemia  soon 
supervenes,  and  disturbances  of  circulation  and  respiration  are  prominent 
in  almost  all  cases.  An  erythematous  rash  often  appears  on  the  face 
and  trunk  about  a  week  after  the  development  of  the  dropsy.  The  dis- 
ease runs  its  course  in  from  three  to  six  weeks.  The  mortality  varies 
from  2  to  40  per  cent.,  and  death  results  from  oedema  of  the  lungs, 
liydrothorax,  hydropericardium,  or  other  cardiac  or  pulmonary  com- 
plications. 

Treatment. — The  treatment  is  purely  symptomatic. 


278  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

NASHA  FEVER. 

{Nakra  Fever.) 

Nasha  fever  is  an  acute  infectious  disease,  peculiar  to  certain  parts 
of  India,  especially  Bengal,  and  characterized  by  fever,  swelling  of  the 
nasal  mucous  membrane,  and  sometimes  coma  and  death. 

Etiology. — ^The  nature  of  the  disease  is  not  known.  Exposure,  un- 
hygienic conditions,  and  poor  food  seem  to  predispose  to  it.  Women 
apparently  are  more  predisposed  than  men;  children  and  the  aged  are 
relatively  immune.  It  prevails  mostly  from  April  to  August.  One  attack 
seems  to  predispose  to  others,  which  sometimes  develop  at  more  or  less 
definite  intervals.  The  disease  is  believed  by  some  observers  to  be  a 
manifestation  of  malaria,  but  this  is  doubtful,  since  the  malarial  parasite 
has  not  been  found  and  the  disease  is  refractory  to  quinine. 

Symptoms. — The  disease  usually  begins  with  congestion  of  the  nasal 
mucous  membrane  and  the  development  of  a  pea-sized,  circumscribed 
swelling  on  the  nasal  septum.  The  patient  soon  complains  of  malaise, 
headache,  severe  neuromuscular  pains  in  the  neck  and  shoulders,  con- 
stipation, and  fever.  The  fever  is  moderate  in  degree  and  usually  sub- 
sides in  from  three  to  five  days,  concurrently  with  subsidence  of  the  nasal 
symptoms.  The  swelling  of  the  nasal  mucous  membrane  never  goes 
on  to  suppuration,  but  cases  have  been  reported  in  which  sudden  sub- 
sidence of  the  sw^elling  has  been  followed  by  grave  cerebral  symptoms, 
such  as  coma,  delirium,  and  death.  The  spleen  is  usually  enlarged  and 
palpable.  A  diffuse  erythematous  eruption  has  occasionally  been 
observed. 

Treatment. — ^The  treatment  is  purely  symptomatic.  Puncture  of  the 
spleen,  which  has  been  recommended  as  affording  relief  to  the  local  and 
general  symptoms,  seems  to  be  unduly  hazardous. 

JAPANESE  RIVER  FEVER. 

Japanese  river  fever  is  an  acute,  infectious  disease,  occurring  in  the 
western  part  of  the  Island  of  Nippon,  and  characterized  by  an  initial 
eschar,  soon  followed  by  ulceration  of  the  skin,  continued  fever,  inflam- 
mation of  the  lymphatics,  and  an  exanthematous  eruption. 

Etiology. — The  nature  of  the  disease  is  unknown,  though  it  affects 
practically  only  those  engaged  in  harvesting  the  corn  and  hemp  in 
a  certain  part  of  the  island  of  Nippon.  The  Japanese  attribute  it  to  the 
bite  of  an  ascarus.  The  primary  eschar  is  not  unlikely  the  point  of 
infection.  Sex  and  age  are  without  etiological  influence.  One  attack 
does  not  confer  immunity,  though  it  seems  to  lessen  the  severity  of  sub- 
sequent attacks. 

Symptoms. — The  period  of  incubation  is  from  four  to  seven  days, 
during  which  the  patient  may  complain  of  malaise  and  repeated  rigors. 


PONOS  279 

The  first  indication  of  the  disease  is  the  initial  eschar,  which  develops 
about  the  genitals,  the  axillae,  or  the  neck.  Soon  an  ulcer  forms — round, 
dark,  tough,  firmly  adherent,  and  surrounded  by  a  painless  area  of  super- 
ficial congestion.  The  regional  lymph  nodes,  and  sometimes  all  the 
lymph  nodes  of  the  body  and  the  spleen,  become  swollen  and  con- 
gested. With  the  onset  of  the  infection,  fever  develops,  pursues  a 
more  or  less  continued  course,  and  ranges  between  103°  and  104°  F. 
Catarrhal  inflammation  of  the  conjunctivae  and  of  the  bronchi  not  in- 
frequently arises.  On  about  the  fifth  to  the  seventh  day  an  eruption, 
consisting  of  large,  dark  red  papules,  appears  on  the  face,  forearms, 
legs,  and  trunk,  and  not  infrequently  at  the  same  time  a  minute  lichenous 
rash  appears  on  the  forearms  and  trunk.  Both  eruptions  disappear 
in  from  four  to  seven  days,  while  the  fever  begins  to  remit  at  the  end 
of  about  two  weeks,  and  the  temperature  soon  reaches  the  normal. 
During  the  second  week  the  ulceration  begins  to  heal,  the  eschar  being 
first  cast  off".     The  mortality  varies  between  15  and  50  per  cent. 

Treatment. — The  treatment  is  purely  symptomatic.  The  ulcer  should 
be  dressed  antiseptically.  Quinine  and  the  salicylates  have  been  recom- 
mended internally.     Hydrotherapy  also  may  be  useful. 


PONOS. 

Ponos  is  a  rare,  chronic,  endemic  disease  of  childhood  that  occurs 
in  the  islands  of  Spetza  and  Hydra,  off  the  coast  of  Argolis,  and  is  char- 
acterized by  irregular  fever,  enlargement  of  the  spleen,  and  emaciation. 

Etiology. — Apparently  ponos  effects  only  children,  and  commonly 
those  under  the  age  of  four  years,  and  of  tuberculous  antecedents.  It 
appears  to  be  uninfluenced  by  climate,  season,  or  social  conditions. 
Its  exciting  cause  is  not  known,  and  in  reality  its  nature  is  ill  understood. 

Pathology. — Apparently  the  necrospy  findings  of  only  one  case  have 
been  reported.  In  this  the  spleen  was  much  enlarged,  the  capsule  firm, 
and  the  stroma  and  trabeculse  considerably  thickened ;  the  liver  exhibited 
early  cirrhosis;  the  kidneys  were  congested;  and  the  bronchial  and  the 
mesenteric  lymph  nodes  were  swollen. 

Symptoms. — The  onset  is  sudden  with  fever,  which,  having  developed, 
pursues  a  remittent  and  irregular  course.  The  spleen  rapidly  enlarges 
and  becomes  tender;  dyspepsia  and  constipation  develop,  and  the  patient 
emaciates  rather  rapidly,  \\lien  the  disease  has  become  well  established 
«>dema  and  ascites  may  develop,  and  hemorrhages  into  and  from  the 
ditt'erent  organs  and  tissues,  especially  the  gums,  may  occur.  Boils 
and  superficial  areas  of  gangrene  have  been  observed.  The  disease 
lasts  for  a  few  months  to  several  years,  and  the  patients  rarely  recover. 

Treatment. — The  treatment  is  unsatisfactory  and  scarcely  more  than 
symptomatic,  consisting  largely  of  careful  dieting  and  the  administra- 
tion of  tonics. 


280  INFECTIONS  OF  UNKNOWN  ETIOLOGY 


HILL  DIARRHCEA. 

Hill  diarrhoea  is  a  peculiar  disorder  of  the  tropics,  especially  India, 
characterized  by  morning  diarrhoea,  copious,  pale,  liquid  stools,  and 
flatulent  dyspepsia. 

Etiology. — The  causative  factors  of  hill  diarrhoea  are  ill  understood. 
The  disorder  is  especially  common  in  colonists  who,  having  become 
acclimated  to  lovi^,  hot  plains,  go  (often  for  a  holiday)  to  the  neighboring 
hills  (5000  feet  or  more).  The  disease  seems  to  be  more  than  an  ordinary 
intestinal  catarrh;  in  some  respects  it  resembles  sprue,  though,  unlike 
it,  it  tends  to  recovery.  By  some  observers  it  is  believed  to  be  dyspeptic 
in  character  and  associated  with  suppression  of  the  function  of  the  liver, 
pancreas,  etc.  Scheube  attributes  it  to  atony  of  the  colon,  and  to  chilling 
of  the  abdomen  due  to  the  cold  and  dampness  of  the  early  morning  hours 
of  tropical  mountainous  countries. 

Symptoms. — ^The  disorder  not  infrequently  begins  with  flatulent 
dyspepsia  soon  after  the  subject  reaches  the  mountains.  Usually  on 
the  following  morning  between  3  and  5  o'clock  diarrhoea  begins,  and 
from  six  to  twelve  stools  or  more  may  be  passed  before  noon,  after 
which  the  diarrhoea  not  infrequently  ceases  for  the  remainder  of  the  day. 
The  stools  are  copious,  watery  or  pasty,  pale,  frothy,  and  have  been 
likened  to  whitewash  (they  contain  no  biliary  coloring  matter).  The 
stools  are,  as  a  rule,  unattended  by  pain  or  tenesmus,  though  there  may 
be  a  vague,  indefinite  tenderness  along  the  course  of  the  colon.  The 
abdomen  is  sometimes  markedly  distended,  and  there  may  be  consider- 
able borborygmi.  The  disease  tends  to  recovery  at  the  end  of  ten  days 
or  two  weeks.     Recurrences  may  attend  repeated  visits  to  the  hills. 

Diagnosis. — Manson  states  that  the  distinctive  features  of  the  disease 
are  the  regular  recurrence  of  morning  diarrhoea,  its  cessation  after  a 
certain  hour  in  the  forenoon,  the  absence  of  color  in  the  stools,  and  the 
attendant  flatulence. 

Treatment. — The  diet  in  the  majority  of  cases  should  consist  of  milk, 
though  one  can  readily  understand  that  some  patients  might  do  better 
on  animal  broths,  etc.,  that  have  less  tendency  to  ferment.  The  patient 
should  remain  in  bed  during  the  morning  hours,  and  should  be  warmly 
clad.  Calomel  is  believed  to  be  useful  to  stimulate  the  hepatic  function. 
Crombie  and  Manson  advise  a  teaspoonful  of  Liquor  hydra rgyri  per- 
chloridi  (B.  P.),  in  water,  fifteen  minutes  after  each  meal.  The  digestive 
ferments  are  sometimes  useful.  If  treatment  is  of  no  avail,  the  patient 
should  return  to  the  lowlands  whence  he  came. 


EPIDEMIC  GANGRENOUS  PROCTITIS  281 


SPRUE. 

(Psilosis;   Chronic  Diarrhoea  of  Warm  Climates;   Chronic  or  Endemic  Diarrhoea  of 
Cochin  China;  Tropical  Diarrhoea;  Ceylon  Sore  Mouth;  Cachexia  Aphthosa.) 

"Sprue,  or  psilosis,  may  be  defined  as  an  insidious,  chronic,  remitting 
inflammation  of  the  whole  or  part  of  the  mucous  membrane  of  the  ah- 
mentary  canal,  occurring  principally  in  Europeans  who  are  residing  or 
have  resided  in  tropical  or  subtropical  climates.  It  is  characterized  by 
irregularly  alternating  periods  of  exacerbation  and  comparative  quies- 
cence; a  peculiar  inflamed,  superficially  ulcerated,  exceedingly  sensitive 
condition  of  the  mucous  membrane  of  the  tongue  and  mouth;  great 
wasting  and  anemia;  pale,  copious,  and  often  loose,  frequent,  and  frothy 
fermenting  stools;  very  generally  by  more  or  less  diarrhoea;  and  also 
by  a  marked  tendency  to  relapse.  Sprue  may  either  be  primary,  or  it 
may  supervene  on  or  complicate  other  affections  of  the  alimentary  canal. 
Unless  properly  treated  it  is  usually  fatal."     (Manson.) 

Etiology. — The  cause  is  unknown.  The  anatomical  lesions  are  not 
characteristic. 

Treatment.— The  treatment  is  largely  hygienic  and  dietetic.  Manson 
prefers  an  exclusive  milk  diet  for  weeks  or  months;  others  prefer  a 
meat  diet. 

EPIDEMIC  GANGRENOUS  PROCTITIS. 

Epidemic  gangrenous  proctitis  is  an  acute  infectious  disease,  character- 
ized by  rapidly  spreading  phagedena  of  the  anus  and  rectum,  progressing 
to  prolapse  and  gangrene  of  the  ulcerated  rectum. 

Etiology. — Epidemic  gangrenous  proctitis  is  more  or  less  widely 
distributed  throughout  the  tropics,  but  it  is  especially  prevalent  in 
Central  and  South  America,  and  in  the  Philippines  and  other  Pacific 
Islands.  Its  exciting  cause  is  not  definitely  known,  but  it  has  been 
attributed  to  bacterial  infection  (Bacillus  dysenterise.  Bacillus  pyocy- 
aneus,  etc.),  and  in  Venezuela  to  the  eating  of  the  green  stalks  of  unripe 
maize.  The  latter  view,  however,  is  scarcely  tenable  (for  all  cases  at 
least),  since  the  disease  occurs  where  maize  does  not  exist.  The  develop- 
ment of  the  disease  seems  favored  in  low-lying,  damp  regions.  In 
South  America  it  is  almost  confined  to  children;  in  other  tropical  regions 
adults  also  are  attacked. 

Pathology. — The  lesions  consist  of  ulceration  attended  by  pseudo- 
membranous formation,  limited  in  some  cases  to  the  region  of  the 
sphincters,  but  often  spreading  to  the  rectum  and  the  sigmoid,  and  soon 
followed  by  prolapse  and  gangrene  of  the  rectum. 

Symptoms. — The  initial  symptoms  consist  of  burning  and  itching 
above  the  anus  and  a  tendency  to  frequent  defecation.  Soon  the  dis- 
charges become  more  frequent  and  are  attended  by  abdominal  pain  and 
constant  and  distressing  tenesmus,  which  frequently  leads  to  extrusion 


282  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

of  the  bowel.  Fever,  anorexia,  and  thirst  supervene.  The  stools  at 
first  consist  of  fecal  matter;  soon,  however,  they  become  mucoid  or  muco- 
sanguineous,  and  extremely  fetid.  Occasionally  even  almost  pure  blood 
is  discharged.  Severe  nervous  symptoms,  such  as  delirium  and  coma, 
and  in  children,  convulsions,  supervene.  The  patient  emaciates  rapidly, 
and,  as  a  rule,  soon  dies — in  some  cases  before  prolapse  of  the  rectum 
has  occurred.  Recovery,  however,  occasionally  ensues,  even  after  the 
advent  of  coma,  prolapse,  and  gangrene  (with  sloughing)  of  the  rectum. 

Diagnosis. — In  the  early  stages  the  disease  is  not  unlikely  to  be  mis- 
taken for  dysentery,  but  an  examination  of  the  anus  and  rectum  serves 
to  prevent  error. 

Treatment. — Opium  is  indicated  to  relieve  pain  and  to  control  the 
intestinal  movements.  It  may  be  given  h^qjodermicly,  but  should  also 
be  applied  locally  to  the  inflamed  and  ulcerated  areas.  Antiseptic  and 
soothing  lotions  to  the  anus  and  rectum  are  also  called  for.  The  local 
use  of  a  portion  of  roasted  lemon  or  of  lemon  juice  has  a  vogue  in  Vene- 
zuela. In  the  event  of  gangrene  the  rectum  must  be  excised,  should  the 
patient's  condition  warrant  it. 


TROPICAL  PHAGEDENA. 

Tropical  phagedena  is  a  rapidly  spreading  gangrene  of  the  skin  and 
subcutaneous  tissues,  leading  to  the  formation  of  a  large  sloughing  sore. 

Etiology. — Tropical  phagedena  is  preeminently  a  disease  of  the  tropics, 
occurring  especially  where  the  climate  is  hot  and  damp.  The  exciting- 
cause  of  the  disease  is  not  known,  though  doubtless  it  is  a  microorganism. 
It  finds  its  readiest  victims  among  the  physically  depressed  and  those  in 
poor  health  from  any  cause.  In  some  subjects  an  insect  bite  or  an  abra- 
sion seems  to  be  the  starting  point  of  the  infection. 

Symptoms. — The  feet  and  legs  are  the  most  common  seat  of  the 
lesions,  though  no  part  of  the  body  is  exempt.  The  first  indication  of 
the  disease,  if  the  skin  has  been  previously  sound,  is  the  development  of 
a  large  blister,  containing  a  serosanguinolent  fluid.  This  ruptures  in 
a  few  hours,  and  exposes  a  sloughing  sore  which  rapidly  spreads  and 
forms  a  horribly  fetid,  yellowish  ulcer,  the  centre  of  w^hich  liquefies 
in  a  few  days,  while  the  periphery  continues  to  spread.  Not  only  is 
there  peripheral  extension,  but  also  extension  in  the  depths,  whereby 
the  muscles,  tendons,  nerves,  vessels,  and  bone  may  become  implicated. 
At  the  end  of  a  week  or  more  the  slough  is  gradually  separated.  When 
the  disease  begins  in  an  already  existing  wound  or  sore,  the  granulating 
surface  dries  and  is  gradually  converted  into  a  slough. 

The  lesions  cause  considerable  pain  which,  together  with  the  drain  on 
the  system,  undermine  the  patient's  health,  and  may  lead  to  death  from 
exhaustion,  hemorrhage,  or  septicemia.  In  some  cases,  however,  the 
constitutional  disturbance  is  relatively  slight  and  cicatrization  proceeds 
— provoking,  as  a  rule,  considerable  deformity  and  mutilation. 


ULCERATING  GRANULOMA   OF  THE  GENITALS  2S3 

Treatment. — Opium  is  indicated  not  only  to  relieve  pain,  but  also 
because  of  a  seeming  beneficial  action  on  the  phagedenic  process. 
The  ulcer  should  be  curetted  or  cauterized  with  pure  carbolic  acid,  and 
then  continuously  irrigated  with  a  tepid  antiseptic  lotion.  The  general 
health  should  be  maintained  bv  tonics  and  nutritious  food. 


TROPICAL  BUBO. 

(Climatic  Bubo;  Tropical  Non-venereal  Adenitis.) 

Tropical  bubo  is  a  non-venereal  inflammatory  enlargement  of  the 
inguinal  lymph  nodes  attended  by  remittent  fever  lasting  from  three 
to  four  weeks. 

Etiology. — Tropical  bubo  is  most  common  in  the  East  Indies  and  China, 
but  occurs  also  in  South  Africa,  Japan,  the  Philippines,  along  the  coast 
of  the  Mediterranean  Sea,  in  the  West  Indies,  Malaga,  etc.  Limited 
epidemics  have  been  observed  among  sailors  and  soldiers.  Age  is  of 
no  etiological  importance.  The  exciting  cause  of  the  disease  has  not 
been  isolated,  though  it  is  doubtless  microorganismal.  Infection  is 
believed  to  occur  through  small  wounds  or  abrasions  of  the  legs  or  genitals 
or  through  the  bites  of  insects. 

Symptoms. — The  onset  of  the  disease  is  often  rather  sudden,  with 
chill,,  fever  (103°  to  104°  F.),  headache,  backache,  and  enlargement, 
tenderness,  and  redness  of  the  lymph  nodes  of  the  groin  of  one  or 
both  sides.  In  some  cases  a  group  of  nodes,  in  other  cases  separate 
contiguous  nodes,  are  involved.  The  nodes  increase  in  size  until 
they  attain  that  of  a  goose  egg,  whereupon  the  fever,  which  has  been 
remittent  in  type,  gradually  lessens  and  the  nodes  decrease  in  size — 
though  they  may  remain  enlarged  for  two  months  or  more.  Usually 
there  is  little  pain,  and  the  constitutional  symptoms,  aside  from  the  fever 
are  slight.  In  some  cases,  however,  the  skin  over  the  enlarged  nodes 
becomes  adherent,  and  the  nodes  soften  and  form  suppurating  sinuses, 
which  lead  not  only  externally  but  often  deeply  into  adjacent  tissues. 
In  this  event  the  pain  and  constitutional  symptoms  may  become  marked. 
The  suppuration  may  continue  several  months. 

Treatment. — If  softening  has  not  occurred,  iodine  and  ichthyol,  or 
an  ointment  of  mercury,  belladonna,  and  iodine,  may  be  applied.  If 
softening  occurs,  the  abscess  should  be  opened  freely,  curetted,  and  treated 
antiseptically.  General  treatment  is  rarely  called  for,  and  at  all  events 
is  to  be  based  upon  general  principles. 


ULCERATING  GRANULOMA  OF  THE   GENITALS. 

Ulcerating  granuloma  of  the  genitals  (pudenda)  is  a  chronic  venereal 
disease  of  the  tropics,  characterized  by  its  granular  character,  its  large 
extent,  and  its  tendency  to  hemorrhage. 


284  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

Etiology, — Ulcerating  granuloma  of  the  genitals  occurs  in  men  and 
in  women  between  the  ages  of  thirteen  and  fifty  years,  and  is  uninfluenced 
by  sex.  The  exciting  cause  has  not  been  isolated,  though  it  is  present  in 
the  secretions  from  the  granulations  which  are  auto-inoculable  and  in- 
fectious to  others.  Wise  has  demonstrated  spirochetes  (resembling  Spiro- 
chgeta  refringens)  in  the  secretions. 

Symptoms. — The  disease  begins  on  the  genitals  as  an  insignificant 
circumscribed  nodular  thickening  and  elevation  of  the  skin,  which  soon 
develops  into  a  light  red,  shiny  mass  of  granulation  tissue  (partaking  of 
the  nature  of  the  infectious  granulomas) ;  this  has  a  fetid  odor,  excretes 
a  thin,  sanguineous  fluid,  and  bleeds  readily.  The  warm,  moist  surfaces 
about  the  scrotum,  or  the  labia,  and  the  thighs,  are  most  susceptible 
of  infection.  The  lesions  spread  slowly  by  peripheral  extension,  as  well 
as  by  auto-inoculation  of  opposed  (and  other)  surfaces,  and  involve 
most  frequently  the  scrotum,  the  perineum,  the  glans  penis,  and  the  upper 
part  of  the  thighs  in  the  male,  and  the  labia,  the  vagina,  and  the  upper 
part  of  the  thighs  in  the  female.  Spontaneous  recovery  is  unusual, 
though  not  infrequently  attempts  at  healing  are  seen — gradual  shrinkage 
and  the  formation  of  a  thin,  somewhat  raised,  cicatrix,  which,  however, 
having  formed,  not  uncommonly  breaks  down  again. 

Treatment. — Complete  excision  is  the  best  treatment  if  the  lesions 
are  not  too  extensive — in  which  event  the  granulation  tissue  should  be 
curetted  and  cauterized. 

VERRUGA. 

Verruga  is  a  chronic  infectious  disease,  characterized  by  initial  (so- 
called)  rheumatoid  pains,  fever,  anemia,  and  the  development  of 
peculiar,  warty,  granulomatous,  protuberances  on  the  skin,  mucous 
membranes,  and  the  internal  organs. 

Etiology. — ^''erruga  is  most  prevalent  in  Peru  (whence  it  is  often  called 
verruga  peruana),  on  the  Pacific  slope  of  the  Andes  ]\Iountains,  and 
in  certain  of  the  mountainous  regions  of  Chili,  Bolivia,  and  Ecuador. 
It  occurs  in  both  sexes,  at  all  ages,  and  is  apparently  favored  by  moisture, 
heat,  and  elevation  (since  it  is  scarcely  if  ever  observed  at  the  level  of 
the  sea).  It  occurs  in  circumscribed  epidemics,  but  is  not  markedly 
contagious.  The  exciting  cause  has  not  been  isolated.  How  infection 
is  spread  is  not  known,  though  the  natives  of  Peru  attribute  it  to  the 
water  of  certain  springs.  Malaria  is  frequently  associated,  and  is 
believed  by  some  to  be  of  etiological  significance.  One  attack  confers 
immunity. 

Symptoms. — The  period  of  incubation  is  usually  from  fifteen  to 
forty  days,  though  rarely  it  may  be  longer  or  even  shorter.  Clinically 
two  well-defined  stages  are  recognized — that  of  invasion  and  that  of 
eruption.  The  onset  is  usually  insidious  and  marked  by  lassitude, 
indisposition,  neuromuscular  pains  in  the  legs,  followed  in  a  few  days  by 
slight  rigors  and  evening  fever,  which  soon  increase  in  severity.     The 


KUBISAGARI  285 

fever  may  reach  102°  to  103°  F.,  and  pursues  usually  a  remittent,  but 
occasionally  an  intermittent  course.  The  fever  is  accompanied  by 
insomnia,  intense  headache,  hemorrhages,  and  pains  in  the  back  and 
the  joints,  of  which  the  knee,  ankle,  and  the  small  joints  of  the  hands 
and  feet  are  most  susceptible. 

Spasmodic  and  painful  contractures  of  certain  muscles,  especially 
of  the  calves  and  of  the  neck,  occur — most  frequently  at  night.  Nausea, 
vomiting,  vertigo,  photophobia,  transient  amblyopia,  dyspnoea,  bronchitis, 
loss  of  appetite,  and  marked  thirst  are  also  commonly  complained  of. 
Early  in  the  disease  the  bowels  are  constipated,  but  later  diarrhoea 
develops.  Marked  anemia  and  emaciation  soon  supervene,  and  con- 
stitute characteristic  features  of  the  disease.  The  liver  is  frequently, 
the  spleen  less  commonly,  enlarged  and  palpable.  The  fever  gradually 
subsides  in  about  thirty  days  (more  or  less)  and  therewith  the  stage  of 
eruption  sets  in.  This  consists  at  first  of  pin-sized  pinkish  papules, 
which  gradually  become  darker  (somewhat  bluish)  in  color,  and  increase 
in  size  until  they  form  c{uite  large  excrescences.  Manson  originally 
regarded  them  as  identical  macroscopically  and  microscopically  with 
the  granulomas  of  yaws,  but  more  recently  other  observers,  notably 
Glogner,  have  pointed  out  noteworthy  differences.  As  in  yaws,  how- 
ever, the  eruption  may  be  sparse  or  abundant,  discrete  or  confluent; 
and  the  swellings  or  granulomas  are  exceedingly  vascular  and  bleed 
freely,  thus  contributing  to  the  anemia.  They  are  found  most  commonly 
on  the  face,  neck,  and  limbs;  in  many  cases  they  develop  on  the  palms 
of  the  hands,  the  soles  of  the  feet,  and  the  hairy  scalp — while  the  trunk 
is  usually  exempt;  they  are  common  also  on  the  mucous  membranes, 
and  in  the  different  organs  of  the  body,  where  they  often  occasion  notable 
hemorrhages.  The  lesions  persist  from  four  to  six  weeks,  and  then  desic- 
cate and  desquamate,  or  sometimes  undergo  ulceration  and  suppuration. 

Prognosis. — Among  natives  the  mortality  is  from  10  to  15  per  cent.; 
it  is  much  higher  among  the  white  race,  and  may  reach  60  to  70 
per  cent. 

Diagnosis. — Though  verruga  much  resembles  yaws,  it  can  usually 
be  distinguished  by  the  involvement  of  the  internal  organs,  which  are 
unaffected  in  yaws,  and  by  the  marked  tendency  to  hemorrhage  mani- 
fested by  the  lesions. 

Treatment. — Treatment,  aside  from  removal  from  mountainous  regions 
to  the  coast,  which  is  indicated  in  all  cases,  is  purely  symptomatic. 
Quinine  has  been  recommended  on  account  of  the  common  association 
of  malaria.     The  removal  of  the  ulcerated  areas  has  also  been  practised. 


KUBISAGARI. 

(Endemic  Paralytic  Vertigo.) 

Kubisagari  is  a  chronic  endemic  disease  of  the  northeastern  part  of 
the  principal   island  of  Japan,  characterized   by  dimness   of   vision, 


286  INFECTIONS  OF   UNKNOWN  ETIOLOGY 

-diplopia,  ptosis,  and  paralysis  of  certain  muscles,  especially  of  the  neck 
(whence  the  name,  kubisagari,  that  is,  one  who  hangs  his  head). 

Etiology. — ^The  nature  of  the  disease  is  ill  understood.  It  is  almost 
confined  to  farming  peasants,  especially  those  who  live  under  the  same 
roof  with  their  cattle,  in  which,  as  well  as  in  many  other  respects,  it  re- 
sembles endemic  paralytic  vertigo  (Gerlier's  disease)  of  Switzerland  and 
certain  parts  of  France.  Miura  believes  that  the  local  horse  plague 
and  cattle  plague  are  in  some  way  related  etiologically  to  the  disease. 
Age  and  sex  are  without  influence.  The  disease  is  most  common  during 
the  warm  season,  and  disappears  during  the  winter. 

Symptoms. — Kubisagari  is  characterized  by  attacks  which  come  on 
at  intervals  of  several  hours  to  several  days,  and  last  for  from  several 
minutes  to  several  hours,  during  which  there  is  dimness  of  vision,  diplopia, 
ptosis,  and  paralysis  of  different  muscles.  Paralysis  of  the  posterior 
cervical  muscles  is  the  most  common,  and  causes  the  head  to  drop  for- 
ward; paralysis  of  the  muscles  of  the  tongue,  of  the  lips,  of  the  cheek, 
and  of  deglutition  interferes  with  speech,  mastication,  and  swallowing; 
and  paralysis  of  the  muscles  of  the  trunk  and  the  extremities,  which 
is  less  common,  interferes  with  station  and  locomotion.  The  attacks 
sometimes  come  on  without  known  cause,  but  in  some  cases  are  induced 
by  physical  exertion  (especially,  it  is  said,  a  stooped  posture  with  the 
stomach  empty),  by  hunger,  by  indigestion,  by  eye-strain,  etc.  In 
some  cases  there  is  considerable  mental  depression;  the  lacrymal, 
nasal,  and  salivary  secretions  may  be  increased;  and  the  reflexes  may 
be  exaggerated.  The  disease  is  not  fatal,  though  it  may  last  for 
years. 

Treatment. — Treatment,  as  a  rule,  is  not  encouraging.  Miura  re- 
ports favorable  results  from  the  use  of  potassium  iodide  and  arsenic, 
and  the  bromides  are  believed  to  be  sometimes  of  some  avail  in  controlling 
the  frequency  of  the  attacks. 


6AN60SA. 

Gangosa  is  a  disease  that  prevails  in  Guam,  where  it  is  said  to  involve 
about  two  per  cent,  of  the  population;  it  occurs  also  in  the  Ithmus  of 
Panama,  the  West  Indies,  the  Philippines,  and  perhaps  in  certain  parts 
of  South  America.  It  is  described  by  Mink  and  McLean  as  being 
characterized  by  a  destructive  ulceration,  usually  beginning  on  the  soft 
palate,  pillars,  or  uvula,  and  extending  by  continuity  to  the  hard  palate, 
the  nasal  cavity,  the  larynx,  and  even  the  face.  Active  ulceration  is  fol- 
lowed, after  a  variable  period,  by  cicatrization  or  chronic  ulceration. 
Mutilation  always  results.  Constitutional  symptoms  are  either  slight  or 
absent.  The  disease  resembles,  but  may  readily  be  differentiated  from, 
leprosy,  syphilis,  tuberculosis,  etc.  A  specific  infectious  agent  has  not 
been  isolated;  but  the  disorder  appears  to  be  infectious,  being  spread  by 
contact. 


PSITTACOSIS  287 


AINHUM. 


Ainhum  is  described  by  Manson  as  a  disease  affecting  the  toes,  espe- 
cially the  little  toes,  of  negroes,  East  Indians,  and  other  dark-skinned 
races,  and  commencing  as  a  narrow  groove  in  the  skin,  almost  invariably 
on  the  inner  and  plantar  side  of  the  foot  of  the  little  toe,  of  one  or  both 
feet.  Once  started,  the  groove  deepens  and  extends  gradually  around 
the  whole  circumference  of  the  toe;  the  distal  portion  of  the  toe  is  likely 
to  swell  to  a  considerable  size,  as  if  constricted  by  a  ligature.  There  is 
little  or  no  pain,  although  there  may  be  inconvenience  from  the  liability 
to  injury  of  the  dangling  and  everted  toe.  In  the  course  of  years  the 
groove  deepens,  and  finally  the  toe  drops  off  as  if  amputated.  The  dis- 
ease has  been  variously  interpreted — as  being  a  manifestation  of  leprosy, 
a  circumscribed  scleroderma,  a  trophoneurosis,  a  congenital  spontaneous 
amputation,  the  result  of  self-mutilation  by  ligatures,  wearing  toe  rings, 
etc.,  and  as  caused  by  injuries  to  the  toes.  Wellman  believes  that  it 
results  from  injuries  to  bare-footed  persons,  caused  by  long  grasses,  and 
that  the  factor  in  prolonging  the  irritation  and  inflammation  is  the  chigger, 
Sarcopsylla  penetrans,  which  seems  to  have  a  predilection  for  the  affected 
spot,  especially  if  the  skin  be  cut  or  torn. 

GOUNDOU. 

(Anakhre.) 

Goundou  is  a  disease  that  occurs  among  the  natives  of  Africa,  and  is 
characterized  by  severe  and  persistent  headache,  later  followed  by  a 
sanguinopurulent  discharge  from  the  nostrils,  and  the  development  of 
painless  symmetrical  swellings  at  the  sides  of  the  nose.  Although  the 
discharge  may  subside,  the  swellings  progressively  increase  in  size  until 
they  may  be  as  large  as  an  ostrich's  egg;  eventually  they  may  obstruct 
the  line  of  vision  or  destroy  the  eyes.  The  disease  has  been  variously 
interpreted  as  a  manifestation  of  yaws,  or  of  syphilis,  as  a  malformation 
due  to  the  non-union  of  the  nasal  and  frontal  bones,  as  a  manifestation 
of  atavism  referable  to  tribal  peculiarities  of  the  original  negro,  as  a 
disease  sui  generis,  and  as  a  disease  caused  by  the  larvae  of  insects  in  the 
nostrils.  Wellman  believes  that  the  growths  are  due  to  an  osteoplastic 
periostitis,  the  definite  cause  of  which  has  not  been  demonstrated. 

PSITTACOSIS. 

Psittacosis  is  a  disease  of  birds,  characterized  by  loss  of  appetite, 
general  weakness,  diarrhoea,  and  death  (often  in  convulsions).  It  is 
believed  to  be  communicable  to  man,  infection  being  commonly  acquired 
from  parrots — in  England,  Germany,  France,  and  Italy.  In  man  it  is 
characterized  by  pneumonia  that  is  often  atypical  in  course,  attended  by 
toxemia,  and  usually  ends  fatally. 


SECTION    II. 
INTOXICATIONS. 


The  intoxications  to  be  here  discussed  comprise  the  series  of  diseased 
conditions,  the  result  of  more  or  less  continued  activity  of  divers  poison- 
ous chemical  substances;  the  acute  poisonings  belong  more  properly  to 
the  subject  of  toxicology. 

ALCOHOLISM. 

Symptoms. — Acute  Alcoholism. — ^The  effect  of  a  large  amount  of 
alcohol  taken  within  a  short  time  is  exerted  chiefly  on  the  nervous 
system;  at  first  there  is  exaltation  of  the  nervous  functions,  which  is  soon 
followed  by  perversion,  and  finally  depression  and  stupor.  In  the  ordi- 
nary case  the  action  of  the  heart  becomes  at  first  accelerated,  respira- 
tion quickened,  the  muscular  force  and  activity  increased,  the  mentality 
active,  the  eyes  brilliant,  and  the  face  flushed  (although  it  may  be  pale) ; 
the  patient  gradually  becomes  loquacious  and  indiscreet  in  his  confi- 
dences, and  care  fades  away.  Soon,  however,  the  perceptive  faculties 
become  confused,  the  intellect  dulled,  the  memory  faulty,  movement 
of  the  limbs  uncertain  and  incoordinate,  the  gait  unsteady,  the  speech 
thickened,  the  facial  flush  deepened,  the  pupils  dilated,  the  conjunctivae 
red  and  watery,  and  the  gaze  staring.  Gradually  depression  of  the  gen- 
eral functional  activities  ensues,  and  the  patient  passes  into  a  more  or  less 
profound  sleep  (from  which,  however,  he  can  be  more  or  less  aroused); 
the  temperature  may  become  subnormal.  In  other  cases  the  subject 
becomes  readily  infuriated  or  maniacal,  and  upon  slight  or  no  provoca- 
tion may  commit  serious  crimes,  such  as  murder,  etc.  Periodical  recur- 
rences of  such  attacks  of  acute  alcoholism  are  common  in  persons  with 
an  inherited  or  acquired  craving  for  alcohol — so-called  dipsomaniacs; 
in  the  intervals  between  attacks  the  subject  may  abstain  entirely  from 
alcohol.  The  ordinary  attack  of  acute  alcoholism  is  readily  recognized, 
but  alcoholic  coma  must  be  distinguished  from  apoplexy,  uremia,  dia- 
betic coma,  morphine  poisoning,  etc. 

Chronic  Alcoholism.— While  it  is  undoubtedly  true  that  many 
persons  can  take  a  moderate  amount  of  alcohol  (whiskey,  wine,  beer) 
and  attain  a  ripe  old  age  in  good  physical  condition,  the  matter  is 
19 


290  INTOXICATIONS 

largely  individual,  and  to  the  majority  of  mankind  the  continuous  or 
daily  consumptiom  of  even  a  moderate  amount  of  alcohol  is  fraught 
with  danger.  Alcohol  brings  inevitably  in  its  wake  disordered  function 
and  altered  structure.  The  bloodvessels  become  sclerosed,  and  the 
heart  hypertrophied  and  dilated  or  fatty;  the  gastro-intestinal  tract 
becomes  congested  and  chronically  inflamed,  giving  rise  to  the  so-called 
morning  sickness  of  alcoholics — anorexia,  nausea,  perhaps  vomiting, 
coated  tongue,  constipation,  etc.;  the  liver  becomes  cirrhotic;  the  kid- 
neys become  the  seat  of  chronic  difi^use  indurative  nephritis;  and  the 
nervous  system  reveals  various  deteriorations.  Of  these,  muscular 
tremor,  involving  the  extremities,  especially  the  hands,  the  lips,  and  the 
tongue,  are  common;  various  disorders  of  sensibility,  including  the 
special  senses,  neuralgiform  pains  and  true  neuritis,  meningitis,  etc., 
may  develop.  The  mind  (will  and  intellect)  and  the  morals  deteriorate. 
The  patient  becomes  irritable  and  suspicious;  his  judgment  becomes 
impaired,  his  memory  enfeebled,  and  sleep  unsatisfying;  lapses  from 
moral  rectitude  (sexual  and  other)  are  common;  hallucinations  and 
delusions  may  supervene,  and  the  patient  may  gradually  pass  into 
irremediable  insanity.  The  association  in  chronic  alcoholics  of  loss 
of  memory,  pseudoreminiscences  (false  notions  as  to  time,  place, 
and  actualities),  and  peripheral  neuritis  is  spoken  of  as  Korsakoff's 
psychosis. 

Delirium  Tremens  (Mania  a  potu). — Delirium  tremens  is  an  inci- 
dent of  chronic  alcoholism,  that  usually  follows  periodical  excessive 
indulgence  in  alcohol,  and  may  be  precipitated  by  a  fright,  shock,  frac- 
ture, or  other  trauma,  acute  infection,  especially  pneumonia,  etc.  The 
symptoms  usually  begin  with  general  restlessness,  mental  activity 
(sometimes  apathy),  and  insomnia — for  which  additional  alcohol  may 
be  taken^without  avail.  In  two  or  three  days  delirium  and  halluci- 
nations of  sight  and  hearing  set  in.  The  patient  talks  incessantly  and 
incoherently;  conducts  imaginary  enterprises,  and  insists  upon  their 
urgency,  so  that  unless  watched  or  restrained  he  avails  himself  of  the 
first  opportunity  to  escape  from  his  bed  and  room — usually  by  way  of 
the  window.  Should  he  doze,  he  may  be  awakened  by  terrifying  dreams, 
and  while  awake  he  is  tormented  by  the  most  distressing  hallucinations 
—of  sight,  such  as  rats,  mice,  demons,  snakes  (a  patient  of  mine  with 
marked  aortic  insuflSciency  was  assured  of  being  infected  with  snakes 
bv  watching  the  violent  pulsations  of  his  very  tortuous  arteries  in  the 
arms);  and  of  hearing,  insulting  remarks,  threats  of  imaginary  enemies, 
etc.  There  is  a  well-marked  muscular  tremor;  the  pulse  is  rapid  and 
soft,  often  very  weak;  and  there  may  be  some  fever,  which,  however, 
is  almost  if  not  always  due  to  a  complication,  such  as  pneumonia,  which 
is  often  overlooked.  '  In  favorable  cases,  at  the  end  of  three  to  five  days 
the  patient  sleeps,  the  restlessness  abates,  the  hallucinations  disappear, 
and  the  patient  begins  to  convalesce.  Very  noticeable  improvement  often 
follows  a  prolonged  sleep,  but  the  tremor  may  continue  for  some  time. 
In  unfavorable  cases  with  increase  of  the  symptoms  and  persisting 
insomnia  the  patient  dies  of  exhaustion. 


ALCOHOLISM  291 

Treatment. — ^The  ordinary  and  recurring  attacks  of  acute  alcoholism 
rarely  require  any  treatment  per  se.  The  effects  of  the  alcohol  pass  off 
during  the  sleep,  and  although  the  patit  nt  shows  for  some  days  the 
grind  of  the  mill  of  the  gods,  he  soon  recovers.  Should,  however,  the 
coma  be  deep,  gastric  lavage  should  be  employed.  If  the  patient  is 
unruly  or  maniacal,  a  hypodermic  injection  of  apomorphine  (^  grain, 
0.01  gram)  usually  induces  not  only  nausea  and  vomiting,  but  also 
quietude.  In  the  event  of  convulsions,  a  few  whiffs  of  chloroform  may 
be  given,  or  chloral  (20  grains,  1.3  gram)  and  bromide  (40  grains, 
2.6  gram)  may  be  administered,  and  repeated  if  necessary  in  two  hours. 
If  the  patient  is  much  depressed  (low  temperature,  etc.),  resort  should 
be  had  to  energetic  frictions,  external  heat,  enemas  of  hot  saline  solu- 
tion and  coffee,  and  coffee  by  the  mouth  (or  stomach  tube),  hypodermic 
injections  of  strychnine  and  atropine,  artificial  respiration,  the  faradic 
current  to  the  respiratory  muscles,  etc. 

The  chronic  alcohol  habit  is  best  treated  in  a  hospital  or  similar 
institution  where  the  physician  has  entire  command  of  the  situation. 
The  alcohol  should  be  withdrawn  as  rapidly  as  possible  (three  to  five 
days) ;  there  is  neither  logic  nor  advantage  in  continuing  it  in  gradually 
decreasing  amounts  for  two  or  three  weeks.  The  following  may  be  given 
as  a  substitute  for  the  alcohol: 

I^ — Tincture  of  nux  vomica 6  drams  25  0 

Tincture  of  capsicum     .  2  drams  81 0 

Ammonium  bromide 5  drams  200 

Elixir  of  ammonium  valerianate 2  ounces  60  0 

Syrup  of  ginger 2  ounces  60  0 

Water,  sufficient  to  make 8  ounces  250  0 — M. 

S. — One  tablespoonful  (15  c.c.)  four  times  a  day. 

Atropine  hypodermicly,  y^  grain  (0.0005  gram),  twice  or  thrice 
daily,  will  keep  in  control  the  nervousness  in  the  early  days  of  absti- 
nence from  the  alcohol.  An  additional  dose  of  a  bromide,  or  chloral 
(20  grains  1.3  gram),  or  hyoscine  (ytw  grain,  0.00065  gram),  or  sul- 
phonal  or  veronal,  etc.,  may  be  given  at  bedtime  to  induce  sleep.  Good 
results  also  attend  frequent  feedings,  perhaps  of  highly  seasoned  food, 
for  a  time  at  least  (to  satisfy  the  craving  for  something  stimulating); 
free  catharsis;  a  daily  or  twice  daily  hot  bath  followed  by  a  cold 
douche;  and  some  outdoor  exercise. 

If  the  alcoholic  subject  is  seen  in  delirium  tremens  or  at  the  end  of 
a  debauch  ("threatened  with  delirium  tremens"),  the  first  essential 
is  to  get  him  asleep;  often  he  will  awake  from  a  prolonged  sleep  entirely 
refreshed,  and  the  danger  has  past.  He  must  be  kept  in  bed  (preferably 
on  a  mattress  on  the  floor)  and  gently  restrained;  the  use  of  wrist-  and 
ankle-straps  may  be  necessary,  but  forcible  personal  restraint  by  nurses 
or  attendants  increases  the  delirium  and  resistance.  The  patient 
should  first  be  given  5  grains  (0.3  gram)  of  calomel  and  10  grains  (0.6 
gram)  of  compound  jalap  powder  dry  on  the  tongue,  and  then  a  hypnotic 
— chloral  (15  grains,  1  gram)  and  morphine  (^  grain,  0.008  gram)  are  the 
best;  these  doses  may  be  repeated  at  the  end  of  an  hour  if  the  patient 


292  INTOXICATIONS 

is  still  wakeful  and  restless,  but  in  the  event  of  a  weak  heart  this  should 
be  fortified  with  strychnine  and  digitalis.  To  the  chloral  and  morphine 
one  may  add  sodium  bromide  (40  to  60  grains,  2.6  to  4  grams);  or  he  may 
give  hyoscine  {j^u  grain,  0.00065  gram),  paraldehyde  (1  to  2  drams, 
4  to  8  grams),  etc.     A.  Lambert  advises : 

I^ — Strychnine  sulphate -3^  grain  0  002 

Hyoscine  sulphate Y^q  grain  0  00065 

Apomorphine  hj^drochloride y^  grain  0  006 

The  use  of  atropine  (j^iF  ^^  eV  grain,  0.00065  to  0.001  gram)  twice  daily 
has  also  been  attended  by  good  results. 

Hypnotics,  such  as  trional,  veronal,  and  the  bromides,  usually  suffice 
after  the  first  prolonged  sleep,  but  none  may  be  needed.  Special  atten- 
tion must  be  given  to  supporting  the  patient's  strength  by  the  use  of 
strychnine  (g^j-  grain,  0.002  gram,  every  four  hours)  or  nux  vomica,  and 
by  an  abundance  of  nutritious  food — preferably  liquid  and  hot  (milk, 
broths,  eggs),  perhaps  highly  seasoned,  for  several  days.  A  weak  heart 
must  be  supported  on  well-known  principles.  Lambert  extols  the  use  of 
the  belladonna,  xanthoxylum  (prickly  ash),  and  hyoscyamus  mixture 
mentioned  under  the  opium  habit. 

OPIUM  HABIT. 

{Morphine  Habit;  Morphinism;  Morphinomonia.) 

Taken,  as  a  rule,  in  the  beginning  to  alleviate  pain  or  to  produce 
sleep,  or,  as  in  the  East,  for  reasons  similar  to  those  that  actuate  the 
Occidental  to  take  alcohol,  opium  or  morphine,  and  to  a  less  extent 
codeine  and  heroin,  gradually  create  an  almost  if  not  quite  uncontrol- 
lable craving.  The  habitues,  both  the  pleasure  seekers  (morphinists) 
and  the  pain-racked  subjects  (morphinomaniacs)  may  take  enormous 
amounts — a  half  to  one  ounce  of  opium,  a  pint  of  tincture  of  opium, 
10  to  30  grains  of  morphine,  etc.,  daily,  and  the  amount  is  usually  in- 
creased with  the  passage  of  time. 

Symptoms. — ^The  opium  (or  morphine)  habitue  usually  has  a  pale, 
grayish-ashen  countenance,  and  deep-sunk,  dreamy,  inexpressive  eyes; 
he  (or  she)  is  withered,  emaciated,  and  prematurely  old-looking,  restless, 
and  irritable.  ^Mien  not  under  the  influence  of  the  drug  the  patient  is 
likely  to  be  depressed,  weak,  and  inactive.  As  a  rule,  the  appetite  is 
impaired  and  capricious,  digestion  deranged,  the  bowels  constipated, 
and  sleep  poor  and  unrefreshing.  Itching  of  the  skin  is  not  uncommon, 
and  there  may  be  oedema,  etc.  Marked  perversion  of  the  moral  sense 
is  common;  the  habitu^  has  no  regard  for  his  word,  either  in  statement  of 
fact  or  promises.  Neurasthenic  and  hysterical  phenomena  are  common 
in  women.  Extraordinary  suffering  and  collapse  may  follow  sudden 
discontinuance  of  the  drug. 

Treatment. — It  is  worse  than  useless  to  attempt  treatment  outside 
of  a  hospital  or  sanatorium  where  the  strictest  supervision  of  the  patient 


COCAINE   HABIT  293 

is  possible;  the  ordinary  morphine  habitue  usually  goes  to  a  hospital 
laden  with  morphine,  and  will  obtain  the  drug  at  all  hazards.  As  a  rule, 
the  patient  should  remain  in  bed  for  ten  days  or  two  weeks.  The  mor- 
phine should  be  withdrawn  rather  rapidly,  that  is,  within  a  week.  At 
the  same  time  the  patient  should  receive  a  cold  tub  bath  or  sponge  bath 
in  the  morning,  and  a  hot  bath  at  night;  and  massage  in  the  middle  of 
the  day,  or  in  the  afternoon.  An  abundance  of  simple  nutritious  diet 
should  be  given  at  short  intervals.  Much  of  the  abdominal  distress, 
and  pain,  nausea  and  vomiting,  diarrhoea,  etc.,  has  been  attributed 
to  hyperchlorhydria,  which  may  be  met  by  the  aforementioned  fre- 
quent feedings,  large  doses  of  sodium  bicarbonate,  etc.  Restlessness 
and  nervousness  may  be  controlled  with  the  bromides,  valerian,  etc.; 
sleep  may  be  promoted  by  an  occasional  dose  of  sulphonal,  veronal, 
chloral,  etc.,  if  required,  but  caution  is  necessary  lest  one  drug  habit 
be  substituted  for  the  other.  The  cardiac  and  general  asthenia  may 
require  the  use  of  strychnine,  aromatic  spirit  of  ammonia,  and  other 
difi'usible  stimulants,  strophanthus,  digitalis,  etc.  Lambert  extols 
the  following  as  a  specific  in  the  treatment  of  drug  (morphine,  cocaine, 
alcohol)  addictions: 

I^ — Tincture  of  belladonna 2  ounces  60 

Fluid  extract  of  xanthoxylum, 

Fluid  extract  of  hyoscyamus         of  each  1  ounce  30 

Lambert  advises  that  the  treatment  be  begun  with  4  compound  cathartic 
pills  and  5  grains  of  blue  mass,  and  a  soapsuds  enema.  When  the  pills 
have  begun  to  act,  6  to  8  minims  of  the  belladonna  mixture  should  be 
given  every  hour,  and  every  six  hours  the  dose  should  be  increased 
2  minims,  until  14  to  16  minims  is  being  taken  hourly,  or  the  patient 
has  shown  signs  of  belladonna  intoxication  (dilated  pupils,  dryness  of 
the  throat,  a  red  rash,  rapidity  and  incisiveness  of  speech,  or  beginning- 
delirium).  Should  these  develop,  they  should  be  allowed  to  subside, 
whereupon  one  should  begin  with  the  mixture  again  in  8  myiim  doses 
hourly.  With  the  first  dose  of  the  mixture,  from  one-half  to  two-thirds 
of  the  total  daily  amount  of  morphine  or  cocaine  to  which  the  patient 
has  become  accustomed,  is  given — in  three  equal  doses  at  half-hour 
intervals.  The  bowels  must  be  opened  thoroughly — with  compoimd 
-cathartic  pills,  blue  mass,  calomel,  castor  oil,  etc.  At  the  end  of  thirty 
hours  strychnine,  digitalis,  or  strophanthus  should  be  commenced.  The 
treatment  is  said  to  take  away  the  desire  for  morphine,  cocaine,  or 
alcohol  in  less  than  five  days,  with  a  minimum  of  discomfort  and 
suffering  to  the  patient. 

COCAINE  HABIT. 

{Cocainism.) 

The  cocaine  habit  is  usually  acquired  in  consequence  of  taking  the 
drug  to  relieve  exhaustion  (sexual,  postalcoholic,  etc.),  or  to  alleviate 


294  INTOXICATIONS 

pain,  neuralgia,  chronic  nasal  catarrh,  etc.  As  much  as  30  or  40  grains 
daily  may  be  taken  by  the  mouth  or  hypodermicly. 

Symptoms. — Cocaine  at  first  produces  a  feeling  of  mental  exhilaration 
and  bodily  vigor,  freedom  from  pain  and  distress,  and  a  subjective 
sense  of  the  ability  to  accomplish  the  mind's  desires  and  the  heart's 
cravings;  but  the  judgment  becomes  perverted  and  accomplishment 
by  no  means  keeps  pace  with  stimulated  imagination.  In  the  course 
of  time  these  feelings  give  way  to  nervousness,  irritability,  introspection, 
apprehension,  and  insomnia.  As  the  use  of  the  drug  is  persisted  in,  the 
periods  of  peace  and  exhilaration  become  shorter,  and  the  restlessness, 
depression,  and  distorted  mentality  more  marked;  the  appetite  fails, 
the  patient  emaciates,  and  even  insanity  may  ensue.  Some  subjects 
exhibit  a  periodicity  in  their  addiction  to  the  drug;  and  others  are  addicted 
also  to  alcohol,  morphine,  etc.,  concurrently  or  intermittently. 

Treatment. — ^The  treatment  in  general  should  follow  the  principles 
suggested  under  morphinism.  Withdrawal  of  the  cocaine  should  be 
moderately  rapid — within  a  week,  the  bromides,  valerian,  hyoscyamus 
being  used  to  control  the  nervousness;  or  one  may  have  recourse  to  the 
belladonna  mixture  advised  by  A.  Lambert.  Care  should  be  taken 
not  to  substitute  the  alcohol,  morphine,  or  chloral  habit  for  the  cocaine 
addiction. 

LEAD  POISONING. 

{Plumbism;  Saturnisim.) 

Lead  poisoning  is  a  common  result  of  one  of  the  so-called  dangerous 
industrial  trades — lead  working.  Lender  like  conditions  women  seem 
to  be  more  susceptible  than  men.  The  lead  usually  enters  the  system 
by  way  of  the  respiratory  tract  (inhalation  of  k ad-dust-laden  atmosphere), 
by  way  of  the  digestive  system  (contaminated  food  and  drink;  pro- 
fessional administration  of  lead),  or  by  way  of  the  skin  (cosmetics, 
hair  dyes^  thread,  etc.).  Less  commonly  poisoning  may  follow  the 
use  of  lead  douches  in  the  vagina,  etc. 

Pathology. — In  acute  and  fatal  cases  the  conspicuous  lesion  is  catarrhal 
gastro-enteritis  and  softening  of  the  brain.  Goadby  and  Goodbody 
believe  that  the  essential  and  primary  action  of  lead  intoxication  is  the 
production  of  minute  and  microscopic  hemorrhages  in  various  portions 
of  the  body,  including  the  nervous  system,  and  that  the  clinical  symp- 
toms of  lead  palsy  and  its  good  prognosis  when  treated  early  are  explain- 
able by  the  presence  of  minute  hemorrhages  in  the  peripheral  nerves. 
In  advanced  cases  the  lesions  are  those  of  multiple  neuritis,  with  atrophy 
and  degeneration  of  the  muscles;  degenerative  lesions  may  also  be 
found  in  the  ganglion  cells  of  the  anterior  cornua  of  the  spinal  cord. 

Symptoms. — Acute  Lead  Poisoning. — Symptoms  may  develop  after 
a  few  weeks  exposure,  or,  rarely,  they  may  not  come  on  until  after  years 
of  exposure.  The  manifestations  are  usually  those  of  severe  gastro- 
intestinal catarrh  (nausea,  vomiting,  colicky  pain,  diarrhoea  or  con- 


LEAD  POISONING  295 

stipation),  which  may  lead  to  collapse  and  death.  There  may  be  asso- 
ciated coma  or  convulsions,  cerebral  or  peripheral  paralyses,  rapidly 
developing  anemia,  suppression  of  urine,  albuminuria,  slow  pulse,  etc. 

Chronic  Lead  Poisoning. — ^The  significant  symptoms  of  chronic 
lead  poisoning  consist  of  lead  colic,  lead  paralysis,  lead  encephalopathy, 
and  lead  cachexia. 

Lead  colic  (^painter  s  colic)  is  the  most  common  manifestation.  The 
pain,  which  may  be  preceded  by  ill-defined  gastro-intestinal  disorder, 
is  usually  very  severe,  paroxysmal  (colicky),  and  is  often  diffuse,  although 
it  may  be  localized  to  the  region  of  the  umbilicus,  the  epigastrium,  or 
hypogastrium;  it  is  usually  relieved  by  firm  pressure.  The  paroxysms 
may  continue  for  a  few  moments  to  an  hour  or  more,  and  when  the 
severe  pain  subsides  more  or  less  dull  aching  pain  continues.  Consti- 
pation is  the  rule,  but  the  paroxysms  of  pain  may  be  associated  with 
diarrhoea.  Relapses  are  common,  and  exposure  may  cause  chronic 
lead  colic. 

Lead  paralyses  (or  palsies)  are  quite  common,  and  may  come  on 
suddenly  or  slowly.  They  are  due  to  peripheral  neuritis,  and  are  asso- 
ciated with  tremors,  wasting  of  the  muscles,  reactions  of  degeneration, 
paresthesias,  neuralgias,  arthralgia,  etc.  The  following  types  have  be 
distinguished:  (1)  The  musculospiral  type  (antibrachial  type,  wris  ~ 
drop),  in  which  involvement  of  the  musculospiral  nerve  leads  to  paralysis" 
of  the  extensor  muscles  of  the  wrist  and  the  fingers  (except  the  supinator 
longus)  and  the  characteristic  wrist-drop.  In  long-continued  cases 
slight  backward  displacement  of  the  cofpus  and  distention  of  the  syno- 
vial bursae  (Griibler's  tumor)  may  occur.  (2)  The  brachial  type,  in 
which  the  deltoid,  biceps,  brachialis  anticus,  and  sometimes  also  the 
pectoral  muscles  are  involved.  (3)  The  Aran-Duchenne  type,  common 
in  tailors,  in  which  the  small  muscles  of  the  hand  and  the  thenar  and 
hypothenar  eminences  are  involved  (resembling  chronic  anterior  polio- 
myelitis). (4)  The  peroneal  type,  in  which  the  lateral  peroneal  and  the 
extensor  muscles  of  the  toes  are  involved  (steppage  gait).  Rarely  there 
may  be  paralysis  of  the  laryngeal  or  intercostal  nerves;  or  a  palsy 
reseml)ling  Landry's  ascending  paralysis  may  occur;  or  hemiplegia 
may  ensue;  or  the  condition  may  resemble  tabes  dorsalis. 

Lead  encephalopathy  may  be  manifested  by  mild  symptoms  such  as 
headache,  dizziness,  excessive  irritability  or  depression,  tremor,  insomnia, 
dimness  of  vision,  tinnitus  aurium,  etc.,  or  by  severe  symptoms,  such  as 
delirium,  coma,  or  convulsions.  The  delirium  is  marked  by  periods 
of  violence  and  intervals  of  somnolence,  which  may  be  followed  by 
true  sleep  and  convalescence.  Coma  may  come  on  suddenly  or  grad- 
ually and  be  preceded  or  attended  by  delirium  or  convulsions.  The 
convulsion  may  be  localized  or  generalized  and  reseml)le  epilepsy. 

Lead  cachexia  is  characterized  by  a  pallid,  sallow  complexion,  coated 
tongue,  a  peculiar  dry,  metallic  taste  in  the  mouth,  fetid  breath,  gastro- 
intestinal derangements,  constipation  perhaps  alternating  with  attacks  of 
diarrhoea,  malaise,  weakness,  and  emaciation. 


296  INTOXICATIONS 

Examination  of  the  blood  reveals  a  well-marked  anemia — oligocythemia 
and  oligochromemia  (50  per  cent,  or  thereabout),  a  characteristic  baso- 
philic degeneration  of  the  erythrocytes,  some  erythroblasts,  and  perhaps 
slight  leukocytosis.  In  most  cases  there  is  a  bluish  or  grayish-black 
line  (2  to  3  mm.  wide)  at  the  margin  of  the  gums,  in  the  papillae  (lead 
sulphide  precipitated  in  the  tissue  by  the  sulphuretted  hydrogen  of  the 
tartar);  it  must  be  distinguished  from  a  somewhat  similar-looking  line 
between  the  gums  and  the  teeth  which  is  readily  removed  with  a  tooth- 
brush. The  HCl  content  of  the  gastric  juice  is  usually  diminished  or 
absent,  and  lactic  acid  may  be  present.  Arteriosclerosis  with  h^-per- 
trophy  of  the  heart  and  chronic  interstitial  nephritis  eventually  ensue. 

Diagnosis. — The  diagnosis  is  easy  in  the  presence  of  any  of  the  char- 
acteristic symptoms,  but  in  a  case  of  coma  it  may  be  exceedingly  difficult. 
The  bluish  line  in  the  gums  and  basophilic  degeneration  of  the  erythro- 
cytes are  of  much  importance.  In  other  cases  the  first  clue  to  the  diag- 
nosis may  be  a  knowledge  of  the  patient's  occupation  or  of  his  exposure 
to  the  poison.     In  some  cases  lead  may  be  detected  in  the  urine. 

Prognosis. — ^The  outlook  is  favorable  in  all  but  the  severe  encephalo- 
pathies, which  often  result  fatally,  or  if  recovered  from  may  eventuate 
'-J  mental  deterioration.  AYrist-drop  if  neglected  may  prove  intractable. 
^^  *^Treatment. — ^As  soon  as  symptoms  become  in  the  slightest  degree 
lanifest,  the  patient  should  be  removed  from  exposure  to  lead  and 
vvarned  against  again  subjecting  himself  to  it,  since  there  is  always 
danger  of  relapse  in  susceptible  individuals.  Workers  in  lead  should 
wear  a  mask,  and  should  be  scrupulously  clean,  especially  in  regard  to 
the  hands  (finger  nails),  which  often  are  the  indirect  source  of  intoxi- 
cation (in  eating,  etc.).  In  the  severe  acute  poisonings,  sodium  and 
potassium  sulphate  should  be  administered  (to  precipitate  insoluble 
lead  sulphate);  opium  should  be  given  for  pain,  and  stimulants  for  the 
collapse.  Lead  colic  should  be  treated  by  magnesium  sulphate,  calomel 
and  compound  jalap  powder;  morphine  and  atropine  hj'podermicly 
for  the  pain  and  to  relax  the  intestinal  musculature;  hot  applications 
to  the  abdomen,  etc.  Potassium  iodide  (15  to  30  grains,  1  to  2  grams, 
daily)  should  be  administered  to  promote  elimination  of  the  lead;  iron 
should  be  given  for  the  anemia,  and  massage,  passive  motion,  exercises, 
and  electricity  for  the  local  paralysis. 

Carles  has  proposed  the  production  of  a  sterile  abscess  (by  the  intra- 
muscular injection  of  1  c.c.  of  turpentine)  with  a  view  to  withdraw 
into  the  abscess  by  means  of  the  phagocytes  the  lead  deposited  in  the 
body;  and  the  later  evacuating  of  the  abscess. 


ARSENICAL  POISONING. 

Arsenic  may  enter  the  system  in  poisonous  amounts  by  the  intestinal 
or  the  respiratory  tracts.  Most  cases  of  poisoning  are  accidental,  the 
poisoning  being  acquired  in  the  pursuit  of  certain  dangerous  trades, 


MERCURIAL  POISONING  297 

such  as  the  manufacture  of  colored  wallpapers,  various  fabrics,  artificial 
flowers,  etc.,  but  poisoning  may  also  follow  the  criminal  administration 
or  taking  of  Rough-on-rats,  Paris  green,  etc.;  occasionally  it  follows  the 
therapeutic  administration  of  arsenic. 

Symptoms. — Beginning  therapeutic  overaction  or  intolerance  of 
arsenic  is  manifest  by  salivation,  epigastric  pain  and  distress,  nausea, 
vomiting,  diarrhoea  and  tenesmus,  oedema  and  itching  of  the  eyelids, 
urticaria,  pityriasis,  psoriasis,  eczema,  muscular  tremors,  and  contrac- 
tions and  stiffness  of  the  joints.  In  w^hat  may  be  called  acute  poisoning 
the  gastro-intestinal  symptoms  are  aggravated,  the  urine  and  the 
feces  may  be  bloody,  and  there  may  be  anuria.  In  some  cases  gastro- 
intestinal symptoms  are  in  abeyance  and  symptoms  resembling  opium 
narcosis  may  come  on;  later  numbness,  sharp  darting  pains,  or  paral- 
yses may  supervene.  In  chronic  arsenical  poisoning,  the  symptoms, 
which  may  develop  insidiously,  are  usually  those  of  increasing  anemia 
and  debility,  pigmentation  (also  keratosis  or  herpes)  of  the  skin,  and 
multiple  neuritis  (paresthesia,  neuralgia,  paralyses),  involving  the 
legs  (extensor  and  peroneal  muscles)  rather  than  the  arms,  and  usually 
associated  wdth  rapid  and  marked  atrophy  of  the  muscles.  There  may 
be  also  divers  gastro-intestinal  disturbances,  redness  and  bleeding  "** 
the  gums,  stiff  joints,  etc. ;  pseudotabes  may  ensue.  ^~ 

Diagnosis. — ^The  diagnosis  may  be  based  upon  known  exposure  to  tt* 
influence  of  the  poison,  pigmentation  and  other  lesions  of  the  skin 
multiple  neuritis,  and  the  detection  of  arsenic  in  the  urine. 

Treatment. — ^The  treatment  consists  in  avoidance  of  the  source  of 
intoxication;  potassium  iodide  to  promote  elimination;  iron  for  the 
anemia;  and  massage,  electricity,  etc.,  for  the  neuritis. 

MERCURIAL  POISONING. 

(Hydrargyrism;  Mercurialism.) 

Mercury  is  extensively  used  in  the  manufacture  of  mirrors,  bronzes, 
thermometers,  decorative  novelties,  cosmetics,  etc.,  so  that  poisoning 
not  infrequently  ensues.  The  poison  may  gain  access  to  the  system 
by  way  of  the  alimentary  tract,  the  respiratory  tract,  or  the  skin.  The 
therapeutic  administration  of  mercury  (calomel,  blue  mass,  etc.)  also 
may  lead  to  poisoning. 

Symptoms. — ^The  acute  symptoms  consist  of  fetid  breath,  a  metallic 
taste  in  the  mouth,  salivation,  swelling,  sponginess,  and  frequently 
hemorrhage  of  the  gums,  sometimes  even  loosening  and  shedding  of  the 
teeth,  with  ulceration  and  necrosis  of  the  jaw.  The  characteristic  of 
the  chronic  cases  is  muscular  tremor  (trembles),  which  at  first  occurs 
only  on  movement  or  excitement,  but  later  becomes  more  or  less  con- 
tinuous, usually  first  involving  the  tongue  and  face  (interfering  with 
speaking)  and  later  the  extremities  (interfering  with  arm  movements 
and  walking).  Physical  strength  lessens  and  mental  deterioration  may 
ensue. 


298  INTOXICATIONS 

Diagnosis. — ^The  symptoms  and  the  history  are  usually  conclusive. 
Multiple  sclerosis,  paralysis  agitans,  and  other  disorders  associated 
with  tremors  should  be  readily  excluded. 

Treatment. — ^The  avoidance  of  the  poison  is  the  first  essential  of  the 
treatment.  Potassium  iodide  should  be  given  to  promote  elimination. 
A  gargle  of  tannic  acid  and  antiseptics  may  be  used  during  salivation. 
Iron,  quinine,  and  strychnine  in  tonic  doses  should  be  given. 

SNAKE-VENOM  POISONING. 

The  common  poisonous  snakes  of  the  United  States  are  the  Crotalus 
(rattlesnake),  the  Ancistrodon  (water  moccasin  and  copperhead),  and 
the  Elaps  (coral  and  harlequin  snake);  in  Europe  only  the  vipers  abound; 
in  Asia,  the  cobra,  vipers,  crotalus,  elaps,  and  other  poisonous  varieties 
are  found.  The  venom  is  contained  in  a  gland  with  a  maxillary  fang 
that  becomes  unsheathed  in  activity;  the  venom  is  viscid,  and  varies  in 
color  from  pale  amber  to  deep  yellow.  Noguchi  states  that  snake  venom 
owes  its  toxicity  to  the  presence  of  several  active  principles,  which  are 
nresent  in  varying  proportions  in    different  venoms,  whence  the  dif- 

ences  in  their  activity.  These  toxic  principles  are:  That  which  pro- 
jces  instantaneous  intravascular  clotting  of  the  blood;  that  which 
"ttacks  the  nervous  system  (neurotoxin);  that  which  causes  rupture 
of  the  walls  of  the  capillary  vessels  and  extensive  hemorrhages  (hemor- 
rhagic principle);  that  which  attacks  the  blood  corpuscles,  causing 
hemolysis  and  agglutination  (hemolytic  and  hemo-agglutinative  prin- 
ciples) ;  those  which  cause  lysis  of  other  body  cells  (cytolytic  principles) ; 
those  which  protect  or  harden  the  erythrocytes;  and  that  which  causes 
a  loss  of  the  bactericidal  property  of  the  blood. 

Symptoms. — Noguchi  states  that  the  symptoms  observed  in  man  may 
be  divided  into  local  and  general.  The  local  symptoms  consist  in  a 
rapidly  appearing,  inflammatory  swelling  at  the  site  of  the  bite,  followed 
by  more  or  less  ecchymosis  and  necrosis,  with  or  without  pain,  and 
often  with  the  appearance  of  lymphangitis  and  local  phlegmon.  The 
constitutional  symptoms  are  fever,  cerebral  and  spinal  disturbances, 
especially  of  the  medulla,  including  paralysis  of  the  respiratory  centre, 
and  rapid  advance  of  motor  paralysis.  Hematuria,  hemoglobinuria, 
hematemesis,  diarrhoea,  vomiting,  amaurosis,  headache,  vertigo,  violent 
dyspnoea,  and  general  convulsions  are  often  observed.  In  viperine 
poisoning  there  may  be  also  cold  perspiration  and  a  small  intermittent 
pulse.  Death  may  ensue  in  two  minutes  (Crotalus  poisoning),  more 
commonly  after  about  fifteen  minutes;  or  it  may  be  delayed  for  from 
twelve  to  forty-eight  hours,  or  longer. 

Treatment. — ^An  attempt  should  be  made  to  retard  the  absorption 
of  the  venom,  by  the  application  of  a  ligature  about  the  region  of 
the  bite,  by  opening  the  wound  and  cupping  or  sucking,  or  otherwise 
mechanically  removing  the  venom.     One  should  also  inject  into  and 


FOOD  POISONING  299 

around  the  bitten  region  potassium  permanganate  (1  per  cent.),  calcium 
chloride  (1 .5  per  cent.),  chromic  acid  (1  per  cent.),  or  ammonia.  Alcohol, 
coffee,  and  tea  may  be  used,  as  well  as  oxygen  inhalations,  and  saline 
intravenous  injections.  Noguchi  states  that  experimentally  strychnine, 
morphine,  nicotine,  and  curare  are  not  only  of  no  value,  but  distinctly 
harmful.  The  specific  treatment  is  Calmette's  antivenin,  which 
should  be  used  immediately  if  it  is  available.  Unfortunately  each 
venom  seems  to  require  for  neutralization  a  specific  antivenin;  an 
efficient  polyvalent  antivenin  has  not  yet  been  prepared. 

FOOD  POISONING. 

{Ptomaine  Poisoning;  Bromatotoxism .) 

Poisoning  may  follow  the  eating  of  food  or  pseudo-food:  (1)  Because 
the  substance  taken  is  in  itself  poisonous,  that  is,  it  contains  an  en- 
dogenous poison,  and,  speaking  strictly,  can  not,  therefore,  be  called 
a  food  (certain  mushrooms,  fish,  etc.);  or  (2)  because  to  an  otherwise 
suitable  food  an  exogenous  poison  may  be  added.  In  addition,  some 
persons  are  unusually  susceptible  to  the  influence  of,  and  become  more 
or  less  ill  from  eating,  certain  foods,  toward  which  mankind  reacts 
in  what  may  be  called  a  standard  manner,  such  as  strawberries,  buck- 
wheat, veal,  liver,  etc.    The  exogenous  poisons  found  in  foods  may  be: 

(1)  Various  chemical  adulterants  added  to  preserve  the  food  or  to  mask 
putrefactive  processes,  such  as  various  sulphites,  salicylic  acid,  boric 
acid,  benzoic  acid  (and  their  salts),  formaldehyde,  potassium  nitrate, 
etc.;  or  coloring  matters,  such  as  salts  of  copper,  lead,  arsenic,  etc. 

(2)  Metals,  such  as  tin,  lead,  copper,  etc.,  derived  from  vessels  con- 
taining food.  (3)  Divers  sorts  of  microorganisms — bacteria,  fungi, 
and  zooparasites  of  specific  infections,  as  well  as  the  organisms  of 
putrefaction.  The  alkaloidal  products  of  putrefaction  are  spoken  of 
as  ptomaines,  and  their  ill  effects  as  ptomaine  poisoning. 

Meat  Poisoning  (Kreatoxism) . — Meat  poisoning  may  result  from  eating 
meat  (especially  sausage,  ham,  and  pork,  but  also  beef,  veal,  game,  and 
all  kinds  of  corned  meat)  infected  with  Bacillus  botulinus  (so-called 
botulism).  Bacillus  enteritidis  (Gartner),  Proteus  vulgaris.  Bacillus 
coli.  Bacillus  paratyphosus,  etc.  The  nature  of  the  poison  (kreatoxicon) 
has  not  been  determined.  The  symptoms  may  be  gastro-intestinal 
or  nervous  (toxemic),  or  both.  Often  there  is  a  period  of  incubation  of 
several  hours  or  more,  in  which  there  may  be  no  symptoms.  The 
onset  is  often  sudden,  with  abdominal  pain,  nausea,  vomiting,  diarrhu'a, 
headache,  wealoiess,  and  neuromuscular  pains;  there  may  be  an  initial 
chill  or  chilliness  and  subsequent  fever  (101°  to  103°);  headache,  vertigo, 
faintness,  and  profuse  sweating  are  common.  In  some  severe  cases 
the  diarrhoea  is  profuse  and  quite  exhausting  (choleraic  form),  and  with 
the  toxemia  may  lead  to  collapse  and  death. 

Milk  Poisoning  (Galactotoxism)  and  Cheese  Poisoning  (Tyrotoxism). — 
Poisoning  may  ensue  from  the  use  of  milk  and  its  derivatives  (cheese, 


300  INTOXICATIONS 

ice-cream,  etc.),  the  toxic  agents  being  tyrotoxicon  (Vaughan)  and  per- 
haps other  ptomaines.  In  some  cases  the  colon  bacillus  has  been  found 
in  the  milk.  The  symptoms  consist  of  nausea,  vomiting,  diarrhoea,  with 
perhaps  bloody  or  cholera-like  discharges,  neuromuscular  pains  and 
cramps  in  the  legs,  fever,  and  collapse.  There  may  be  a  rash  resem- 
bling that  provoked  by  belladonna. 

Fish  Poisoning  (Ichthyotoxism)  and  Shellfish  Poisoning  (Mytilotoxism). — 
Fish  poisoning  may  follow  the  eating  of  fish  that  has  undergone  putre- 
faction, or  of  certain  parts  (roe,  testicles,  poison  glands  connected  with 
the  fins,  etc.)  of  otherwise  wholesome  fish.  The  symptoms  may  be 
gastro-intestinal  (pain,  nausea,  vomiting,  and  diarrhoea),  or  nervous, 
with  collapse,  or  they  may  resemble  those  of  belladonna  poisoning 
(dryness  and  constriction  of  the  throat,  dilatation  of  the  pupils,  ptosis, 
delirium,  convulsions,  coma).  Shell-fish  poisoning  may  follow  the  eating 
of  unwholesome  mussels,  oysters,  lobsters,  crabs,  etc.  A  poisonous 
principle  (mytilotoxin)  has  been  isolated  in  certain  cases.  The  symp- 
toms are  largely  gastro-intestinal  (pain,  nausea,  vomiting,  and  diar- 
rhoea), with  which  a  rash  and  other  symptoms  suggesting  belladonna 
poisoning  are  often  added.  The  pulse  may  become  rapid  and  the 
patient  collapsed,  or  he  may  pass  into  coma. 

Grain  Poisoning  (Sitotoxism). — Eegotism. — Ergotism  results  from 
eating  rye  and  other  grain  infected  with  Claviceps  purpurea  (the  ergot 
fungus).  Kobert  has  isolated  three  poisonous  substances — sphacelinic 
acid,  cornutin,  and  ergotinin;  to  these  Jacoby  has  added  sphacelotoxin, 
which  he  believes  to  be  the  specific  poison.  The  symptoms  may  be 
acute  or  chronic.  The  acute  symptoms  are  largely  gastro-intestinal  with 
collapse.  The  chronic  disorder  may  be  of  the  gangrenous  or  the  con- 
vulsive type.  The  gangrenous  type  is  characterized  by  pain,  paresthesias, 
anesthesias,  blood  stasis,  and  gangrene  of  the  fingers,  toes,  nose,  ears,  etc. 
The  convulsive  type  is  characterized  by  a  prodromal  period  of  from 
ten  to  fourteen  days,  during  which  there  may  be  pains  and  paresthesias, 
and  perhaps  fever;  these  are  followed  by  muscular  spasms  and  contrac- 
tures, especially  of  the  arms  and  legs,  that  may  last  for  a  few  hours  or 
days  and  recur.  Delirium  and  convulsions  may  supervene.  Eventually 
a  pseudotabes  (posterior  spinal  sclerosis)  ensues. 

Lathyrism  (Lupinosis).— Lathyrism  results  from  eating  meal 
(and  bread)  to  which  vetch  seed  (Lathyrus  sativus  and  Lathyrus  cicera) 
has  been  added,  usually  as  a  substitute  for  wheat.  It  occurs  in  Italy, 
Austria,  Africa,  and  India.  The  nature  of  the  poison  is  not  known. 
The  chief  symptoms  consist  of  paresthesias,  spastic  paraphlegia  (involv- 
ing the  legs),  increased  reflexes,  etc. 

Pellagra  (Maidism). — Pellagra  results  from  eating  corn  (maize) 
that  has  become  in  some  unknown  way  unwholesome  or  spoiled.  It 
is  common  in  Italy,  France,  Spain  and  in  the  southern  and  western 
parts  of  the  United  States.  The  symptoms  develop  insidiously,  the 
earliest  manifestations  usually  being  gastro-intestinal — anorexia,  stoma- 
titis, salivation,  epigastric  pain  or  distress,  diarrhoea,  and  a  gradually 


FOOD  POISONING  301 

increasing  anemia,  asthenia,  disinclination  to  exertion,  and  psychic 
depression.  The  fully  developed  disease  is  characterized  by  cutaneous, 
digestive,  and  nervous  symptoms.  There  is  at  first  a  characteristic 
pellagrous  erythema  that  usually  comes  on  first  in  the  spring,  tends  to 
subside  and  recur  (in  the  fall  and  spring).  It  develops  bilaterally 
especially  on  the  exposed  surfaces,  the  hands,  arms,  face,  and  neck;  that 
is,  it  seems  to  be  related  to  the  action  of  the  actinic  rays  of  the  sun;  it 
may  be  dry  (usually  early)  or  wet;  the  lesions  become  pigmented  (liver- 
yellow  or  chocolate  color)  and  usually  progress  to  desquamation,  exfolia- 
tion, and  gangrene  of  the  skin,  which  are  followed  by  cicatrization. 
The  characteristic  digestive  symptoms  consist  of  stomatitis,  the  cardinal- 
red  tongue  (Watson),  the  bald  tongue  (Sandwith),  or  the  stippled,  bluish- 
black  tongue  (Lavender) ;  salivation,  pyrosis,  and  diarrhoea  (fetid,  slimy, 
greenish  stools),  sometimes  bloody  stools,  may  occur.  The  nervous 
symptoms  consist  of  neuromuscluar  pains  in  the  back  and  legs,  spinal 
tenderness,  headache,  vertigo,  unilateral  or  bilateral  mydriasis,  muscular 
spasms,  exaggerated  reflexes,  later  paralysis  with  lessened  or  absent 
reflexes,  mental  depression,  delusions,  hallucinations,  melancholia,  and 
insanity.  Mild  cases  may  be  afebrile,  but  fever  (102°  to  105°  or  more) 
is  not  uncommon.  Improvement  may  occur  after  the  lapse  of  several 
months,  but  recurrences  especially  in  the  fall  and  spring  are  common. 

Vegetable  Poisoning. — Poisonous  symptoms  sometimes  follow  the 
eating  of  potatoes  that  have  "sprouted."  The  symptoms  are  attributed 
to  solanin,  which,  under  the  influence  of  Bacillus  solaniferum,  increases 
from  the  normal  0.06  per  cent,  to  as  much  as  0.4  per  cent.  The  symp- 
toms consist  of  digestive  disturbances  (pain,  nausea,  vomiting,  diarrhoea), 
jaundice,  headache,  chills,  fever,  and  prostration. 

Treatment. — ^The  treatment  of  food  poisonings  consists  primarily 
in  avoiding  the  source  of  the  intoxication,  the  proper  preservation  of 
food,  careful  agricultural  supervision  to  avoid  contamination  of  grain, 
etc.,  and  in  the  cases  of  pellagra,  etc.,  removal  from  the  region  of  endemic 
intoxication.  In  the  acute  ptomaine  poisonings  the  stomach  should  be 
washed  out,  and  the  bowels  thoroughly  evacuated  by  a  brisk  cathartic; 
following  this  the  diarrhoea  should  be  controlled  by  bismuth,  lead, 
opium,  etc.  Stimulants,  such  as  alcohol  and  strychnine,  are  often 
required.  Hypodermoclysis  and  enteroclysis  also  may  prove  useful 
in  reviving  a  prostrated  patient  and  favoring  elimination  of  the  pto- 
maines. Arsenic  and  quinine  have  proved  of  value  in  pellagra;  tonics 
also  are  indicated.  Recently,  Cole  and  Winthrop  have  recommended 
the  transfusion  of  pellagrinous  blood  (believed  to  contain  antibodies), 
or,  if  this  be  not  obtainable,  of  normal  blood. 


SECTION   III. 
DISORDERS  OF  METABOLISM. 


Pathological  Physiology. — The  disturbances  of  metabolism  to  which 
the  l)ody  is  subject  are  many  and  various.  Some  of  these  constitute 
cHnical  entities  and  are  discussed  under  appropriate  headings,  such  as 
diabetes,  gout,  obesity,  etc.;  others  in  a  broad  sense  inchide  many  of  the 
disorders  of  the  ductless  glands  and  of  internal  secretion,  which  also  are 
discussed  under  appropriate  headings;  others  are  not  so  well  defined  nor 
so  well  understood.  These  have  not  attained  the  dignity  of  clinical  enti- 
ties, being,  as  a  rule,  merely  more  or  less  obtrusive  manifestations  of  a 
wide  variety  of  diseased  conditions;  they  are  alike,  however,  in  that  they 
lead  ultimately  to  more  or  less  pronounced  poisoning  of  the  body,  and 
since  the  toxic  agent  is  elaborated  within  the  body,  they  are  distinguished 
as  endogenous  poisonings  or  auto-intoxications.  In  the  majority  of  cases 
the  poisonous  agent  has  not  been  identified  with  certainty,  so  that  these 
auto-intoxications  are  still  the  subject  of  more  speculation  than  of  dem- 
onstrated fact.  Nevertheless,  three  types  of  auto-intoxications  may  be 
distinguished,  although  they  are  not  sharply  delimitable  the  one  from 
the  other  nor  from  other  diseased  states,  of  which  often  they  are  merely 
a  manifestation:  (1)  Gastro-intestinal  auto-intoxications;  (2)  acidosis 
and  acid  intoxications;  and  (3)  retention  auto-intoxications. 

Gastro-intestinal  Auto-intoxications. — Gastro-intestinal  auto- 
intoxications conceivably  may  result  from  the  absorption  of:  (1)  Poisonous 
intermediate  products  of  digestion;  (2)  poisonous  end  products  of  meta- 
bolism that  normally  are  detoxified  in  the  body  or  excreted  therefrom ; 
and  (3)  certain  products  of  putrefaction.  It  is  difficult,  if  not  impossible 
to  sepai-ate  these  from  the  results  of  the  activity  of  bacteria — those 
normal  in  the  intestine  as  well  as  those  foreign  thereto,  since  it  is  not 
improbal)le  that  bacterial  activity,  of  much  importance  in  the  orderly 
performance  of  some  of  the  intestinal  functions,  if  perverted,  may  injuri- 
ously affect  the  intestinal  enzymes.  Abeyance  of  the  detoxifying  func- 
tion of  the  liver  is  often,  at  least  in  part,  answerable  for  the  gastro- 
intestinal auto-intoxications.  The  evidence  that  intermech'ate  and  end 
|)ro(lucts  of  digestion,  such  as  peptones,  ])urins,  luicleo-proteins,  etc., 
may  be  absorbed  and  give  rise  to  toxic  symptoms  is  very  unsatisfactory 
and  inconclusive  and  for  the  present  may  be  disregarded.  Putrefactive 
changes  in  the  intestine  involve  almost  solelv  the  aromatic  and  sulj)hur 


304  DISORDERS  OF  METABOLISM 

groups  of  the  protein  molecule.  The  aromatic  bodies  yield  indol,  phe- 
nol, and  skatol,  which  uniting  with  sulphuric  acid,  may  appear  in  the 
urine  (indoxyl-sulphate,  so-called  indicanuria,  etc.)-  This  occurs  in  the 
event  of  protein  decomposition  elsewhere  than  in  the  intestine,  and  it  is 
doubtful  whether  of  itself  it  gives  rise  to  symptoms;  but  with  reserve  it 
may  be  interpreted  as  a  measure  of  intestinal  putrefaction:  it  occurs 
most  rapidly  and  in  greatest  amount  in  obstruction  or  paralysis  of  the 
small  intestine.  Various  other  disorders  are  attributed,  with  more  or 
less  reason,  to  gastro-intestinal  intoxication:  senescence  and  ultimately 
death  (Metchnikoff) ;  the  headache  and  general  malaise  of  chronic  con- 
stipation; chlorosis  (Sir  Andrew  Clark);  pernicious  anemia,  attributed 
by  William  Hunter  to  oral  and  gastro-intestinal  toxemia;  tetany,  some- 
times associated  with  gastric  dilatation,  and  due  apparently  at  least 
indirectly  to  the  absorption  of  a  poison  from  the  stomach;  the  toxemia 
and  death  of  high  intestinal  obstruction  (duodenal  auto-intoxication, 
disturbance  of  the  balance  of  physiological  intra-enteric  enzymotic  bal- 
ance, Maury);  cirrhosis  of  the  liver;  chronic  disease  of  the  joints;  a 
so-called  intestinal  infantilism,  described  by  Herter  and  attributed  by 
him  to  chronic  intestinal  infection  due  to  the  overgrowth  and  persistence 
of  the  bacterial  flora  of  the  intestine  belonging  normally  to  the  nursling 
period;  and  a  rare  form  of  cyanosis,  known  as  enterogenous  cyanosis, 
due  in  the  one  series  of  cases  to  methemoglobinemia,  the  result  of  the 
absorption  of  nitrites  from  the  intestine  in  chronic  diarrhoea,  and  amen- 
able to  a  milk  diet,  and  due  in  another  series  of  cases  to  sulph-hemoglo- 
binemia,  the  result  apparently  of  putrefaction  of  the  proteins  in  chronic 
constipation,  and  amenable  to  treatment  directed  toward  the  constipa- 
tion. The  treatment  of  these  gastro-intestinal  auto-intoxications  com- 
prises attention  to  any  demonstrable  focus  of  intoxication,  such  as 
pyorrhoea  alveolaris  or  other  form  of  oral  sepsis,  chronic  ulceration  of 
the  bowel,  rectum,  etc.;  regulation  of  the  diet,  especially  restricting  the 
amount  of  meat,  and  giving  in  the  one  case  milk,  as  well  as  milk  soured 
with  the  lactic  acid  bacillus  (Bacillus  bulgarius) ;  in  another  case  food 
that  leaves  sufficient  residue  to  promote  free  evacuation  of  the  bowels; 
medicinal  and  other  treatment  of  constipation,  if  it  be  present;  the 
use  of  so-called  intestinal  antiseptics,  such  as  salol,  /3-naphthol,  bismuth 
sulphocarbolate,  resorcin,  etc.;  and  high  colonic  irrigations 

Acidosis  and  Acid  Intoxications. — Acidosis  is  a  diseased  condition 
in  which  organic  acids,  notably  /3-oxybut}Tic  acid,  diacetic  acid,  and 
acetone  (the  so-called  acetone  bodies)  appear  in  abnormal  amounts  in 
the  blood  and  the  urine  (ketonuria) ;  acid  intoxication  is  a  diseased  con- 
dition in  which  in  addition  toxic  symptoms  develop.  There  is  still  some 
discussion  as  to  whether  these  acetone  bodies  are  toxic  per  se,  or  whether 
they  exert  their  deleterious  action  merely  because  they  are  acid,  robbing 
the  body  of  native  alkali,  diminishing  the  power  of  the  blood  to  take  up 
carbon  dioxide,  and  leading  to  tissue  asphyxiation;  perhaps  both  factors 
are  operative  in  human  pathology.  These  acetone  bodies  are  derived 
largely,  if  not  exclusively,  from  the  lower  fatty  acids;  perhaps  in  small 


DIABETES  305 

part  from  the  fatty  acid  moiety  in  protein,  such  as  leucin.  Tiie  condi- 
tion of  acid  intoxication  may  be  the  result  of  an  augmented  formation 
of  these  acetone  bodies,  or  of  a  deficiency  of  bases;  and  it  is  found  in: 
(1)  Diabetes,  of  which  it  forms  a  conspicuous  and  serious  feature,  and 
under  which  heading  it  is  discussed;  (2)  starvation  of  whatsoever  sort: 
insuflSciency  of  food;  inability  to  take  or  utilize  food,  as  in  stricture  or 
carcinoma  of  the  oesophagus,  stomach,  or  intestine;  diseased  conditions 
of  the  gastro-intestinal  tract  leading  to  long-continued  rectal  feeding, 
etc.;  it  is  especially  likely  to  supervene  if  oxidation  is  deficient  and 
little  or  no  carbohydrate  is  taken;  (3)  the  febrile  state,  in  which  in 
addition  to  destruction  of  the  body  fat  and  protein,  the  supply  of  food 
is  often  insufficient  and  cannot  be  properly  metabolized;  (4)  certain 
ill-understood  conditions  of  the  gastro-intestinal  tract,  usually  associated 
with  constipation,  in  which  I  have  seen  it  present  in  high  grade;  (5) 
after  anesthesia;  (6)  in  young  children,  and  in  excessive  degree  in  the 
recurrent  vomiting  of  unknown  cause  in  children;  and  (7)  in  some  cases 
of  pernicious  vomiting  of  pregnancy.  The  treatment  of  the  acidosis  con- 
sists, in  brief,  in  preventing,  if  possible,  the  formation  of  the  acetone 
bodies  by  a  judicious  combination  of  fat,  protein,  and  carbohydrate 
(discussed  under  diabetes),  by  neutralizing  the  circulating  acids  (by 
administering  large  amounts  of  sodium  bicarbonate  or  other  alkali), 
and  by  supplying  deficient  bases,  such  as  calcium  and  magnesium. 

Retention  Auto-intoxications. — To  the  retention  of  excrementi- 
tious  products,  auto-intoxications,  such  as  uremia,  puerperal  eclampsia, 
and  so-called  cholemia  are  often  attributed;  but  the  nature  of  the  sup- 
posed excrementitious  products  have  not  been  determined,  and  there  is 
considerable  evidence  tending  to  support  the  view  that  in  these  condi- 
tions the  detoxifying  function  of  the  liver  is  the  major  factor  at  fault: 
the  complete  elucidation  of  the  many  problems  herewith  concerned  must 
await  future  investigations.  Asphyxia  may  be  looked  upon  as  a  form 
of  auto-intoxication  due  to  the  retention  of  carbon  dioxide.  The 
toxemia  that  follows  extensive  burns  may  be  due  to  the  retention  of 
toxic  substances  incapable  of  elimination  by  the  burned  skin,  or  to  the 
absorption  of  a  toxic  substance  from  the  burned  areas.  Retention  of 
sodium  chloride  is  at  least  one  factor  in  the  production  of  the  oedema 
of  nephritis,  and  perhaps  of  other  oedemas. 


DIABETES. 

(Diabetes  M  ell  it  us.) 

Diabetes  is  a  disorder  of  metabolism,  involving  chiefly  the  carbohy- 
drates, and  characterized  clinically  by  hyperglycemia,  glycosuria,  and 
ultimately  ketonuria  and  acid  intoxication. 

Etiology. — Diabetes  occurs  at  all  ages,  but  is  most  common  after  the 
fortieth  year;  almost  one-third  of  the  cases  develop  in  the  sixth  decade, 
and  about  one-fifth  prior  to  the  thirtieth  year;  but  it  may  develop  in 
20 


306  DISORDERS  OF  METABOLISM 

advanced  life  as  well  as  in  infancy.  It  is  more  common  in  males  than  in 
females  in  the  proportion  of  3  to  2.  In  general,  it  is  less  common  in 
this  country  (though  increasing)  than  it  is  in  Europe;  it  is  especially 
common  among  Hebrews,  and  comparatively  rare  among  negroes.  It 
is  a  disease  of  the  well-to-do,  rather  than  of  the  poor  (in  the  proportion 
of  10  to  1,  von  Noorden).  Hereditary  influences  are  active  in  some  cases, 
diabetes  itself,  gout,  obesity,  and  neuropathies  being  common  in  the 
antecedents,  as  well  as  in  the  immediate  family  of  diabetic  subjects. 
It  is  not  uncommon  in  husband  and  wife  (conjugal  diabetes),  which 
without  much  reason  has  suggested  an  infectious  cause  to  some 
observers. 

The  direct  cause  of  diabetes  is  not  known.  An  unhygienic  mode  of 
life,  exposure  to  wet  and  cold,  overeating,  excessive  indulgence  in  car- 
bohydrates and  in  meat,  alcoholism,  sedentary  habits,  prolonged  anxiety, 
mental  strain,  emotional  and  other  nervous  disturbances,  etc.,  have 
been  credited  with  etiological  significance.  The  combination  of  seden- 
tary habits,  excessive  eating  (carbohydrates  and  meats)  and  drinking 
(alcoholism),  and  prolonged  mental  strain  (absorption  in  business 
pursuits,  large,  financial,  and  other  responsibilities)  is  common  in  those 
who  develop  diabetes.  Disorders  that  are  sometimes  attended  by  tem- 
porary glycosuria  seem  sometimes  also  to  lead  to  true  diabetes,  such 
as:  pregnancy;  infections  (diphtheria,  scarlatina,  malaria,  influenza, 
syphilis,  etc.)  which  perhaps  act  by  setting  up  pancreatitis;  injury  and 
disease  of  the  brain  and  spinal  cord  (epilepsy,  chorea,  organic  disease 
especially,  but  not  alone,  of  the  medulla  and  the  floor  of  the  fourth 
ventricle),  etc. 

Pathology. — The  important  lesions  occur  in  the  pancreas — for  our 
knowledge  of  which  fact  we  are  indebted  to  Minkow^ski,  von  Mering, 
Opie,  etc.  Cecil  recently,  studying  90  cases,  found  lesions  of  the  pan- 
creas in  79  (87.4  per  cent.);  in  these  the  islands  of  Langerhans  were 
always,  sometimes  alone,  diseased  (sclerosis,  hyaline  degeneration,  leuko- 
cytic infiltration,  and  h^'pertrophy).  97  per  cent,  of  the  cases  occurring 
after  the  age  of  thirty  years  were  associated  with  lesions  of  the  pan- 
creas, and  87  per  cent,  occurred  in  association  with  chronic  inter- 
acinous  pancreatitis  accompanying  arteriosclerosis.  50  per  cent,  of  the 
cases  occurring  before  the  age  of  thirty  years  were  associated  with  lesions 
of  the  pancreas;  and  75  per  cent,  of  all  cases  of  diabetes  in  which  the 
pancreas  was  normal  occurred  before  the  age  of  thirty  years.  In 
addition  to  disease  of  the  pancreas,  the  liver  is  usually  enlarged;  fatty 
changes  are  common;  there  maybe  cirrhosis,  which  is  usually  associated 
with  pigmentation  of  the  liver,  pancreas,  skin,  etc.  (hemochromatosis, 
bronzed  diabetes).  The  nervous  system  shows  divers  but  inconstant 
lesions:  sclerosis,  cysts,  or  tumors  in  the  medulla  and  sometimes  else- 
where; meningitis  and  the  lesions  of  different  organic  diseases;  degenera- 
tion of  the  posterior  columns  of  the  cord  and  peripheral  neuritis  (the 
cause  of  so-called  diabetic  tabes),  etc.  Usually  there  is  arteriosclerosis 
and  hypertrophy  of  the  heart.    Hyperglycemia  (as  much  as  0.5  per  cent. 


DIABETES  307 

instead  of  the  normal  0.1  to  0.15)  is  constant,  and  the  opsonic  index  is 
reduced.  The  thyroid,  pituitary,  and  adrenals  are  sometimes  enlarged 
or  otherwise  diseased.  Tuberculosis,  especially  of  the  lungs,  broncho- 
pneumonia, croupous  pneumonia,  chronic  nephritis,  gangrene,  pyococcic 
infections,  such  as  furuncles,  carbuncles,  etc.,  are  common  complica- 
tions, and  may  be  the  cause  of  the  fatal  issue.  Chronic  nephritis 
occurs  in  about  one-half  of  the  cases,  and  is  attributable  to  the 
polyuria  and  ketonuria. 

The  ultimate  nature  of  diabetes  is  not  yet  perfectly  understood,  largely 
because  the  fate  of  carbohydrates  in  the  body  in  health  has  not  been 
fully  elucidated.  It  is  known  that  normally  the  carbohydrates  of  the  food 
are  converted  into  glycogen  and  warehoused  in  the  liver  and  the  muscles ; 
and  that  under  some  circumstances  glycogen  may  be  formed  from  the 
non-nitrogenous  moiety  of  the  food  protein  as  well  as  the  body  protein. 
As  required  by  the  body  for  heat  and  energy,  the  glycogen  undergoes 
destruction,  being  converted  largely  into  alcohol  and  carbon  dioxide. 
How  this  glycolysis  is  effected  is  still  the  subject  of  study.  The  tendency 
of  modern  studies  is  to  minimize  the  significance  of  the  liver,  which  is 
believed  to  act  chiefly  as  a  storehouse,  liberating  the  stored  glycogen 
as  it  is  required  and  preventing  an  excess  going  over  into  the  circulation 
at  any  one  time  (which  would  result  in  hyperglycemia).  There  is, 
however,  an  intimate  relationship  between  the  pancreas  and  the  muscles. 
The  islands  of  Langerhans  in  the  pancreas  produce  a  secretion  con- 
taining a  ferment  or  zymogen,  which,  reaching  the  muscles  by  way  of 
the  blood  stream,  encounters  there  another  ferment  or  proferment; 
an  interaction  occurring  between  the  two  results  in  the  production  of  an- 
other ferment,  which  has  the  specific  property  of  destroying  dextrose 
(glucose).  In  pancreatic  diabetes  the  pancreatic  ferment  or  zymogen 
is  deficient  or  absent;  the  muscular  ferment  or  zymogen  is  not  acti- 
vated, the  glycolytic  ferment  is  not  formed,  and  glucose  is  not  combusted, 
but  passes  over  in  the  blood  in  excess  (hyperglycemia),  and  is  excreted 
in  the  urine  (glycosuria).  By  some  investigators  it  is  believed  that  the 
pancreas,  rather  than  supplying  a  substance  requisite  for  the  proper 
metabolism  of  sugar,  has  the  property  of  neutralizing  a  poison  which, 
not  detoxified,  leads  to  the  accumulation  of  sugar  in  the  blood.  In  many 
cases  the  ability  properly  to  utilize  fats  also  is  more  or  less  impaired,  and 
/3-oxybutyric  acid  and  its  derivatives  (oxidation  products),  diacetic  acid 
and  acetone,  intermediary  products  of  fat  metabolism  (derivatives  of  the 
lower  fatty  acids),  are  excreted  in  the  urine  (ketonuria),  and  acetone 
also  with  the  expired  air.  This  occurs  especially  in  conditions  of  carbo- 
hydrate starvation;  and,  often  in  the  early  stages  of  the  disease,  at  least, 
can  be  prevented  by  feeding  carbohydrates,  which  are  concerned  in  pro- 
viding the  oxygen  necessary  for  the  ultimate  oxidation  of  the  fatty  acids 
to  carbon  dioxide  and  water;  later,  however,  this  becomes  impossible, 
and  a  dangerous  acid  intoxication  ensues  and  may  lead  to  a  fatal 
termination. 

Associated  disturljance  in  the  carbohydrate  and  fat  metabolism  is 


308  DISORDERS  OF  METABOLISM 

found  in  some  cases  of  diabetes  in  the  obese,  in  some  of  which  the 
conversion  of  carbohydrates  into  fat  is  not  seriously  disturbed,  ahhough 
the  carbohydrate  tolerance  may  be  low  (alimentary  glycosuria,  latent 
diabetes);  in  some  of  these  true  diabetes  may  subsequently  develop.  Dis- 
order of  the  protein  metabolism  is  apparent  in  the  fact  that  an  excess  of 
protein  increases  the  glycosuria  in  some  cases;  some  observers  believe 
that  an  excess  of  protein  is  at  least  partly  responsible  for  the  disease 
(said  to  stimulate  the  thyroid). 

There  is  in  diabetes  some  relationship  between  the  pancreas  and  the 
ductless  glands — the  thyroid,  the  adrenals,  and  the  pituitary  body. 
These,  particularly  the  thyroid  and  the  pituitary,  may  be  found  enlarged; 
and  diabetes  clinically  is  found  associated  with  more  or  less  well-developed 
Graves'  disease  and  akromegaly.  There  is  believed  to  be  an  antagonism 
between  the  pancreas  and  the  thyroid;  hyperactivity  of  the  thyroid 
may  produce  glycosuria.  It  has  been  found  also  that  the  injection  of 
adrenalin  results  in  hyperglycemia  and  glycosuria  (adrenal  diabetes), 
and  an  adrenal  influence  in  human  diabetes  has  been  postulated  (inter- 
ference with  the  oxidizing  power  of  the  pancreas,  or  an  action  upon  the 
sympathetic  nervous  system,  resulting  in  the  non-warehousing  or  the 
release  of  glycogen,  with  ensuing  h}'perglycemia  and  glycosuria).  The 
administration  of  phloridzin  (a  glucoside)  also  results  in  glycosuria 
without  hyperglycemia;  it  is  attributed  to  a  toxic  influence  on  the  renal 
epithelium,  and  is  used  as  a  test  of  the  functional  capacity  of  the  kidney. 
The  influence  exerted  by  the  nervous  system  in  some  cases  is  not  well 
understood.  Some  observers  believe  that  the  disturbance  in  diabetes 
is  not  so  much  in  the  pancreas  and  its  internal  secretion  as  in  the  nerves 
that  pass  through  the  pancreas;  others  believe  that  the  nervous  influ- 
ence results  in  the  imperfect  storage  or  liberation  of  glycogen  in  the 
body.  H}^erglycemia  is  a  constant  feature — an  increase  in  the  sugar 
content  of  the  blood  from  the  normal  0.1  to  0.15  per  cent,  to  0.3  or  0.5 
per  cent.  To  it  is  attributable  indirectly  the  fatigue  and  emaciation, 
on  account  of  the  calories  thus  lost.  A  daily  excretion  of  100  grams  of 
sugar,  representing  400  calories  (16  per  cent,  of  the  calories  required  for 
a  man  weighing  70  kilograms),  must  be  met  by  increased  protein  and 
fats,  whence  the  hyperglycemia  indirectly  results  in  increased  appetite. 

Symptoms.^ — In  the  great  majority  of  cases  the  onset  is  insidious  and 
the  disease  often  has  made  considerable  progress  by  the  time  obtrusive 
symptoms  become  manifest — chronic  cases,  which  may  last  for  years  and 
are  especially  common  in  subjects  past  middle  life;  rarely  the  onset  is 
abrupt,  or  the  disorder,  having  been  existent  though  ill-declared  for  some 
time,  suddenly  (perhaps  following  an  injury,  shock,  or  some  emotional 
disturbance)  becomes  very  acute  and  rapidly  progressive — acute  cases, 
which  are  especially  common  in  young  subjects  and  may  soon  lead  to 
death.  There  is,  however,  no  essential  difference  between  the  two 
classes  of  cases.  As  a  rule,  the  early  symptoms  consist  of  malaise, 
readily  induced  languor,  or  loss  of  flesh  and  strength ;  or  frequent  micturi- 
tion, polyuria,  or  excessive  thirst  attracts  attention.     The  fully  developed 


DIABETES  309 

disease  is  characterized  by  hyperglycemia,  polyuria,  glycosuria,  and 
ultimately  ketonuria,  acid  intoxication,  and  fatal  coma;  polydypsia 
and  polyphagia;  often  but  not  always  marked  emaciation;  and  a  number 
of  variable  and  inconstant  symptoms  referable  to  the  different  systems 
of  organs  (complications). 

Major  interest  and  significance  attaches  to  the  urine — which  is  in- 
creased in  amount,  pale  in  color,  acid  in  reaction,  of  increased  specific 
gravity,  and  contains  sugar,  and  often  one  or  more  of  the  acetone  bodies. 
The  total  twenty-four-hour  amount  of  urine  averages  between  three  and 
six  liters;  but  enormous  amounts  (twenty  to  thirty  or  more  liters)  may 
be  excreted,  and  in  other  cases  the  amount  may  be  scarcely,  if  at  all, 
above  the  normal  (mild  cases;  cases  markedly  improved;  under  the  in- 
fluence of  infectious  processes;  prior  to  the  fatal  issue).  The  specific 
gravity  varies,  as  a  rule,  between  1025  and  1040,  but  it  is  sometimes 
quite  low  (1015  or  less),  and  rarely  it  may  be  very  high  (1050  to  1070). 
The  sugar  content  varies — from  0.5  to  2  or  3  per  cent,  in  mild  cases,  to 
5  to  10  per  cent,  in  severe  cases.  The  total  amount  of  sugar  excreted 
daily  varies  from  50  to  200  grams  or  thereabout  in  mild  cases  to  500 
to  1000  grams  or  more  in  severe  cases;  but  it  is  markedly  influenced  by 
the  diet,  the  mode  of  life,  the  form  of  treatment,  and  approaching 
fatality  and  coma. 

The  total  nitrogen  of  the  urine  (normally  10  to  15  grams  daily)  is 
usually  increased  (15  to  20  grams  or  more);  this  is  due,  as  a  rule,  to  the 
increased  protein  ingestion,  but  in  severe  cases,  especially  with  high 
glycosuria  and  during  coma,  it  is  due  also  to  destruction  of  the  body 
protein.  The  total  urea  is  increased  (for  the  reasons  just  mentioned); 
the  percentage  of  urea  is  usually  unchanged  in  the  absence  of  acidosis; 
it  is  diminished  when  acidosis  is  present  (on  account  of  the  increased 
ammonia) .  The  creatinin  may  be  increased ;  the  uric  acid  may  be  normal 
or  increased.  Of  special  importance  and  significance  is  the  increased 
output  of  ammonia.  Normally  this  varies  from  0.5  to  1  gram  daily,  up 
to  1.5  grams  on  a  meat  diet;  in  diabetes  it  is  often  increased  to  3  to  6 
grams,  and  may  reach  8  to  10  grams  or  more;  and  instead  of  forming  2  to 
5  per  cent,  of  the  total  nitrogen,  it  may  form  10  to  20  per  cent.  This 
increase  is  to  be  interpreted  as  an  effort  on  the  part  of  nature  to  neutralize 
the  existing  acidosis — the  result  of  the  acid  derivatives  of  the  proteins  and 
the  fats.  The  sulphur  and  phosphorus  of  the  proteins  normally  are 
oxidized  to  HjSO^  and  PgOj,  but  encountering  sufficient  fixed  bases  they 
are  neutralized;  when  in  excess,  however,  they  unite  with  some  of  the 
ammonia  (a  product  also  of  protein  katabolism)  and  are  carried  oft' 
in  the  urine.  In  addition,  the  acetone  bodies,  when  present,  are  also, 
at  least  in  part,  neutralized  by  ammonia.  The  anunonia  excretion 
thus  is  a  trustworthy  indication  of  the  degree  of  existing  acidosis,  and  is 
more  readily  determined.  The  acetone  bodies,  /3-oxybutyric  acid,  dia- 
cetic  acid,  and  acetone  (of  which  the  succeeding  is  the  oxidation  product 
of  the  preceding)  are  often  present  in  the  urine  (ketonuria)  in  variable 
amounts.     Normally  a(;etone  is  present  in  the  urine  (0.01  to  0.03  graui 


310  DISORDERS  OF  METABOLISM 

in  the  twenty-four  hours) ;  in  diabetes  this  may  be  increased  to  2  or 
more  grams,  and  the  total  excretion  of  acetone  and  diacetic  acid  may 
reach  5  to  8  grams,  while  that  of  ;3-oxybutyric  acid  may  reach  50  to  70 
grams.  The  acetone  bodies  are  derived  from  the  lower  fatty  acids  of 
the  organism  and  the  food,  but  they  occur  in  the  urine  only  in  the  event 
of  disordered  carbohydrate  metabolism,  the  katabolism  of  80  to  100  grams 
of  carbohydrates  being  ordinarily  sufficient  to  prevent  the  ketonuria. 
This  rather  than  the  glycosuria  is  the  important  index  of  the  severity 
of  the  diabetes :  the  acetone  bodies  are  absent  in  mild  cases  for  a  long 
time,  and  acetone  is  the  first  to  appear;  later,  diacetic  acid  is  added, 
and  in  advanced  and  severe  cases  (absolute  loss  of  carbohydrate  toler- 
ance, with  the  excretion  in  the  urine  not  only  of  all  the  ingested  carbo- 
hydrates, but  also  of  sugar  derived  from  the  non-nitrogenous  portion  of 
the  proteins),  all  three  bodies  may  be  encountered. 

Albuminuria  is  encountered  sometime  in  at  least  one-half  of  the  cases. 
It  is  usually  slight  in  grade,  and  may  be  due  to  local  catarrhal  disorders 
of  the  urinary  tract,  general  infections,  arteriosclerosis,  degeneration  of 
the  renal  epithelium  (overwork,  from  long-continued  polyuria,  glycosuria, 
and  ketonuria) ;  in  some  cases  there  may  be  also  casts  and  other  evidences 
of  true  nephritis.  Albuminuria,  previously  absent,  is  likely  to  appear 
as  a  more  or  less  immediate  forerunner  of  coma;  indeed,  it  is  not  un- 
likely that  some  of  the  cases  of  coma  are  uremic  rather  than  diabetic 
in  nature. 

Most  of  the  other  important  symptoms  are  referable  to  the  digestive 
tract  and  the  nervous  system.  Thirst  may  be  the  first  obtrusive  symp- 
tom, and  is  often  exceedingly  distressing;  it  is  probably  due  to  the  systemic 
demands  for  fluids;  the  intake  is  usually  in  direct  ratio  to  the  output. 
The  appetite  may  or  may  not  be  inordinate.  Despite  the  large  amount  of 
food  taken,  digestion  is  often  good,  although  indigestion  (sometimes 
associated  with  gastrectasia)  and  constipation  (sometimes  alternating 
with  attacks  of  diarrhoea)  are  not  uncommon.  Despite  the  large  amount 
of  food  taken  the  patient  may  emaciate  rapidly.  The  tongue  is  usually 
dry,  red,  and  glazed,  perhaps  fissured;  the  saliva  is  scanty;  there  may  be 
aphthous  and  other  forms  of  stomatitis;  and  the  teeth  readily  decay. 
The  liver  may  l)e  enlarged — in  ordinary  diabetes,  as  well  as  in  bronzed 
diabetes  (hemochromatosis). 

Of  the  nerv^ous  sjniiptoms,  pruritus,  especially  of  the  genitalia,  is 
often  exceedingly  distressing.  In  addition  there  may  be  paresthesias, 
neuralgias,  or  peripheral  neuritis  (single  or  multiple).  Bilateral  sciatica 
is  common.  In  almost  one-half  the  cases  the  knee-jerks  are  diminished 
or  lost;  this  may  be  associated  with  paresthesias,  irregular  pains,  and 
neuromuscular  cramps  in  the  legs.  Some  of  these  cases  present  a  char- 
acteristic steppage  gait,  degeneration  of  the  posterior  columns  of  the 
spinal  cord,  perhaps  optic  atrophy,  and  other  evitlence  of  tabes  (so-called 
diabetic  tabes).  The  cranial  nerves  (especially  the  abducens,  the 
oculomotor,  the  facial,  etc.)  and  the  spinal  nerves  also  may  be  affected 
(paresthesia,  paresis,   trophic  disturliances,  herpes   zoster,   perforating 


DIABETES  311 

ulcer  of  tiie  foot,  etc.).  Epileptiform  attacks  occasit)nally  occur.  Im- 
potence (probably  due  to  spinal  degeneration)  is  common,  and  may  l)e 
an  early  symptom.  The  patient  is  likely  to  become  nervous,  restless, 
irritable,  hypochondriacal,  or  melancholic. 

The  most  important  of  the  nervous  phenomena  is  coma — which  is  the 
direct  cause  of  the  fatal  issue  in  almost  all  of  the  young  subjects  and  in 
from  one-half  to  three-fourths  of  the  older  subjects  (in  unusual  cases  the 
coma  may  be  not  diabetic,  but  uremic,  or  due  to  meningitis,  cerebral 
hemorrhage  or  softening,  etc.).  Diabetic  coma  is  attributed  to  acid 
intoxication  (^-oxybutyric  acid),  of  which  it  is  the  final  stage,  and  it  is 
to  be  feared  in  all  cases  in  which  ketonuria  occurs  and  when  the  daily 
output  of  ammonia  (the  index  of  the  acidosis)  exceeds  3  grams.  The 
coma  may  develop  suddenly  in  the  midst  of  comparatively  good  health; 
or  it  may  be  precipitated  by  severe  exertion,  excitement,  local  infection, 
etc. ;  or  without  exciting  cause  it  may  come  on  gradually  with  weakness, 
headache,  restlessness,  anxiety,  somnolence,  nausea,  vomiting,  syncope, 
Kussmaul's  dyspnoea,  or  air-hunger  (deep,  energetic,  long-drawn  inspira- 
tion, contrasting  strongly  with  the  general  asthenia,  and  short,  sighing 
expiration,  unassociated  with  cyanosis,  at  the  beginning  at  least), 
a  sweetish,  fruity  odor  to  the  breath  (excretion  of  acetone  and  diacetic 
acid  with  the  breath),  and  gradually  deepening  coma.  The  pulse  is 
usually  small  and  rapid,  the  pupils  dilated,  the  reflexes  abolished,  and 
the  temperature  subnormal;  convulsions  are  rare.  Death  usually  ensues 
in  from  a  few^  hours  to  a  few  days;  rarely  the  patient  may  recover,  and 
perhaps  succinnb  to  a  subsequent  attack. 

Complications. — Complications  are  quite  common,  being  due  to  the 
h\'perglycemia  and  its  attendant  impaired  nutrition  and  lessened 
resistance  to  bacterial  infection,  acidosis,  etc.  Diminished  resistance 
to  bacterial  infection  (lessened  opsonic  index)  is  answerable  for  the  com- 
mon furunculosis,  boils,  and  carbuncles  (usually  staphylococcic  infection), 
tuberculosis,  pneumonia,  and  bronchopneumonia  (perhaps  followed  by 
abscess  or  gangrene),  which  are  responsible  for  most  of  the  fatal  issues 
not  due  to  coma,  but  which  also  may  induce  the  fatal  coma.  There  are 
many  sorts  of  skin  eruption,  eczema  (set  up  sometimes  by  intolerable 
itching),  urticaria,  xanthoma,  purpura,  etc.  Gangrene,  especially  of 
the  leg,  is  not  uncommon  in  middle-aged  or  elderly  subjects,  even  in  mild 
cases;  it  is  due  to  atheroma  or  obliterating  endarteritis. 

Generalized  arteriosclerosis  is  common  and  may  be  associated  with 
hypertrophy  of  the  heart;  rarely,  toward  the  end,  in  cases  of  failing  heart 
or  advanced  nephritis,  oedema  may  supervene,  but  it  is  uncommon — 
on  account  of  the  marked  polyuria  and  consequent  "dryness"  of  the 
tissues.  Amenorrhoea  is  common.  Conception  may  occur,  but  is 
likely  to  be  followed  by  abortion  or  aggravation  of  the  disease.  Vulvitis, 
vaginitis,  urethritis,  etc.,  are  common  in  the  female,  and  balanitis, 
phimosis,  etc.,  in  the  male.  The  special  senses  may  l)ecome  involved — 
aml)lyopia,  amaurosis,  retinitis,  cataract  (especially  in  young  subjects), 
chronic  catarrhal  deafness  (otitis  media),  etc. 


312  DISORDERS  OF  METABOLISM 

Diagnosis. — The  diagnosis  comprises  not  only  the  mere  recognition  of 
the  disease  and  its  differentiation  from  other  disorders  that  resemble  it, 
but  also  the  determination  of  the  type  and  severity  of  the  disorder,  of  the 
degree  of  carbohydrate  tolerance,  of  the  presence  and  the  degree  of 
acidosis,  and  of  the  general  nutrition  of  the  patient.  Polyuria,  poly- 
dypsia,  polyplagia,  emaciation,  and  such  suggestive  phenomena  as  genital 
pruritus,  impotence,  bilateral  sciatica,  recurring  boils,  etc.,  may  suggest 
the  disease;  but  the  diagnosis  usually,  and  in  the  early  stages  always, 
depends  upon  an  examination  of  the  urine.  Too  much  importance  can- 
not be  attached  to  the  routine  examination  of  the  urine,  in  all  cases  of 
diseases,  if  the  early  stages  of  diabetes  are  to  be  diagnosticated. 

The  carbohydrates  include:  (1)  The  monosaccharides  or  glucoses — 
glucose  (dextrose,  grape  sugar),  levulose  (fruit  sugar),  and  galactose 
(invert  milk  sugar);  (2)  the  disaccharides  or  saccharoses — saccharose 
(cane  sugar),  maltose  (malt  sugar),  and  lactose  (milk  sugar);  (3)  the 
polysaccharides  or  amyloses — starch,  glycogen,  dextrin,  cellulose,  and 
certain  gums ;  and  (4)  the  pentoses  or  five-carbon  sugars — arabinose  and 
xylose;  and  glycuronic  acid.  Of  these,  only  glucose,  lactose,  maltose, 
levulose,  pentose,  and  glycuronic  acid  possess  clinical  importance  in  the 
present  connection.  Glucose  (dextrose)  may  be  determined  by  Fehling's 
test,  the  fermentation  test,  the  phenylhydrazin  test,  and  dextrorotation 
of  polarized  light  (in  the  polariscope) ;  but  one  must  also  exclude  certain 
non-carbohydrate  reducing  substances,  such  as  uric  acid,  creatinin, 
alkapton,  and  certain  drugs  (for  details  one  should  refer  to  books  on 
clinical  laboratory  diagnosis). 

Having  determined  the  presence  of  glucose  in  the  urine,  it  is  advisable 
to  ascertain  whether  the  condition  is :  (1)  Toxic  glycosuria,  such  as  may 
follow  the  administration  of  anesthetics,  or  certain  drugs  and  poisons, 
such  as  phloridzin,  chloral,  morphine,  coal-tar  products,  etc.,  or  develop 
in  the  course  of  or  following  pregnancy,  some  infection,  etc. ;  (2)  neurotic 
glycosuria,  such  as  may  be  due  to  divers  emotional  or  other  disturbances, 
shocks,  etc.;  or  occur  in  association  with  different  nervous  diseases; 
(3)  alimentary  glycosuria  (the  inability  to  metabolize  100  grams  of 
glucose  taken  at  one  time  without  the  appearance  of  glucose  in  the 
urine);  or  (4)  true  diabetic  glycosuria.  The  toxic,  neurotic,  and  ali- 
mentary cases  are  transitory  and  intermittent;  as  a  rule,  the  amount 
of  sugar  excreted  is  small,  and  the  condition  may  entirely  disappear: 
but  many  of  the  cases  bear  a  more  or  less  intimate  relationship  to  true 
diabetes,  of  which  they  may  be  an  early  stage  or  ill-developed  form,  and 
to  which  they  may  progress. 

From  a  diagnostic,  prognostic,  and  therapeutic  standpoint  it  is  im- 
portant in  the  case  of  true  diabetes  (continuous  glycosuria  associated 
with  the  other  mentioned  symptoms)  to  determine  the  t;y^e,  whether 
mild,  intermediate,  or  severe;  that  is,  to  determine  the  carbohydrate 
tolerance.  Mild  cases  are  those  in  which  some  degree  of  carbohydrate 
tolerance  is  maintained;  that  is,  100  grams  of  glucose  can  be  metab- 
olized without   the  development  of   glycosuria,    and    no   disturbance 


DIABETES  313 

in  fat  metabolism  is  present;  that  is,  there  is  no  ketonuria.  Inter- 
mediate cases  are  those  in  which  the  carbohydrate  tolerance  is  almost 
if  not  quite  lost  (less  than  30  to  50  grams) ;  that  is,  the  urine  becomes 
aglycosuric  on  a  carbohydrate-free  diet  continued  for  a  week  or  more ; 
and  there  is  also  some  disturbance  of  fat  metabolism,  shown  in  aceto- 
nuria  and  diaceturia  from  time  to  time,  but  especially  when  the 
patient  is  on  a  carbohydrate-free  diet.  Severe  cases  are  those  in  which 
the  carbohydrate  tolerance  is  entirely  lost;  that  is,  the  urine  does 
not  become  aglycosuric,  even  when  a  carbohydrate-free  diet  has  been 
continued  for  several  weeks,  although  aglycosuria  may  be  produced 
by  restriction  of  the  protein  intake;  and  ketonuria  (including  often 
/9-oxybutyric  acid)  is  a  constant  feature.  The  severity  of  the  case  is  to 
be  determined  not  so  much  by  the  output  of  glucose,  assuredly  not 
by  the  percentage  output,  as  by  the  output  compared  with  the  carbo- 
hydrate intake.  In  some  cases  of  total  carbohydrate  intolerance  sugar 
may  be  found  in  the  urine  on  a  fat-protein  diet  in  the  proportion  of 
3.65  to  1  of  nitrogen  (the  fatal  ratio,  Mandel  and  Lusk).  The  majority 
of  eases  of  diabetes  are  mild,  but  they  are  most  common  in  elderly  and 
obese  subjects;  intermediate  cases  are  common  in  middle  life;  severe 
cases  are  most  common  in  youthful  and  in  thin  subjects. 

The  acidosis  may  be  determined  by  Gerhardt's,  Arnold's,  or  Hart's  tests 
(for  diacetic  acid  and  acetone),  by  the  Huppert-Messinger  quantitative 
test,  by  levorotation  of  polarized  light  after  complete  fermentation  of  the 
urine,  by  determining  the  ammonia  output,  and  roughly  by  the  amount  of 
sodium  bicarbonate  required  to  render  the  urine  alkaline  (normally  5  to 
10  grams,  Blum).  The  general  condition  of  the  patient  is  to  be  determined 
by  repeated  physical  examination  and  determination  of  the  body  weight. 
Diabetic  coma  may  be  distinguished  from  uremic  coma  by  ketonuria,  per- 
haps glycosuria,  fruity  odor  to  the  breath,  and  the  characteristic  Kuss- 
maul  dyspnoea;  albuminuria  and  the  cardiovascular  and  other  signs  of 
chronic  nephritis  are  often  present,  and  may  at  first  be  confusing. 

Prognosis. — ^The  course  of  the  disease  is  rarely  acute  (several  weeks); 
usually  it  is  chronic — several  years  to  many  years  (twenty  or  more). 
The  prognosis  varies  with  the  severity  of  the  case :  it  is  bad  in  youthful 
subjects  (in  infancy,  childhood,  and  adolescence);  in  thin  rather  than 
obese  subjects;  in  the  event  of  marked  and  rapid  loss  of  flesh  (despite 
the  ingestion  of  a  large  amount  of  food);  in  the  event  of  carbohydrate 
intolerance,  marked  glycosuria,  ketonuria,  non-response  to  treatment, 
and  infectious  complications.  Coma  is  almost  invariably  fatal.  The 
prognosis  is  favorable  in  eklerly  obese  subjects;  in  cases  with  fair  or 
moderate  carl)ohydrate  tolerance,  slight  glycosuria,  and  no  ketonuria; 
in  the  absence  of  complications;  and  in  the  event  of  response  to  treat- 
ment ^lessening  of  glycosuria  and  increase  in  weight). 

Treatment. — The  treatment  is  almost,  if  not  (juite,  wholly  dietetic. 
General  hygienic  measures;  a  life  of  comparative  ease  and  quiet,  free  from 
undue  professional  or  business  exactions,  worry,  and  emotional  and  other 
disturbances;  a  moderate  amount  of  regulated  exercise  (whicli  in  some, 


314  DISORDERS  OF  METABOLISM 

especially  mild,  cases  appears  to  increase  sugar  metabolism,  but  which 
may  have  a  contrary  effect  in  severe  cases);  now  and  then  a  course  of 
treatment  at  some  one  of  the  well-known  spas;  and  drugs — each  has  its 
place  in  treatment,  but  the  physician  must  individualize;  he  must  treat 
the  patient,  not  the  disease. 

Diet. — Since  the  patient  has  more  or  less  lost  the  ability  to  metabo- 
lize carbohydrates,  and  we  are  unable  directly  to  influence  the  carbohy- 
drate metabolism,  it  becomes  necessary  to  nourish  him  largely  on  a 
fat-protein  diet.  The  difficulty  in  doing  this  is  apparent  from  the  fact 
that  a  healthy  subject  ordinarily  derives  almost  one-half  of  his  heat  and 
energy  from  carbohydrates;  that  this  is  largely  or  wholly  lost  to  the  dia- 
betic through  the  glycosuria;  that  it  is  difficult  to  supply  this  deficiency 
with  a  fat-protein  diet  (which  is  not  the  most  palatable);  and  that 
continuation  of  the  h}^erglycemia  results  in  a  decreased  tolerance  of  the 
tissues  for  carbohydrates — as,  on  the  contrary,  lessening  of  the  h}^er- 
glycemia  results  in  an  increased  tolerance;  and  that  a  carbohydrate-free 
diet  is  likely  to  lead  to  a  dangerous  acid  intoxication.  The  permissible 
and  the  prohibited  foods  are  mentioned  in  Table  I,  which  as  well  as 
the  other  tables  appended  have  been  arranged  by  T.  C.  Janeway. 

In  the  treatment  of  every  diabetic  subject  the  first  essential  is  to  deter- 


Table  I. — General  Diabetic  Diet  List. 

May  take  freely:  Soups — aJl  meat  soups  and  broths;  may  add  vegetables  allowed,  egg,  or 
cheese.  Meats — all  fresh,  smoked,  or  cured  meats  (except  liver),  poultry,  and  game,  T^athout 
sauces  or  gravies  containing  flour;  pate  de  foie  gras.  Fish — all  kinds  of  fish,  except  oysters, 
clams,  and  scallops,  cooked  without  bread  crumbs  or  meal;  dried,  salted,  smoked,  or  pickled 
fish.  Eggs — prepared  in  any  way  without  flour.  Fats — butter,  lard,  suet,  olive  oil,  or  other 
fats.  Cheeses — all  kinds,  especially  cream,  Swiss,  English,  and  pineapple  cheese.  Vegetables 
and  salads — asparagus,  beet  greens,  Brussels  sprouts,  cabbage,  cauliflower,  celery,  chicorj', 
cresses,  cucumbers,  egg-plant,  endive,  kohl-rabi,  leeks,  lettuce,  okra,  pumpkin,  radishes, 
rhubarb,  salsify,  sauerkrout,  spinach,  string  beans,  tomatoes,  vegetable  marrow.  Pickles  made 
from  the  above-mentioned  vegetables,  unsweetened;  ripe  olives.  Fungi — mushrooms  and 
truffles.  Cream — not  over  three  ounces  a  day.  Condiments — salt,  pepper,  cayenne,  paprika, 
curry,  cinnamon,  cloves,  English  mustard,  nutmeg,  caraway,  capers,  vinegar,  and  the  piquant 
sauces  in  small  quantities,  unless  specially  forbidden.  Desserts — jellies  made  from  gelatine; 
custards  and  ice  cream  made  with  eggs  and  cream;  all  sweetened  with  saccharin  and  flavored 
with  vanilla,  coffee,  or  brandy.  The  following  recipes  for  desserts  are  suggested:  Baked  cus- 
tard— 1  egg,  1^  ounces  of  cream,  2J^  ounces  of  water;  two  or  three  J^^-grain  saccharine  tablets, 
8  drops  of  vanilla  essence;  beat  up  well,  pour  into  a  buttered  dish,  grate  a  little  nutmeg  on 
top,  and  bake  twenty  minutes.  Coffee  ice  cream — 13^  oujices  of  cream,  IJ^  ounces  of  water, 
1  ounce  of  strong  coffee,  two  or  three  J^-grain  saccharine  tablets;  dissolve;  add  1  egg,  well 
beaten;  mix  in  a  saucepan  and  beat  slowly  with  stirring  until  it  thickens;  set  aside  until  cool; 
then  freeze.  Nuts — butternuts.  Beverages — tea  or  coffee,  sweetened  with  saccharin,  and 
with  the  portion  of  cream  allowed;  whiskey,  brandy,  rum,  and  other  distilled  liquors  up  to  3 
ounces  a  day;  light  Rhine  or  Moselle  wine,  claret,  or  Burgundy  up  to  16  ounces  a  day;  mineral 
waters  of  all  kinds;  lemonade  in  small  quantity,  sweetened  with  saccharin. 

Articles  prohibited,  except  as  prescribed  in  the  accessory  diet  (carbohydrate  equivalents.  Table  IV) : 
Sugars  and  sweets  of  every  kind;  pastry,  puddings,  preserves,  cake,  and  ice  cream;  bread  and 
biscuit  of  all  kinds,  toast,  crackers,  and  griddle  cakes;  cereals,  such  as  rice,  oatmeal,  sago, 
hominy,  tapioca,  and  barley;  macaroni,  potatoes,  carrots,  parsnips,  beans,  peas,  beets,  green 
corn,  and  turnips;  fruit  of  all  kinds,  fresh  and  dried;  .soups,  sauces,  or  gravies  thickened 
with  flour  or  meal,  or  made  with  milk;  beer,  ale,  porter,  all  sweet  wines,  sherry,  or  port 
wine,  sparkling  wines,  cider,  and  liqueurs;  milk,  chocolate,  or  cocoa;  all  sweet  drinks  and 
goda  water. 


DIABETES  3l5 

mine  the  carbohydrate  tolerance  and  the  degree  of  acidosis  (if  there  be 
any) ;  the  carbohydrate  tolerance  should  be  redetermined  at  least  every 
two  months  in  mild  and  intermediate  cases,  and  perhaps  more  fre- 
quently in  the  severe  cases.  To  determine  the  carbohydrate  toler- 
ance, the  patient  should  be  put  upon  a  fixed  fat-protein  diet  of  suffi- 
cient caloric  value  to  maintain  strength  and  body  weight;  that  is,  35 
large  calories  per  kilogram  of  body  weight  (a  man  weighing  70  kilo- 
grams— 150  pounds — requires  about  2500  calories  per  day).  The  carbo- 
hydrates should  be  withdraw^n  gradually  (three  to  seven  days,  depending 
upon  the  severity  of  the  case),  since  sudden  withdrawal  may  result  in  a 
severe,  perhaps  fatal,  acidosis,  ^^^lile  determining  the  carbohydrate 
tolerance,  the  presence  and  the  degree  of  acidosis  should  be  inquired 
into,  and  if  present  the  patient  should  be  given  one-half  to  one  ounce  of 
sodium  bicarbonate  daily.  A  suitable  fat-protein  diet  is  indicated  in 
Table  II.  To  this  fat-protein  diet  100  grams  (3  ounces)  of  white  bread 
(55  per  cent,  of  carbohydrate)  in  three  equal  portions  should  be  added. 
The  bread  should  be  gradually  w^ithdrawn  until  the  urine  has  become 
sugar-free;  if  the  patient  is  not  aglycosuric  when  the  bread  has  been 
entirely  withdrawn,  the  diet  without  bread  should  be  continued  for  one 
week  or  more,  in  the  hope  that  the  urine  will  become  sugar-free.     If  the 

Table  II. — Standard  Strict  Diet. 

Breakfast:   Coffee  with  13^  ounces  cream;  2  eggs  cooked  with  H  ounce  butter;  3  ounces  ham. 
Luncheon:  Bouillon  with  1  raw  egg;   3  ounces  sirloin  steak,  chicken,  or  leg  of  lamb;    1  ounce 
bacon;  vegetable  from  list,  2  tablespoonfuls,  with  }^  ounce  butter;  dessert  made  with  1  egg  and 
IJ^  ounces  cream;   6  ounces  wine,  or  1  ounce  whiskey  or  brandy. 
Afternoon  tea  with  }^  ounce  cream. 

Dinner:  Any  clear  soup;  3  ounces  fish  (.salmon,  shad,  or  mackerel),  with  J^  ounce  butter; 
14  pound  roast  pork,  beef,  mutton,  turkey,  or  lamb  chops;  vegetables  from  list,  2  tablespoon- 
fuls, with  }4  ounce  butter;  salad  with  3^  ounce  oil  in  dressing;  1  ounce  cheese,  English,  pine- 
apple, Swiss,  or  full  cream;  6  ounces  wine,  or  1  ounce  whiskey  or  brandy;  demitasse  of  coffee. 

Protein =    126  grams;     515  calories 

Fat =   222  grams;  2065  aalories 

Carbohydrate =15  grams;       60  calories 

Alcohol =      .30  grams;     210  calories 

2850 
Table  III. — Standard  Diet  with  Restricted  Protein. 

Breakfast:  Coffee  with  IJ^  ounces  cream;  2  eggs  with  }4  ounce  butter;   1  ounce  bacon. 
Luncheon:  2  eggs;   1  ounce  bacon;  2  ounces  lamb  chops  (1),  ham  (2),  beefsteak  (3),  chicken 
(4),  or   fish   (5)   broiled  with   }4  ounce  butter    (each    day    select   meat    with    same    number   for 
luncheon  and  dinner);   vegetable  from  list,  2  tablespoonfuls,  with  J^  ounce  butter;  dessert  made 
with  1  egg  and  114  ounces  cream;   6  ounces  wine  or  1  ounce  whiskey  or  brandy. 
Afternoon  tea  with  }^  ounce  cream. 

Dinner:  .\ny  clear  soup;  14  pound  roast  pork  (5),  beef  (4),  mutton  (3),  turkey  (2),  chicken 
(1),  or  lamb  (1);  (each  day  select  meat  with  same  number  for  luncheon  and  dinner);  vegetables 
from  list,  2  tablespoonfuls,  with  }4  ounce  butter;  salad  with  }4  ounce  oil  in  dressing;  1  ounce 
cream  cheese;  6  ounces  wine  or  1  ounce  whiskey  or  brandy;  demitasse  of  coffee. 

Protein =82  grams;     334  calories 

Fat =    215  grams;   2008  calories 

Carboliydrate =15  grams;        GO  calories 

."Vlcohol =      .30  grams;     210  calories 

2612 


316  DISORDERS  OF  METABOLISM 

urine  becomes  sugar-free,  gradually  increasing,  weighed  amounts  of  white 
bread  may  be  added  to  the  diet  until  sugar  is  again  excreted.  Should 
the  patient  continue  to  excrete  sugar  on  the  fat-protein  diet  (without 
bread),  the  protein  intake  must  be  reduced,  since  considerable  protein 
intake  increases  the  glycosuria.  A  suitable  diet  with  restricted  protein 
is  that  of  Table  III. 

The  foregoing  procedures  will  determine  the  carbohydrate  tolerance 
(expressed  in  weighed  amounts  of  white  bread),  as  well  as  the  presence 
or  absence  of  acidosis,  and  permit  of  a  classification  of  the  case — mild, 
intermediate,  or  severe.  As  regards  the  acidosis,  subjects  who  tolerate 
100  grams  or  more  of  bread  rarely  have  acidosis;  those  who  tolerate 
less  carbohydrate  may  or  may  not  exhibit  ketonuria,  but  the  ketonuria 
that  develops  during  this  experimental  withdrawal  of  carbohydrates 
lasts  only  a  few  days,  as  a  rule;  the  diacetic  acid  disappears,  and  the 
amount  of  acetone  is  not  in  excess  of  the  normal. 

The  subsequent  treatment  of  the  patient  varies  with  the  type  of  the 
disease,  but  the  main  indications  are  to  maintain  nutrition  and  body 


Table  IV. — Table  of  Carbohydrate  Equivalents. 

Amount  in  ounces 

Per  cent,  equal  to  1  ounce 
Article.                                                                         carbohydrates.       white  bread. 

Breads:  White 51-55  1 

All  other 47-53  1 

Eolls  and  biscuit 52-60  1 

Corn  bread 46  IJ^ 

Crackers,  average 69-72  M 

Cereals:  Oatmeal,  boiled 11.3  5 

Hominy,  boiled 17.8  3 

Macaroni,  boiled        .       .       .       .       .       .       .           15.8  3K 

Rice,  boiled 24.4  2J^ 

Tubers  and  Legumes:  Potatoes,  cooked  ....           18-20  3 

Parsnips 13  4 

Beans,  baked 20  2M 

Beans,  lima,  cooked 20  2^ 

Peas,  green,  cooked 15  3J^ 

Milk 4-5  10 

Fruits:  Apples,  apricots,  and  pears 12-14  4 

Cherries 15  3J4 

Huckleberries 16  3J^ 

Plums 20  214 

Bananas 22  2J^ 

Nuts:  Filberts 12  iVi 

Almonds 15  3)^ 

Peanuts 22  2}4 

Table  V. — Green  Days. 

Breakfast:   1  egg,  boiled  or  poached;  cup  of  black  coffee. 

Dinner:  Spinach  with  a  hard-boiled  egg;  H  ounce  bacon;  salad,  with  }4  ounce  oil;  0  ounces 
of  wine  or  1  ounce  of  whiskey  or  brandy. 

4.30  P.M.:  Cup  of  beef  tea  or  chicken  broth. 

Supper:  1  egg,  scrambled,  with  tomato  and  a  little  butter;  M  ounce  bacon;  cabbage,  sauer- 
kraut, string-beans,  or  asparagus;  cup  of  tea;  or  white  wine,  4  <>\ince.s;  or  whiskey  or  brandy, 
1  ounce. 

}4  ounce  of  sodium  bicarbonate  in  the  twenty-four  hours. 

Carbohydrates  =  about  5  grams.      Calories  =  575. 


DIABETES  .  317 

weight,  to  lessen  the  h}^erglycemia  (of  which  the  glycosuria  affords  a 
clinical  measure),  and  to  prevent  or  control  the  acidosis.  Mild  cases, 
in  which  the  carbohydrate  tolerance  is  100  grams  or  more  of  white 
bread,  should  be  kept  within  their  limit.  Physicians  who  prefer  gluten 
bread  should  not  prescribe  it  under  the  misapprehension  that  it  is  harm- 
less; most  of  those  on  the  market  contain  from  30  to  70  per  cent,  of 
carbohydrate ;  ordinarily  it  is  better  to  give  a  weighed  amount  of  white 
bread  of  known  carbohydrate  content.  The  patient  may  be  permitted 
to  vary  the  carbohydrates  of  his  diet  in  accordance  with  his  desires  and 
his  metabolic  activities — which  in  individual  cases  is  not  alike  for  all 
carbohydrates.  Table  IV  shows  some  permissible  carbohydrates  and 
their  equivalents  in  terms  of  white  bread.  In  the  intermediate  cases, 
the  diet  in  general  should  conform  to  that  of  Table  II,  with  the  addition 
of  such  small  amount  of  carbohydrate  as  may  be  found  to  be  within  the 
patient's  capabilities  to  metabolize.  Considerable  bacon,  fat  meats  (fat 
beef,  pork,  mutton,  etc.),  and  fish  (salmon,  etc.),  up  to  a  total  of  not 
more  than  150  grams  (5  ounces)  daily,  butter,  thick  cream,  cheese,  oil, 
etc.,  are  especially  to  be  used.  The  digestion  of  the  considerable  amount 
of  fat  and  the  prevention  of  diarrhoea  from  imperfect  digestion  of  fat  may 
be  facilitated  by  a  moderate  amount  of  alcohol,  as  suggested  in  Tables  I, 
II,  and  III.  In  severer  cases  the  difficulties  are  increased;  the  protein 
must  be  reduced,  and  one  may  not  add  carbohydrates.  Study  and  re- 
arrangement of  the  diet,  however,  will  permit  one  to  nourish  the  patient 
sufficiently  on  a  very  low  protein  diet  (100  grams  or  less).  Idiosyncrasies, 
however,  must  be  met — some  patients  cannot,  others  will  not,  adhere  to  the 
prescribed  diet,  others  fail  in  nutrition,  or  acidosis  develops,  in  which 
cases,  heterodoxical  as  it  may  seem,  it  is  better  that  the  patient  have  a 
little  sugar  in  his  urine  than  that  he  fail  in  flesh  and  strength  or  run 
the  risks  of  acid  intoxication.  Now  and  then  a  diet  containing  very  little 
protein  is  serviceable:  largely  broths  (the  hunger  days  of  Naunyn),  or 
green  vegetables,  eggs,  bacon,  butter,  black  coffee,  and  alcohol  (the  green 
days  of  von  Noorden,  Table  V). 

Good  results  have  been  reported  from  time  to  time  by  a  milk  cure, 
Mosse's  potato  cure,  and  von  Noorden's  oatmeal  cure.  The  last- 
mentioned  consists  of  250  grams  of  oatmeal,  salted  to  suit  the  taste,  and 
three  to  four  quarts  of  water,  cooked  for  two  hours  on  a  moderate  fire; 
thereupon  250  to  300  grams  of  butter  and  100  grams  of  a  vegetable 
albumin,  such  as  roborat,  gliden,  rice  albumin,  etc.,  is  added  (six  to 
eight  eggs  may  be  substituted  for  the  albumin  in  the  country).  This  is 
to  be  taken  in  divided  portions  during  the  twenty-four  hours,  with  a  little 
black  coffee  or  alcohol.  Von  Noorden  recommends  the  treatment  in 
cases  of  moderate  severity,  four  or  five  times  a  year,  for  a  week— thus : 
one  vegetable  day,  three  oatmeal  days,  two  vegetable  days.  The  return 
to  the  usual  diabetic  diet  must  be  gradual,  since  otherwise  increased 
glycosuria  and  coma  may  ensue. 

Drugs. — The  drug  treatment  of  diabetes  is  notoriously  inefficient, 
although  drugs  have  their  place  in  the  treatment;  but  without  proper 


318  .  DISORDERS  OF  METABOLISM 

dietetic  regulation  drugs  are  worse  than  useless.  Opium,  codeine, 
and  arsenic  often  seem  to  be  of  much  service;  they  appear  to  favor 
oxidation,  lessen  glycosuria  (perhaps  by  preventing  protein  destruction), 
and  increase  the  general  well-being  of  the  patient.  The  bromides  are 
of  service  in  many  of  the  nervous  manifestations.  Tonics,  such  as 
iron,  quinine,  strychnine,  etc.,  are  often  useful.  Jambul,  chimophila,  the 
salicylates,  etc.,  have  been  extolled  from  time  to  time.  The  alkalies 
are  of  distinct  service — the  alkaline  mineral  waters  and  the  carbonate, 
bicarbonate,  citrate,  tartrate  of  sodium.  In  the  event  of  acetonuria  one- 
half  to  one  ounce  of  sodium  bicarbonate  should  be  given  daily,  and 
twice  or  thrice  as  much  in  impending  coma.  Developed  coma  is  usually 
fatal,  but  it  is  sometimes  relieved  by  intravenous  injections  of  2  to  4  per 
cent,  of  sodium  carbonate  in  physiological  saline  solution.  The  compli- 
cations are  to  be  treated  on  general  principles. 

DIABETES  INSIPIDUS. 

(Polyuria.) 

Diabetes  insipidus  is  a  chronic  disorder  characterized  by  the  passage 
of  large  amounts  of  non-saccharine  and  non-albuminous  urine  of  low 
specific  gravity. 

Etiology. — The  disorder  is  most  common  in  males  between  the 
twentieth  and  the  thirtieth  year;  more  than  half  of  the  cases  occur  be- 
tween the  tenth  and  the  fortieth  year.  Some  cases  seem  to  be  hereditary, 
or  several  cases  occur  in  the  same  family.  Two  types  of  polyuria  may 
be  differentiated — the  secondary  or  symptomatic  and  the  primary  or 
idiopathic.  Symptomatic  polyuria  is  especially  common:  (1)  In  diabetes, 
chronic  interstitial  nephritis,  after  drinking  large  amounts  of  water,  etc., 
in  organic  and  functional  disorders  of  the  cerebrospinal  and  sympathetic 
nervous  system,  such  as  trauma,  syphilis  (gumma,  basilar  meningitis), 
tumors  (especially  of  the  floor  of  the  fourth  ventricle),  hemorrhage, 
hydrocephalus,  lesions  of  the  medulla,  of  the  trapezoid  body  of  the  pons, 
or  of  the  middle  cerebellar  lobe,  etc.,  fright,  emotional  disturbances, 
hysteria,  neurasthenia,  psychoses,  epilepsy,  alcoholism,  etc.;  (2)  during 
or  after  infections  (typhoid,  typhus,  malarial  or  scarlet  fever,  tuberculosis, 
diphtheria,  measles,  etc.);  and  (3)  in  conditions  of  general  ill  health 
from  overwork,  mental  anxiety,  poor  nutrition,  etc.  The  idiopathic 
cases  are  those  that  develop  without  obvious  or  discoverable  cause. 

The  nature  of  the  disease  is  not  well  understood.  The  basis  of  it  is 
believed  to  be  a  functional  incapacity  of  the  kidneys  (unassociated  with 
noteworthy  structural  alterations),  due  to  disturbance  of  the  nervous 
or  vascular  mechanism  (vasodilatation  unaccompanied  by  rise  of  the 
general  arterial  pressure),  in  consequence  of  which  the  kidneys  are 
unable  to  excrete  urine  containing  a  normal  percentage  of  solids;  the 
normal  amount  of  solids  can  be  excreted  only  in  association  with  the 
passage  of  a  large  amount  of  urine,  in  the  absence  of  which  concentration 
of  the  blood  occurs.    Increase  in  the  protein  intake  does  not  cause,  as  it 


DIABETES  INSIPIDUS  319 

does  in  health,  an  increase  in  the  specific  gravity  of  the  urine,  but  an 
increase  in  the  amount  of  urine,  the  proportion  of  urea  remaining  con- 
stant. Similar  results  follow  variations  in  the  sodium  chloride  intake. 
Occasionally  diabetes  insipidus  is  said  to  develop  into  diabetes  mellitus, 
and  vice  versa,  but  usually  this  is  a  misinterpretation  of  surface 
phenomena. 

Pathology. — There  are  no  constant  or  characteristic  lesions.  Divers 
lesions  of  the  brain  are  found  in  about  one-third  of  the  cases.  The  kid- 
neys may  be  enlarged  and  congested,  and  the  renal  pelves,  ureters,  and 
bloodvessels  dilated  and  hypertrophied. 

Symptoms. — As  a  rule,  the  onset  of  the  disease  is  insidious;  in  some 
cases,  as  after  a  fright,  etc.,  there  may  be  a  sudden,  usually  transitory 
polyuria;  in  other  cases,  as  after  trauma,  the  onset  may  be  abrupt,  but 
the  course  protracted.  The  characteristic  phenomenon  is  the  passage  of 
a  large  amount  (5,  10,  20,  or  more  liters  daily)  of  urine,  which  is  pale  in 
color  and  of  low  specific  gravity  (1005  to  1001  or  less);  the  total  solids  are 
about  normal;  albumin  and  sugar  are  absent,  except  in  rare  circum- 
stances, and  then  are  present  only  in  traces  and  temporarily.  Thirst  is 
an  almost  constant  symptom  and  may  be  the  first  noteworthy  manifes- 
tation; it  is  the  result  and  not  the  cause  of  the  polyuria.  The  appetite 
may  be  poor,  normal,  or  excessive;  the  stomach  may  become  dilated; 
the  mouth  and  the  skin  usually  are  dry;  constipation  is  common.  Head- 
ache, nervousness,  irritability,  loss  of  sexual  power,  and  other  nervous 
manifestations  may  occur,  the  general  health  may  remain  for  a  long 
time  unaftected  (depending  upon  the  actuating  cause);  but  emaciation 
and  loss  of  strength  sometimes  supervene. 

Diagnosis. — The  diagnosis  is  easy.  Symptomatic  cases  should  be 
readily  recognized  by  attention  to  the  causative  factors;  the  frequency  of 
syphilis  as  an  etiological  factor  should  be  borne  in  mind.  Diabetes 
mellitus  may  be  excluded  by  the  absence  of  hyperglycemia,  glycosuria 
(and  high  specific  gravity),  carbohydrate  intolerance,  ketonuria,  and  the 
common  complications.  Chronic  interstitial  nephritis  may  be  excluded 
by  the  absence  of  albuminuria,  casts,  and  the  cardiovascular,  retinal,  and 
uremic  manifestations  of  nephritis;  in  addition,  the  specific  gravity  of  the 
urine  is  usually  higher  and  the  amount  less  than  in  diabetes  insipidus. 

Prognosis. — The  duration  and  prognosis  vary  with  the  cause  and  type 
of  the  disease.  Recovery,  except  in  the  obviously  transitory  cases,  is 
unlikely,  but  the  patient  may  live  for  many  years.  Death  often  ensues 
from  complicating  infections. 

Treatment. — As  low  a  protein  and  sodium  chloride  intake  as  is  con- 
sistent with  the  maintenance  of  strength  and  weight  should  be  given. 
It  is  not  necessary  or  advisable  to  restrict  the  fluid  intake,  since  it  results 
in  retention  of  the  urinary  solids  and  other  harmful  consequences.  The 
iodides  are  often  of  marked  benefit  even  in  a})parently  non-syphilitic 
cases.  Strychnine  and  vasoconstrictors,  such  as  ergot,  behadonna,  etc., 
are  often  followed  l)y  benefit;  adrenalin  hypodermidy  or  intravenously 
may  be  tried.    Opium  and  valerian  also  are  of  value  in  some  cases. 


320  DISORDERS  OF  METABOLISM 

GOUT. 

(Podagra.) 

Gout  is  a  chronic  disorder  of  metabolism  attended  by  marked  excess 
of  uric  acid  in  the  blood,  and  the  deposition  in  and  about  the  joints,  as 
well  as  in  other  cartilaginous  and  fibrous  tissues  of  the  body,  of  crystalline 
sodium  biurate. 

Etiology. — While  the  exact  disturbances  of  metabolism  occurring  in 
gout  are  still  the  subject  of  much  study  and  discussion,  certain  predis- 
posing factors  are  commonly  recognized.  Of  these,  heredity  is  probably 
the  most  important.  ^-Utliough  it  is  generally  conceded  that  gout  may  be 
acquired,  that  is,  tliat  it  occurs  in  the  absence  of  gouty  ancestry,  and 
although  not  all  descendants  (children  and  grandchildren)  of  gouty 
subjects  become  gouty,  the  common  opinion  is  that  at  least  50  to  60  per 
cent,  of  gouty  patients  suffer  for  the  sins  of  their  ancestors.  Futcher, 
however,  who  states  that  gout  is  much  more  common  in  this  country  than 
is  generally  believed,  being  often  unrecognized,  believes  that  it  is  much 
more  frequently  acquired  than  inherited,  since  not  more  than  31  per  cent, 
of  his  patients  had  gouty  ancestors.  Gout  is  much  more  common  in 
males  than  in  females,  and  transmission  is  through  the  male  rather 
than  the  female  members  of  the  family.  In  the  female  the  disease  is 
almost  always  inherited.  It  is  more  common  in  the  white  than  in  the 
colored  race.  It  usually  makes  its  appearance  during  the  fourth  decade, 
and  then  continues  more  or  less  through  the  remainder  of  life;  it  may 
however,  develop  later,  and  rarely  earlier,  sometimes  during  the  second, 
and  even  the  first  decade.  Continued  overindulgence  in  alcoholic  bever- 
ages is  an  important  etiological  factor,  fermented  liquors,  such  as  beer, 
ale,  and  porter,  and  wines,  such  as  sherry,  port,  and  champagne,  being 
much  more  injurious  than  distilled  liquors,  such  as  whiskey,  brandy,  gin, 
rum,  etc.  Something  more  than  the  mere- percentage  of  alcohol  seems  to 
be  of  significance.  Overeating  combined  with  insufficient  exercise 
strongly  conduce  to  gout;  and  it  is  more  the  mere  overeating  as  such, 
rather  than  the  special  kind  of  food  (such  as  red  meats,  for  instance, 
long  but  perhaps  erroneously  too  much  blamed),  that  does  the  harm. 
Gout  is  by  no  means  confined  to  the  wealthy  and  idle  class,  since  "in 
England  the  combination  of  poor  food,  defective  hygiene,  and  an  exces- 
sive consumption  of  malt  liquors  makes  'the  poor  man's  gout'  a  common 
affection"  (Osier).  Chronic  lead  poisoning  is  also  an  important  etiolog- 
ical factor,  though  less  so  in  this  country  than  in  England;  how  it  acts, 
whether  by  causing  arteriosclerosis,  l)y  lessening  the  alkalinity  of  the 
blood  (most  saturnine  patients  seem  to  have  an  excess  of  uric  acid  in  their 
blood),  or  by  provoking  trophic  changes  through  the  medium  of  the 
nervous  system,  is  not  definitely  known. 

Despite  considerable  patient  inquiry  and  investigation,  the  ultimate 
factor  in  the  disorder  of  metabolism  provoking  the  gouty  manifestations 
has  not  yet  been  definitely  determined.     It  is  generally  conceded  that 


GOUT  321 

gout  results  from  faulty  metabolism  (largely  defective  oxidation)  of  the 
nitrogenous  foodstuffs  and  of  the  nitrogenous  products  of  tissue  waste, 
and  that,  in  some  way  or  other  disturbances  in  the  formation  or  elimi- 
nation (or  both)  of  uric  acid  is,  directly  or  indirectly,  in  large  part  at 
least,  the  proximal  causative  factor.  Uric  acid  (CjH^N^Og),  as  well  as 
othei-  nitrogenous  compounds,  xanthin,  hypoxanthin,  adenin,  and  guanin, 
are  derived  from  the  nuclei  of  the  leukocytes  and  other  cells  of  the  body 
(endogenous  purin  bodies)  and  from  the  nuclei  of  ingested  food  (exo- 
genous purin  bodies).  Closely  related  to  these  are  other  substances 
(containing  carbon,  hydrogen,  nitrogen,  and  oxygen  (?)),  known  as 
heteroxanthin,  paraxanthin,  episarkin,  carnin,  and  epiguanin.  Collec- 
tively, that  is,  including  uric  acid,  they  are  known  as  the  xanthin  bodies, 
the  nuclein  bodies  (because  of  their  derivation),  the  alloxuric  bodies 
(because  they  contain  an  alloxan  and  a  urea  nucleus),  and  the  purin 
bodies  (because  they  are  derived  from  or  may  be  prepared  synthetically 
from  purin,  CgH^Nj) ;  excluding  uric  acid,  they  are  known  as  the  xanthin, 
nuclein,  alloxuric,  or  purin  bases.  Their  derivation  may  be  thus  repre- 
sented graphically : 

Nuclein 


I  1 

Albumin  Nucleic  acid 

I 


I  I 

Phosphoric  acid  Mother  substance 

I 


Uric  acid  Xanthin  ,   nuclein,  alloxuric,  or  purin  bases 

How  uric  acid  circulates  in  the  blood  under  normal  conditions  is  not 
definitely  known.  It  is  said  to  form  three  groups  of  salts,  which,  with 
sodium  as  the  base,  are  as  follows:  (1)  Neutral  sodium  urate,  merely  a 
laboratory  compound;  (2)  acid  sodium  urate,  or  sodium  biurate,  which 
does  not  occur  physiologically,  though  this  is  the  form  in  which  the 
uric  acid  is  deposited  in  the  gouty  tophi;  and  (3)  sodium  quadriurate, 
which  is  loosely  combined,  readily  soluble,  and  the  form  in  which  Sir 
^^  illiam  Roberts  and  many  others  believe  the  uric  acid  circulates  in  the 
blood.  Minkowski  believes  that  the  uric  acid  circulates  in  combination 
with  the  purin  base,  nucleotin-phosphoric  acid.  In  health  an  adidt  of 
average  weight  on  a  mixed  diet  excretes  from  0.4  to  1  gram  of  uric 
acid,  approximating  0.7  gram  on  an  average;  and  the  ratio  of  uric  acid 
to  urea,  though  it  varies  much,  averages  from  1  to  50  to  1  to  70. 

In  gout,  according  to  Minkowski:  (1)  The  daily  excretion  of  uric  acid 
in  the  intervals  between  the  acute  attacks  ranges  within  the  same  limits 
as  does  the  excretion  in  healthy  individuals;  (2j  in  chronic  gout,  even 
in  those  cases  in  which  there  is  marked  deposition  of  biurates  in  the 
tissues,  a  constant  variation  from  the  normal  amount  of  uric  acid 
excretion  in  any  one  direction  has  not  been  definitely  proved;  and  (3) 
immediately  preceding  an  acute  attack  there  is  regularly  a  diminution  in 
21 


322  DISORDERS  OF  METABOLISM 

the  amount  of  uric  acid  eliminated  in  the  urine,  whereas  during  and  after 
the  attack  the  uric  acid  output  is  increased.  Futcher  disagrees  with 
these  statements  in  having  found  almost  always  a  marked  diminution  in 
the  uric  acid  excretion  in  the  intervals  between  acute  attacks  in  chronic 
tophaceous  gout.  The  blood  in  gout  contains  a  marked  excess  of  uric 
acid,  and  although  there  has  been  and  still  is  much  discussion  as  to 
whether  this  is  due  to  increased  formation,  diminished  destruction  or 
oxidation,  or  diminished  excretion  by  the  kidneys,  the  weight  of  opinion 
recently  tends  to  support  the  view  that  it  is  due  to  deficient  excretion  by 
the  kidneys,  and  this  in  turn  has  been  attributed  to  "functional"  dis- 
turbances independent  of  apparent  organic  disease,  to  the  nephritic 
lesions  so  common  in  gout,  and  by  Minkowski  and  His  to  the  circum- 
stance (not  proved)  that  the  uric  acid  in  gout  may  circulate  in  combina- 
tion different  from  that  of  health  and  more  difficult  of  elimination  by  the 
kidneys. 

Heretofore  too  little  attention  has  been  paid  to  the  excretion  of  the 
purin  bases  in  gout.  Since  it  has  been  shown  that  normally  about  nine- 
tenths  of  the  purin  bodies  eliminated  is  uric  acid,  and  about  one-tenth 
the  purin  bases,  and  since  there  is  no  evidence  that  this  relationship  is 
disturbed  in  gout,  it  is  not  unlikely,  as  maintained  by  Kolish,  that  at 
least  certain  of  the  gouty  phenomena  may  be  due  to  these  purin  bases. 
As  regards  the  phosphoric  acid  elimination,  Futcher  has  shown  that  in 
the  intervals  between  the  attacks  in  chronic  gout  it  falls  far  below  the 
lower  limits  for  the  normal,  and  that  with  the  onset  of  the  acute  attack, 
concurrently  with  the  increase  in  the  uric  acid  elimination,  there  is  a 
parallel  rise  of  the  phosphoric  acid  elimination  to  the  average  or  even  to 
the  upper  limits  for  the  normal.  Others,  however,  have  obtained  some- 
what divergent  results. 

Pathology. — In  addition  to  a  marked  increase  of  the  uric  acid  in  the 
blood,  a  constant  feature  of  the  disease  first  pointed  out  by  Garrod,  the 
joints  present  the  most  characteristic  lesions  of  the  disease — the  deposi- 
tion of  crystalline  sodium  biurate  in  the  cartilages,  synovial  membranes, 
tendons,  ligaments,  and  bursse.  The  metatarsal-phalangeal  joint  of  the 
great  toe  is  most  frequently  involved,  and  the  lesions  may  remain  confined 
to  this  joint  for  a  long  time;  later,  however,  the  metatarsal,  the  ankle,  the 
small  joints  of  the  hands  and  fingers,  and  the  knee  and  the  wrist  may 
become  involved,  but  sometimes  the  lesions  aft'ect  only  the  lower  extremi- 
ties. Similar  deposits  occur  also  in  the  helix  of  the  ear,  as  well  as  in  the 
cartilages  of  the  nose,  eyelids,  and  larynx ;  they  have  been  observed  in  the 
periosteum  (over  the  sacrum  and  elsewhere),  and  in  the  tendons  (the 
tendons  of  the  hand  and  forearm,  Achilles  tendon,  plantar  surface  of  the 
foot,  etc.).  The  deposits  of  sodium  biurate  occur  in,  rather  than  on, 
the  surface  of  cartilage,  being  always  covered  by  a  thin  layer  of  carti- 
lage, through  which  they  present  as  white,  "chalky"  deposits,  or  tophi. 
Wliether  there  is  a  primary  tissue  necrosis  with  a  secondary  deposition  of 
the  sodium  biurate,  as  maintained  by  Ebstein,  or  vice  versa,  as  maintained 
by  His  and  Mordhorst,  has  not  been  definitely  determined.     Ebsteju 


GOUT  323 

maintains  that  the  tissue  necroses  are  always  primary,  that  he  has  found 
them  without  any  uratic  deposits,  and  that  they  are  acid  in  reaction — 
whence  the  ready  deposition  of  the  soluble  and  loosely  combined  quadri- 
urate  as  the  insoluble  crystalline  biurate.  Sir  William  Roberts  believes 
that  the  deposits  occur  especially  in  the  cartilages,  because  in  them  the 
nutritional  currents  are  slowest  and  least  abundant,  the  temperature 
lowest,  and  in  the  articulating  surfaces  the  percentage  of  sodium  chloride 
highest.  As  the  disease  advances  the  periarticular  tissues  (ligaments 
and  fibrous  tissues)  become  invaded,  and  often  large  tophi  or  "chalk 
stones"  are  formed,  which,  together  with  the  fibrous  thickenings,  lead  to 
fixation  and  much  distortion  of  the  joints.  Though  usually  covered  by 
skin,  the  tophi  may  cause  ulceration  of  overlying  structures,  and  small, 
nodular,  "chalky"  masses  may  be  discharged  externally.  True  bony 
outgrowths  are  found  about  the  margins  of  certain  joints  in  far  advanced 
cases. 

The  kidneys  show  the  changes  of  chronic  interstitial  nephritis  (the 
gouty  kidney)  or  sometimes  the  type  described  as  the  arteriosclerotic 
kidney.  Whitish  streaks,  evidences  of  deposits  of  sodium  biurate,  may  be 
found  in  the  papillae,  and  in  and  between  the  uriniferous  tubules.  Gen- 
eral arteriosclerosis  is  common;  indeed,  gout  is  one  of  the  most  frequent 
causes  of  arteriosclerosis.  Hypertrophy  of  the  left  ventricle  is  a  usual 
concomitant.  Not  infrequently  myocardial  degeneration  leading  to 
dilatation  of  the  heart  follows,  and  is  quite  often  associated  with  unusual 
atheroma  of  the  arch  of  the  aorta  and  the  orifices  of  the  coronary  arteries. 
Deposits  of  sodium  biurate  have  been  found  in  the  heart  valves.  Gouty 
pericarditis  sometimes  occurs  toward  the  close  of  life,  and  may  be  the 
direct  cause  of  death.  Emphysema  of  the  lungs  is  common,  and  chronic 
bronchitis  and  asthma  may  supervene.  Crystals  of  sodium  biurate  may 
be  found  in  the  sputum.  Neusser's  perinuclear  basophilic  granules  are 
now  known  to  be  artefacts.  Despite  the  chronic  course  of  the  disease,  no 
noteworthy  anemia,  as  a  rule,  develops. 

Symptoms. — Three  varieties  of  gout  are  usually  distinguished,  acute 
gout,  chronic  gout,  and  irregular  gout. 

Acute  Gout. — Acute  gout  may  be  abrupt  on  onset,  but,  as  a  rule,  it 
is  preceded  for  several  days,  or  at  least  a  few  hours,  by  vague  pains  in  the 
joints  or  muscles,  irritability  of  temper,  mental  depression,  insomnia, 
dyspepsia,  and  scantiness  of  urine  (containing  a  deficiency  of  uric  acid). 
Occasionally,  however,  such  prodromal  manifestations  are  absent.  The 
attack  usually  begins  abruptly  in  the  early  morning  hours,  the  patient 
being  awakened  by  a  sharp  excruciating  pain  in  the  ball  of  the  great  toe. 
The  joint  swells  rapidly,  and  becomes  red,  hot,  extremely  tender,  and  the 
surrounding  skin  oedematous  and  shiny.  Fever,  102°  to  108°  F.,  usually, 
but  not  always,  accompanies  the  attack.  As  the  morning  Avears  on  the 
symptoms  abate,  and  the  patient  may  become  tolerably  comfortable; 
but  the  morning  of  the  succeeding  day,  usually  of  each  succeeding  day 
for  a  week  or  tlierea!)outs,  witnesses  a  recurrence  of  the  severe  symptoms, 
which,  however,  progressively  diminish  in  intensity.    Just  prior  to  and 


324  DISORDERS  OF  METABOLISM 

during  the  early  part  of  the  attack  the  uric  acid  output  is  diminished, 
but  later  and  for  a  short  time  after  the  attack  it  becomes  increased.  In 
addition,  the  urine  is  scanty,  acid  in  reaction,  of  increased  specific  gravity, 
and  heightened  color,  and  it  may  contain  a  trace  of  albumin  or  of 
sugar  (transitory).  Following  the  subsidence  of  the  acute  manifestations, 
the  patient  soon  regains  his  former  health — indeed,  he  may  feel  much 
improved.  The  affected  joint  soon  returns  to  its  normal  condition, 
except  in  cases  of  chronic  gout,  in  which  deformity  sooner  or  later  ensues. 
The  acute  attack  does  not  always  involve  the  great  toes;  occasionally 
other  joints,  such  as  the  wrist,  knee,  or  the  small  joints  of  the  fingers  may 
suffer;  and  the  lesions  are  not  always  confined  to  a  single  joint,  both 
great  toes,  for  instance,  being  occasionally  affected.  The  attacks  recur 
at  varying  intervals —  weeks,  months,  or  even  years — but  with  the  lapse  of 
time  the  intervals,  as  a  rule,  become  progressively  less,  and  the  patient 
gradually  develops  chronic  gout. 

Occasionally  the  local  manifestations  of  gout  disappear  or  improve 
rapidly,  and  concurrently  herewith  serious  symptoms  referable  to  the 
internal  organs  develop — a  condition  to  which  the  term  retrocedent  or 
suppressed  gout  is  applied.  The  symptoms  may  be  gastro-intestinal — 
abdominal  -pain,  vomiting,  diarrhea,  with  weakness,  faintness,  and  a 
rapid,  feeble  pulse,  progressing  occasionally  to  death;  or  they  may  be 
cardiac — precordial  pain,  dyspnea,  and  palpitation  (doubtless  in  some 
cases  true  angina  pectoris) ;  or  they  may  be  cerebral — mental  excitement 
or  depression,  apoplexy,  delirium,  or  coma — in  many  cases  probably 
uremic. 

Chronic  Gout. — In  consequence  of  repeated  attacks  of  acute  gout, 
commonly  with  gradually  decreasing  intervals,  the  symptoms,  though 
less  acute,  become  more  continuous.  Urates  become  deposited  in  the 
articular  cartilages,  later  in  and  about  the  ligaments  and  periarticular 
fibrous  tissues;  these  tophi,  which  often  become  extreme,  together  w^ith 
fibrous  thickenings,  occasion  fixation  and  marked  swelling  and  deformity 
of  the  joints.  Usually  the  feet  are  first  involved;  later  the  hands,  fingers, 
wrists,  knees,  etc.,  may  show  most  extensive  changes.  As  already 
observed,  the  tophi  may  ulcerate  through  the  skin,  and  chalky  deposits 
may  be  exposed  or  even  discharged  externally.  Similar  deposits  are 
found  in  the  cartilages  of  the  ear,  and  elsewhere  in  the  tendinous  and 
fibrous  tissues  throughout  the  body.  The  patient  is  usually  dyspeptic. 
Gradually  arteriosclerosis  develops,  and  the  patient  presents  the  com- 
mon cardiac  and  vascular  manifestations  of  this  condition.  Soon  also 
the  evidences  of  chronic  interstitial  nephritis  present  themselves:  the 
urine  increases  in  amount,  is  of  low  specific  gravity,  and  contains  a  slight 
amount  of  albumin  and  a  few  hyaline  casts.  Aside  from  the  incapacities 
attendant  upon  the  joint  deformities,  the  patients  often  exhibit  unusual 
physical  and  bodily  vigor  for  a  long  time.  The  chronic  course  of  the  dis- 
ease is  sometimes  interrupted  by  acute  exacerbations  of  unusual  severity. 
The  final  end  is  not  infrequendy  determined  by  inflammations  of  any  of 
the  serous  membranes,  or  by  uremia. 


GOUT  325 

Irregular  Gout. — Irregular  gout  is  a  term  applied  to  an  ill-assorted 
group  of  symptoms  that  are  found  in  persons  who  once  have  had  gout, 
or  who,  though  they  may  never  have  suffered  from  gout,  yet  are  pre- 
disposed by  heredity  or  other  factors  to  its  development:  a  condition  to 
which  the  term  gouty  diathesis  or  lithemia  is  often  applied,  but  which 
more  than  anything  else  represents  a  hodge-podge  of  diagnostic  errors. 
Thus,  there  may  be  manifestations  of  catarrh  of  the  gastro-intestinal 
tract,  and  the  gouty  stomach,  the  torpid  liver,  and  biliousness  are  favorite 
ailments  of  certain  physicians  skilled  in  their  treatment.  In  other  cases 
the  urine  is  lessened  in  amount,  high  colored,  and  uric  acid  crystallizes 
out  on  standing — a  circumstance  to  which  undue  importance  has  been 
attributed.  Other  disorders  ascribed  to  the  same  condition  comprise 
eczema,  headaches,  paresthesias,  itching  of  the  palms  of  the  hands  and 
the  soles  of  the  feet,  cramps  in  the  legs,  itching  eyeballs,  conjunctivitis, 
iritis,  retinitis,  tonsillitis,  etc. 

Diagnosis. — Typical  acute  gout  can  scarcely  be  mistaken  for  anything 
else.  In  at\'pical  cases,  as,  for  instance,  when  the  feet  are  not  involved, 
or  when  there  is  polyarthritis,  the  differentiation  from  rheumatic  fever 
may  be  determined  by  a  tophus  in  the  ear,  but  the  mode  of  life,  the 
occupation,  hereditary  factors,  the  absence  of  fever,'  and  the  condition 
of  the  urine  may  be  of  contributing  diagnostic  importance.  Systematic 
search  for  tophi  in  all  cases  would  prevent  many  diagnostic  blunders,  but 
small  fibroid  nodules,  Woolner's  tip,  or  small  sebaceous  cysts  should  not 
be  mistaken  for  them.  Difficulty  may  sometimes  be  experienced  in 
separating  arthritis  deformans,  but  the  antecedent  family  and  personal 
history  and  the  habits  of  the  patient,  together  with  the  absence  of  chalky 
deposits,  serve  to  distinguish  the  one  from  the  other  disease. 

Prognosis. — ^The  likelihood  of  permanent  cure  is  not  encouraging,  but 
by  observing  proper  hygienic  and  dietetic  measures,  the  attacks  may 
be  rendered  infrequent  and  mild,  and  the  development  of  severe 
internal  lesions  may  be  postponed — whereby  the  gouty  subject  may  live 
the  allotted  time  of  man.  The  outlook,  however,  is  bad  when  gout 
develops  in  a  young  subject  under  thirty  years,  and  when  arteriosclerosis 
and  renal  changes  are  advanced. 

Treatment. — Attention  to  hygienic  regulations  is  important.  The 
patient  should  have  plenty  of  fresh  air;  he  should  exercise  regularly,  but 
not  too  violently  or  sufficiently  to  cause  exhaustion,  since  this  may  deter- 
mine an  attack  of  acute  gout,  besides  being  otherwise  objectionable.  He 
should  bathe  frecjuently — a  morning  cold  bath  or  an  evening  warm  bath, 
as  best  suits  the  individual  patient.  An  occasional  Turkish  bath,  as  well 
as  temporary  sojourns  at  certain  spas,  are  often  very  beneficial.  The 
patient  should  drink  freely  of  water — to  the  insistence  upon  which  the 
high  repute  of  certain  "cures"  is  largely  due.  The  drinking  of  the  water 
itself,  promoting  free  diuresis,  rather  than  its  alkaline  contents,  consti- 
tutes the  useful  part  of  the  treatment.  The  waters  that  enjoy  the  greatest 
vogue  are  Saratoga,  Bedford,  and  White  Sulphur,  in  this  country; 
Carlsbad,    Homburg,    Ems,    Kissingen,    in    Germany;    Aix-les-Bains, 


326  DISORDERS  OF  METABOLISM 

Contrexeville,  and  Vichy,  in  France;  and  Buxton  and  Bath,  in  England. 
Sir  William  Roberts  believes  that  the  alkalescence  of  these  waters  is 
without  influence  on  sodium  biurate,  and  that  the  sodium  salts  are 
especially  harmful;  but  since  the  drinking  of  large  quantities  of  water 
in  the  solitude  of  one's  room  is  a  weariness  to  the  flesh,  while  the  same 
process  at  the  spas  not  only  requires  considerable  pecuniary  outlay,  but 
also  promotes  a  healthy  state  of  the  mind,  largely  on  account  of  the 
"accessories,"  such  as  regulated  life,  restricted  diet,  controlled  exercise, 
baths,  etc.,  the  spas  will  continue  to  enjoy  a  well-merited  repute. 

Since  most  gouty  subjects  eat  too  much,  the  diet  must  be  restricted, 
but  the  matter  of  regulation  of  the  diet  is  entirely  individual.  In  general 
the  meats  should  be  reduced,  and  the  white  meats  should  be  preferred  to 
the  red,  though  the  red  meats  need  not  be  prohibited.  Milk  and  eggs 
are  usually  well  borne  and  may  be  given  in  large  amounts.  Green  vege- 
tables, such  as  lettuce,  spinach,  cauliflower,  Brussel  sprouts,  asparagus, 
etc.,  are  quite  permissible.  Though  opinions  differ  with  reference  to 
carbohydrates  and  fats,  they  may  be  given  in  moderate  amount.  Ebstein 
favors  the  use  of  considerable  butter,  even  in  obese  subjects,  stating  that 
not  only  do  they  improve  in  general  condition,  but  actually  lose  some  fat. 
Highly  seasoned  food,  pastry,  cheese,  hot  cakes  and  bread,  tea,  coffee,  as 
well  as  liver,  kidney,  brain,  sweetbread  (rich  in  nuclear  elements),  and 
beef  extracts  (rich  in  derivatives  of  the  xanthin  group)  must  be  prohibited. 
Sir  William  Roberts  advises  restriction  of  the  sodium  chloride  of  the 
food,  believing  that  it  favors  the  crystallization  out  of  sodium  biurate. 
In  general  alcohol  must  be  strictly  interdicted,  especially  the  fermented 
beverages,  such  as  beer,  porter,  ale,  sweet  and  sour  wines,  champagne, 
etc.  When  really  indicated,  a  small  amount  of  whiskey  or  brandy,  well 
diluted,  may  be  permitted. 

During  the  acute  attack  the  patient  should  remain  at  rest,  preferably 
in  bed,  and  the  diet  should  be  restricted  to  a  minimum  of  milk,  eggs, 
and  broths.  The  affected  member  should  be  enveloped  in  cotton  wool 
or  hot  fomentations,  or  a  30  to  50  per  cent,  ichthyol  ointment,  or  a 
saturated  solution  of  magnesium  sulphate,  and  then  elevated.  A  blue 
mass  pill  or  a  purgative  dose  of  calomel  should  be  administered  at  the 
outset.  Custom  sanctions  the  use  of  the  wine  or  the  tincture  of  colchi- 
cum  in  20  to  30  minim  (1.25  to  2.0  c.c.)  doses,  combined  with  potassium 
acetate  or  citrate,  30  to  60  grains  (2  to  4  grams),  every  four  hours,  imtil 
the  acute  symptoms  subside.  The  colchicum  should  be  stopped  imme- 
diately improvement  is  effected.  Colchicine,  y^-q-  grain  (0.0006  gram) 
or  more,  every  two  or  three  hours,  has  recently  been  recommended  as  a 
substitute  for  the  wine  or  the  tincture.  In  some  cases  morphine  may 
be  necessary  to  relieve  the  pain. 

In  the  subacute  and  irregular  forms  of  gout  the  salicylates  have 
long  enjoyed  a  widespread  reputation  and  undoubtedly  do  good  in 
many  cases.  In  chronic  cases,  in  addition  to  the  foregoing  measures, 
the  use  of  potassium  iodide,  piperazin,  guaiacum,  quinine,  and  the  bitter 
tonics,  is  sometimes  attended  by  good  results.  The  extract  of  thymus 
has  been  recommended. 


OBESITY  327 


OBESITY. 


Obesity  is  a  disorder  of  metabolism  characterized  by  the  excessive 
deposition  of  fat  in  the  tissues. 

Etiology. — Ordinary  obesity  is  more  common  in  women  (especially 
Hebrews)  than  in  men,  and  develops  usually  during  the  fifth  decade 
(at  or  about  the  time  of  the  menopause  in  women).  In  some  cases  there 
is  an  hereditary  predisposition,  in  which  event  the  obesity  may  develop 
during  infancy,  childhood,  adolescenc^e,  or  adult  life.  In  the  majority  of 
cases  the  disorder  is  due  directly  to  a  sedentary  life,  indolence,  deficient 
exercise,  overeating,  or  excessive  indulgence  in  alcohol;  but  especially 
to  these  combined.  Many  diseases  that  prevent  adequate  exercise,  such 
as  gout,  chronic  heart  or  lung  disease,  etc.,  or  interfere  with  oxidation, 
such  as  anemia,  etc.,  may  lead  indirectly  to  obesity. 

Pathology. — The  lesions  consist  in  excessive,  sometimes  enormous, 
deposition  of  fat,  not  only  in  regions  where  fat  is  found  normally,  as  the 
subcutaneous  tissues,  mesentery,  about  the  kidneys,  etc.,  but  also  in 
organs  normally  almost,  if  not  quite,  free  from  fat,  especially  the  heart, 
the  liver,  etc.  The  fatty  accumulation  results  from  imperfect  metabolism 
in  general — perhaps  lessened  vitality  of  the  cells  in  general  or  lessened 
requirement  for  food  to  form  sufficient  heat  and  energy.  The  fat  is 
derived  from  the  fat  and  the  carbohydrate  (starchs  and  sugars)  of  the 
food — that  amount  ingested  in  excess  of  the  body  needs  being  thus  stored 
up;  the  non-nitrogenous  moiety  of  the  proteins  imperfectly  oxidized  also 
goes  to  the  formation  of  fat. 

Symptoms. — The  obvious  manifestation  is  the  excessive  accumulation 
of  fat  in  general,  but  especially  in  the  chin,  the  back  of  the  neck,  the 
abdomen,  the  hips,  etc.  For  a  time,  at  least,  there  may  be  no  symptoms 
aside  from  those  due  directly  to  the  great  bulk  of  tissue,  and  inconve- 
nience in  moving  it  about  (walking,  etc.).  Sooner  or  later,  however, 
dyspna>a,  especially  on  exertion,  muscular  asthenia,  and  other  evidences 
of  embarrassed  cardiac  action  (pulmonary  congestion,  bronchitis, 
cyanosis,  oedema,  oliguria,  etc.)  develop,  and  the  physical  signs  of  fatty 
heart  may  be  elicited.  Digestion  may  become  impaired,  constipation  is 
common;  the  liver  is  often  enlarged;  amenorrhoea,  sterility,  and  other 
disorders  may  occur.  Arteriosclerosis,  gout,  diabetes,  etc.,  are  often 
associated,  and  there  is  a  special  predilection  to  secondary  infection 
(lessened  resistance  to  bacterial  infection). 

Diagnosis. — The  diagnosis  is  easy,  as  a  rule;  myxcrdema  should  be 
readily  excluded.  Other  types  of  fatty  accumulations  sometimes 
must  be  taken  into  consideration,  such  as,  (1)  Adiposis  dolorosa 
(Dercum),  a  disorder  most  common  in  middle  life,  in  which,  usually 
associated  with  more  or  less  general  obesity,  irregular,  symmetrical, 
painful,  fatty  masses,  1  to  3  or  4  inches  in  diameter  (symmetrical  lipo- 
matosis), develop  on  the  trunk  and  extremities  (but  not  (he  hands, 
feet,    or    face).      Pain    may   precede    the    development    of    the    fatty 


328  DISORDERS   OF  METABOLISM 

masses;  and  there  may  be  paresthesias,  anesthesias,  and  h\-peresthe- 
sias.  Asthenia,  mental  apathy,  and  psychoses  may  ensue.  The 
disease  is  progressive,  though  of  long  duration,  and  not  especially 
amenable  to  treatment.  (2)  Adiposis  tuberosa  simplex  (Anders),  a 
disorder  resembling  adiposis  dolorosa,  characterized  by  the  develop- 
ment in  the  abdominal  fat  of  fatty  growths,  sometimes  painful  to 
pressure.  Unlike  adiposis  dolorosa,  they  are  amenable  to  the  ordinary 
dietetic  regulations  of  obesity  in  general.  (3)  Adiposis  cerebralis 
(dystrophia  adiposo  genitalis,  Frohlich),  a  condition  of  marked  obesity 
developing  in  the  course  of  tumor 'of  the  brain  (especially  the  pituitary 
body,  pineal  gland),  and  associated  with  defective  development  of  the 
genital  organs.  (4)  Multiple  lipomatosis — multiple  symmetrical  fatty 
tumors  occurring  in  association  with  divers  diseases  of  the  nervous 
system  (tabes,  general  paresis,  etc.).  (o)  Symmetrical  adenolipomatosis 
(MacCormac),  a  condition  characterized  by  the  development  of  fatty 
growths  (containing  sclerosed  lymph  nodes)  in  the  neck,  axilla,  etc.,  and 
often  associated  with  asthenia,  emaciation,  rapid  pulse,  enlarged  spleen, 
etc.  The  nature  of  these  disorders  is  not  well  understood.  The  lesions 
found  have  consisted  of  interstitial  neuritis  in  the  fatty  masses,  atrophy 
and  compensatory  hyperplasia  of  the  thyroid,  tumors  of  the  pituitary, 
lymphoid  hyperplasia,  h\-poplasia  or  retrogression  of  the  sexual  organs, 
and  divers  diseases  of  the  central  nervous  system.  Perhaps  the  cases 
are  much  related  (disorders  of  internal  secretion). 

Prognosis. — The  prognosis  depends  upon  the  nature  of  the  under- 
Iving  factors  and  the  amenability  of  the  subject  to  dietetic  and  other 
regulations. 

Treatment. — ^The  essence  of  successful  treatment  consists  in  bringing 
the  diet  within  the  requirements  of  the  body  as  regards  heat  and  energy, 
and  in  promoting  oxidation  and  the  destruction  of  fat  by  carefully  regu- 
lated and  graduated  exercise,  massage,  and  bath.s — all  of  which  must 
be  carefully  supervised  on  account  of  the  frecjuency  of  associated  cardiac 
weakness.  There  are  several  systems  of  dietetic  regulation,  of  which 
the  best  known  are  Ebstein's,  Oertel's,  von  Xoorden's,  and  Banting's 
(for  details  of  which  one  may  refer  to  special  treatises).  In  general, 
however,  the  amount  of  food  should  be  reduced,  especially  the  starches 
and  sugars;  the  fluid  intake  should  be  greatly  restricted,  and  the  small 
amount  (2  to  3  pints  daily)  allowed  should  be  taken  preferably  two 
hours  after  meals  than  with  food;  alcohol  should  be  prohibited  in  most 
cases.  Care  should  be  taken  to  see  that  the  nitrogen  output  does  not 
exceed  the  intake,  since  this  (destruction  of  the  body  protein)  is  answer- 
able for  most  of  the  weakness  that  attends  many  "cures."  Medicinal 
treatment  is  of  secondary  importance;  a  weak  heart  sometimes  has  to 
be  stimulated,  general  weakness  suggests  the  use  of  tonics,  anemia 
requires  the  use  of  iron,  etc.  Thyroid  extract  is  sometimes  of  service, 
but  it  must  be  employed  with  caution,  since  it  leads  to  breaking  down  of 
the  body  protein  as  well  as  fat,  and  may  induce  thyroidism  in  those  ill 
able  to  withstand  its  effects. 


RICKETS  329 

RICKETS. 

(Rachitis.) 

Rickets  is  a  disease  of  infancy  characterized  by  defective  calcification 
of  the  growing  bones  and  general  disturbances  of  nutrition. 

Etiology. — Rickets  occurs  in  the  great  majority  of  cases  before  the 
end  of  the  second  year  of  life;  it  is  uncommon  before  the  sixth  month, 
although  cases  in  the  newborn  have  been  described  (more  likely  achon- 
droplasia); it  is  said  rarely  to  develop  about  the  time  of  puberty, 
rachitis  tarda  (rather  osteomalacia  of  puberty).  It  is  almost  limited  to 
the  children  of  the  poor  and  those  Avho  live  amidst  general  mihygienic 
conditions;  but  it  may  occur  under  the  best  hygienic  circumstances. 
Parental  syphilis  or  tuberculosis,  poor  nutrition  of  the  mother,  and 
rapidly  succeeding  pregnancies,  may  be  etiological  factors.  A  faulty 
is  diet  the  prime  causative  factor,  whence  the  disease  occurs  in  children 
fed  on  condensed  milk,  cow's  milk,  and  proprietary  foods,  as  well  as  in 
those  nursed  by  the  mother  too  long  or  when  she  has  again  become  preg- 
nant. Excess  of  carbohydrates  (deficiency  of  fats  and  animal  proteins) 
is  believed  to  be  the  important  factor. 

Pathology. — The  chief  lesions  occur  in  the  bones,  and  consist  of  hyper- 
emia of  the  cartilage,  bone  marrow,  periosteum,  and  bony  tissue  itself — 
which  results  in  abnormal  development  of  the  growing  bone,  as  well  as 
changes  in  the  bone  already  formed.  In  the  long  bones,  ossification 
of  the  cartilage  at  the  junction  of  the  epiphysis  and  diaphysis  is  delayed 
and  irregular;  the  outer,  bluish,  proliferative  cartilaginous  area  exhibits 
irregular  multiplication  of  the  cells  and  a  soft  fibroid  matrix  invaded  by 
bloodvessels;  the  inner  yellowish  ossifying  layer  becomes  irregularly 
thickened  and  shows  imperfectly  calcified  areas;  the  two  layers  are  no 
longer  sharply  defined,  but  gradually  merge.  The  osteoblastic  layer  of 
the  periosteum  of  the  shaft  of  the  bone  becomes  thickened  and  nodular, 
the  medullary  cavity,  continuously  enlarging,  results  in  lessening  of  the 
thickness  of  the  osseous  shaft.  In  consequence,  then,  of  delayed  and 
irregular  ossification  (less  than  one-half  of  the  normal  amount  of  lime 
salts  may  be  present)  the  ends  of  the  long  bones  are  softened  and  nodu- 
larly  enlarged  and  the  shafts  irregularly  thickened — whence  they  readily 
become  bent,  distorted,  or  fractured.  Ultimately  they  become  ossified 
and  hard,  but  tiiey  are  likely  to  remain  deformed.  The  liver,  spleen,  and 
mesenteric  lymph  nodes  may  become  enlarged.  The  nature  of  the  pro- 
cess is  not  well  understood;  it  is  not  due  to  deficiency  of  lime  salts  in 
the  food,  nor  to  bacterial  infection. 

Symptoms. — The  onset  of  the  disease  is  insidious.  The  early  symp- 
toms, which  usually  develop  about  the  time  of  dentition,  consist,  as  a 
rule,  of  general  disturbances  rather  than  obtrusive  changes  in  the  bones, 
so  that,  especially  among  the  well-to-do,  the  disease  may  be  overlooked 
for  some  time.  The  child  is  nervous,  restless,  irritable,  sleeps  poorly, 
and   may  have  attacks  of  fever;  he  cries  when  touched,  seems  to  be 


330  DISORDERS  OF  METABOLISM 

generally  hyperesthetic  (bony  prominences  and  soft  parts),  and  throws 
off  the  bedclothes;  he  does  not  thrive,  he  sweats  considerably,  espe- 
cially about  the  head  and  neck  when  asleep;  dentition  is  delayed  or 
irregular;  the  development  of  the  speech  function  is  retarded;  gastro- 
intestinal disturbances,  such  as  poor  appetite,  vomiting,  flatulence,  and 
diarrhoea,  are  common;  emaciation  and  anemia  supervene,  the  muscu- 
lature becomes  soft  and  flabl)y,  and  the  child  is  unable  to  sit  erect  or 
walk. 

In  the  course  of  time  characteristic  changes  appear  in  the  bones.  The 
skull  is  relatively  large,  the  sutures  and  the  fontanelles  remain  unclosed 
(even  in  the  third  and  fourth  years),  and  the  forehead  is  high,  wide,  and 
prominent;  in  young  infants  the  bones  are  soft  and  thin  (craniotabes) 
and  yield  readily  to  pressure.  A  systolic  murmur  may  be  audible  over 
the  open  anterior  fontanelle.  The  costochondral  junctions  being  swollen 
occasion  the  characteristic  bending  of  the  ribs  (rachitic  rosary),  which 
usually  disappears  by  the  fourth  to  the  sixth  year;  atmospheric  pressure 
on  the  softened  ribs  (especially  if  associated  with  difficulty  in  breathing) 
may  give  rise  to  a  groove  along  the  costochondral  junction,  which  when 
associated  with  a  prominent  sternum  gives  rise  to  the  so-called  pigeon 
breast  or  chicken  breast  or  keel-shaped  thorax;  there  may  also  be  a 
groove  (Harrison's)  along  the  attachment  of  the  diaphragm.  The  lower 
ends  of  the  radius  and  ulna  (junction  of  the  epiphysis  and  diaphysis) 
become  thickened,  enlarged,  and  deformed.  Similar  changes  may  occur 
in  the  clavicle,  the  tibia  (especially  the  lower  end),  and  the  other  bones 
of  the  arms  and  legs,  in  the  vertebrae  (kyphosis,  scoliosis,  lordosis),  and  in 
the  pelvis  (rickety  pelvis;  subsequent  difficulties  in  parturition).  The 
changes  in  the  bones  of  the  legs  (occasioning  pain)  and  the  associated 
muscular  weakness  lead  to  delay  in  walking,  and  may  simulate  paralysis 
(pseudoparalysis  of  rickets);  if  the  child  does  walk,  bow-leg  or  knock- 
knee  is  an  almost  inevitable  result.  Greenstick  fractures  of  the  long- 
bones  are  common. 

In  addition,  rickety  children  are  often  the  subject  of  night  terrors 
(pavor  nocturnus),  convulsions,  tetany,  laryngismus  stridulus,  enuresis, 
etc.  The  liver  and  spleen  are  often  enlarged — which  together  with  the 
marked  intestinal  disturbance  (flatulence  and  muscular  atony)  gives 
rise  to  the  characteristic  "pot-belly."  Bronchopneumonia  and  other 
pulmonary  complications  are  common. 

Diagnosis. — The  characteristic  changes  in  the  bones  make  the  diagnosis 
easy;  but  special  efforts  should  be  made  to  recognize  the  disease  early: 
open  fontanelle,  craniotabes,  head  sweating,  throwing  oft'  of  the  bed- 
clothes, delayed  dentition,  and  crying  when  touched,  are  important 
diagnostically.  Infantile  scurvy  (misnamed  acute  rickets)  may  be 
excluded  by  the  aforementioned  signs  and  symptoms,  especially  the 
changes  in  the  cranium,  and  by  the  absence  of  the  characteristic  scorbutic 
changes  in  the  gums  and  the  bones  of  the  legs.  S}-philis  may  be  excluded 
by  the  absence  of  other,  especially  cutaneous  and  mucous  membrane, 
evidences  of  svphilis,  and  should  the  epiphysis  l^e  involved,  by  the  absence 


SCURVY  331 

of  tender,  painful  doughy  swellings,  and  perhaps  dissociation  of  the 
epiphyses  and  diaphyses. 

Prognosis. — The  disease  is  chronic  in  course,  but  tends  to  spontaneous 
recovery  within  a  year  or  more;  under  proper  treatment  cure  may  be 
effected  within  several  months.  Deaths  are  usually  due  to  complications, 
especially  secondary  infections. 

Treatment. — The  best  hygienic  conditions  should  be  procured — fresh 
air,  sunlight,  suitable  clothing,  frequent  bathing,  cool  breezes,  low 
temperature  during  the  summer,  etc.  If  the  child  is  young,  and  the 
mother  cannot  satisfactorily  nurse  it,  or  if  she  is  ill  or  pregnant,  a  wet 
nurse  may  be  procured.  Otherwise  proper  attention  nmst  be  paid  to 
the  diet;  cow's  milk  properly  modified  to  suit  the  age  and  digestive 
abilities  of  the  child  is  the  best;  barley  water,  oatmeal  gruel,  albumin 
water,  and  beef  juice  may  be  added.  Phosphorus  is  the  best  remedy;  it 
leads  to  calcium  retention  in  rachitis,  and  exerts  a  specific  effect  on 
rachitic  bones,  increasing  their  calcium  content;  j-Jq^  grain  (0.0006 
gram)  thrice  daily  may  be  given  in  olive  oil  or  cod-liver  oil;  and  cod-liver 
oil  may  be  rubbed  into  the  skin.  The  hypophosphites,  arsenic,  syrup  of 
iron  iodide,  and  other  iron  preparations  also  are  of  service,  especially  in 
anemic  cases.  The  child  should  not  be  allowed  to  walk  until  the  con- 
dition is  cured. 

SCURVY. 

(Scorbutus.) 

Scurvy  is  a  chronic  disorder  of  nutrition  associated  with  dietetic  errors 
(deprivation  of  fresh  food),  and  characterized  by  weakness,  anemia, 
spongy  gums,  and  hemorrhages. 

Etiology. — Formerly  the  disease  was  prevalent  among  sailors,  soldiers, 
miners,  prisoners,  and  others  deprived  for  a  long  time  of  fresh  food; 
at  present  it  is  rare,  but  occasionally  seen  in  seaports,  in  famine-stricken 
districts,  and  among  the  poor.  Epidemics  have  been  observed.  Un- 
hygienic conditions,  debilitating  influences,  exposure  to  wet  and  cold 
are  believed  to  be  predisposing  factors;  but  the  chief  factor  is  in  some 
way  connected  with  the  prolonged  lack  of  fresh  food,  especially  of  fresh 
meat  and  vegetables;  that  is,  it  follows  a  diet  consisting  largely  of  dried 
or  salt  meat,  dried  vegetables,  cereals,  etc.  Infantile  scurvy  (Barlow's 
disease,  incorrectly  called  acute  rickets)  occurs  among  the  well-to-do 
as  well  as  among  the  poor,  but  in  artificially  fed  infants,  those  fed  on 
condensed  milk,  sterilized  milk,  proprietary  food,  etc.  The  ultimate 
etiological  factor  has  not  been  determined;  it  is  believed  to  be  due  to 
deficiency  of  potassium  salts,  especially  the  citrate,  but  also  the  tartrate 
and  maltate  (Buzzard);  and  to  diminished  alkalinity  of  the  blood  from 
an  insufficient  supply  of  vegetable  salts  (llolfe).  Recently  Wright  has 
contended  that  the  condition  is  an  acid  intoxication  due  to  an  excess 
of  foodstuffs  yielding  an  acid  ash  after  incineration.  These,  which  he 
calls  scorbutic,  are  oats,  barley,  fresh  meats,  salt  meats,  ship  biscuit, 
wheat,  eggs,  rice,  maize,  peas,  and  beans;  the  neutral  or  non-scorbutic 


332  DISORDERS  OF  METABOLISM 

foodstuffs  comprise  sugar,  vegetable  oils,  and  animal  fat;  and  the 
alkaline  or  antiscorbutic  foodstuffs  comprise  carrots,  turnips,  potatoes, 
onions,  milk,  blood  or  meat  containing  blood,  lime  juice,  orange  juice, 
wood,  and  green  herbage.  Hoist  contends  that  the  disease  is  not  an  acid 
intoxication,  but  is  due  to  the  lack  in  the  food  of  some  unidentified  but 
easily  decomposable  constituents  (perhaps  of  the  nature  of  an  enzyme) 
— present  in  antiscorbutic  foods,  but  lacking  in  cereals  (flour,  grains), 
because  they  are  dry. 

Pathology. — The  chief  lesions  are  hemorrhagic  in  nature:  ecchymoses 
in  and  beneath  the  skin  and  mucous  (sometimes  also  the  serous)  mem- 
branes ;  larger  intermuscular  and  sometimes  intra-articular  hemorrhages ; 
subperiosteal  hemorrhages  (most  common  about  the  femur,  but  also 
elsewhere,  as  beneath  the  alveolar  periosteum,  etc.);  and  hemorrhages 
into  the  epiphyseo-diaphyseal  junction  of  the  long  bones,  associated  with 
the  deposition  of  fibrillated  or  reticular  tissue  which  may  soften  and  lead 
to  separation  of  the  epiphyses  and  diaphyses  (which,  however,  may  be 
retained  in  position  by  the  periosteum).  There  may  be  some  absorption 
of  lime  salts  or  decalcification  (acidosis)  and  consequent  fragility  and 
ready  fracturing.  The  gums  become  swollen,  spongy,  hemorrhagic,  and 
sometimes  ulcerated,  and  the  teeth  may  become  loosened.  Ulcerations 
may  develop  in  the  ileum  and  colon.  The  spleen  may  be  enlarged  and 
the  liver,  kidneys,  and  heart  reveal  the  usual  results  of  marked  anemia 
(parenchymatous  and  fatty  degeneration). 

Symptoms. — The  onset  is  insidious,  the  early  symptoms  consisting 
usually  of  general  ill  health,  weakness,  anemia,  and  loss  of  flesh.  The 
hemorrhagic  manifestations  usually  begin  in  the  gums,  which  (often 
first  about  the  canine  teeth)  become  soft,  swollen,  spongy,  hemorrhagic, 
and  perhaps  ulcerated;  the  teeth  may  fall  out;  the  breath  is  very  offen- 
sive, and  the  adjacent  lymph  nodes  become  swollen.  Petechise  and 
ecchymoses  develop  in  and  beneath  the  skin,  especially  of  the  legs; 
larger  hemorrhages  may  develop  in  and  between  the  muscles,  especially 
of  the  calves,  thighs,  buttocks,  abdominal  wall,  shoulder,  etc.  (scurvy 
induration  or  sclerosis);  or  beneath  the  periosteum,  especially  of  the 
femur  (painful  nodular  protuberances).  Epistaxis,  gastro-intestinal 
hemorrhage,  hematuria,  and  other  mucous  membrane  bleedings,  and 
serous  membrane  hemorrhages  (especially  into  the  larger  joints)  may 
occur;  parenchymatous  (visceral)  hemorrhages  are  rare.  The  hemor- 
rhagic effusions,  as  a  rule,  become  absorbed,  but  may  break  down  into 
foul  ulcerations.  There  may  be  erythematous,  urticarial,  and  other  skin 
eruptions.  Cardiovascular  and  pulmonary  symptoms  of  anemia  (dysp- 
noea, palpitation  of  the  heart,  oedema,  etc.);  headache,  mental  depres- 
sion and  apathy,  or  delirium,  etc.,  may  supervene.  The  total  acidity  of 
the  gastric  juice  is  usually  lessened,  and  the  free  HCl  may  be  entirely 
absent.  Necrosis,  fracture,  epiphyseal  separation  of  the  bones  (femur, 
clavicle,  ribs)  may  occur.  Usually  there  is  constipation,  but  there  may 
be  diarrhoea  (scorbutic  dysentery).  The  temperature  is  usually  normal 
or  subnormal  (in  the  absence  of  complications). 


SCURVY  333 

Diagnosis. — The  diagnosis  is  easy  from  a  knowledge  of  the  etiological 
factors  (especially  in  the  event  of  epidemics),  the  gingival  sponginess 
and  hemorrhage,  deep-seated  intramuscular  and  subperiosteal  hemor- 
rhages, especially  in  the  legs,  and  speedy  cure  under  the  influence 
of  an  antiscorbutic  diet.  These  serve  to  exclude  purpura  and  hemo- 
philia. 

Infantile  scurvy  (Barlow's  disease,  formerly  incorrectly  described  as 
acute  rickets)  is  quite  the  same  as  the  disease  in  the  adult.  In  the  be- 
ginning there  is  usually  at  least  some  slight  wasting  or  obviously  impaired 
nutrition,  apathy,  disinclination  to  movement,  and  general  irritability. 
Soon  the  child  is  observed  to  cry  when  disturbed  or  touched  (especially 
the  lower  limbs);  pseudoparalysis  of  the  legs  seems  to  have  developed, 
and  an  irregular,  painful,  and  tender  swelling  of  one  or  both  thighs, 
beginning  above  the  epiphyses,  becomes  apparent  (subperiosteal  hemor- 
rhage). Similar  phenomena  may  develop  elsewhere — in  the  vertebrae, 
the  scapula^,  the  bones  of  the  arms,  etc.,  and  the  process  shows  a  tendency 
to  become  symmetrical.  The  epiphyses  may  become  separated  from  the 
shafts  of  the  long  bones  (femur,  costal  cartilages,  etc.),  and  crepitus  may 
be  elicited.  Swelling  of  the  gums  (if  the  child  has  teeth),  and  other 
mucous  membrane,  cutaneous,  and  intermuscular  hemorrhages  may 
supervene;  hematuria  may  be  the  only  noteworthy  symptom.  (Edema 
of  the  eyelids  associated  with  ecchymosis  of  the  lids  or  conjunctiva  is  not 
infrequent.  Asthenia  is  usually  marked ;  anemia  and  pallor  are  moderate; 
there  may  be  slight  fever  (101°  to  102°).  Rickets  may  be  excluded  by 
the  tender  painful  swellings  of  the  shafts  of  the  bones,  especially  of  the 
legs,  and  the  sponginess  and  hemorrhage  of  the  gums.  Rickets. is  some- 
times believed  to  be  associated  with  scurvy  (scurvy-rickets);  perhaps  it 
predisposes  to  scurvy. 

Prognosis. — The  prognosis  is  good  if  the  disease  is  recognized  and  the 
proper  treatment  is  instituted.  In  neglected  cases  death  may  ensue  from 
hemorrhage,  asthenia,  anemia,  secondary  infections,  etc. 

Treatment. — Nowadays  the  supplying  of  sailors,  soldiers,  and  others 
with  a  suitable  antiscorbutic  diet  effectually  prevents  the  disease,  \\nien 
the  disease  has  developed,  a  generous  supply  of  fresh  meat,  fresh  vege- 
tables, and  the  juice  of  two  or  three  lemons,  oranges,  or  limes  daily 
(sweetened  if  desired)  commonly  lead  to  cure.  If  the  gums  are  much 
swollen  the  diet  should  be  liquid  or  semisolid  for  a  time;  the  gums 
should  he  painted  with  silver  nitrate  (2  to  5  per  cent.);  and  boric 
acid  (3  per  cent.),  or  the  solutions  mentioned  on  page  51,  should  be 
used  as  a  mouth  wnsh.  Hydrochloric  acid,  stomachics,  bitter  tonics, 
strychnine,  alcohol,  iron,  etc.,  are  sometimes  re(|uired  for  obvious  indi- 
cations. Children  should  be  given  mother's  milk  if  possible,  or  fresh 
unsterilized  cow's  milk  suitably  modified,  and  orange  juice  or  lemon 
juice,  other  fruit  juices,  and  meat  juice,  perhaps  with  mashed  potatoes 
and  vegetable  purees.  Iron,  arsenic,  cod-liver  oil,  l)randy,  etc.,  are 
useful  adjuvants.  In  the  event  of  separation  of  the  epiphyses,  splints 
should  be  applied. 


334  DISORDERS  OF  METABOLISM 

AMYLOIDOSIS. 

{Ainyloid  Disease;  Lardaceous  Disease;  Waxy  or  Bacony  Degeneration.) 

Amyloidosis  is  a  disorder  of  metabolism  that  develops  in  the  course  of 
prolonged  suppuration,  especially  tuberculous  or  syphilitic  disease  of  the 
bones,  and  is  characterized  by  the  formation  in  the  tissues  and  organs 
of  lardacein,  a  combination  of  chondroitin-sulphuric  acid  and  a  protein. 

Etiology. — Amyloidosis  follows  prolonged  suppuration  and  long- 
continued  loss  of  the  body  proteins.  It  is  most  common  in  advanced 
tuberculosis,  especially  of  the  bones  and  joints  ("Pott's  disease  of  the 
vertebra,  hip  disease,  etc.);  it  occurs  also  in  advanced  s\^hilis,  some- 
times even  in  the  absence  of  suppuration;  in  non-tuberculous  and  non- 
syphilitic  suppurative  processes,  such  as  osteomyelitis,  empyema,  etc.; 
in  non-suppurative  disorders  leading  to  anemia  and  cachexia,  such  as 
malaria,  leukemia,  carcinoma,  chronic  nephritis,  prolonged  lactation, 
etc.;  and  sometimes  it  occurs  without  obvious  cause.  The  disorder  is 
most  common  in  young  adults  (before  the  fortieth  year),  and  in  males, 
since  they  are  more  subject  than  females  to  the  initiating  causes. 

Pathology. — The  lesions  are  sometimes  confined  to  a  single  organ; 
usually  they  are  widespread,  being  most  common  in  the  kidneys,  spleen, 
and  liver  (which  often  are  involved  concurrently) ;  they  occur  also  in  the 
small  intestine,  the  lymph  nodes,  the  adrenals,  the  stomach,  the  large 
intestine,  the  heart  the  pancreas,  the  thyroid,  the  bone-marrow,  etc. 
The  solid  viscera  become  enlarged,  firm,  dense,  and  heavy;  they  take  on 
a  homogenous,  semitranslucent  or  wax-like  appearance,  and  give  a 
characteristic  reaction  with  iodine  and  other  substances.  The  lardacein 
is  not,  as  was  formerly  supposed,  an  infiltration  derived  from  the  blood, 
but  is  a  formation  developed  in  situ  in  consequence  of  an  interaction 
between  chondroitin-sulphuric  acid  brought  by  the  blood  or  the  lymph- 
atics and  the  local  protein;  the  process  is  in  some  way  determined  or 
influenced  by  bacterial  (and  perhaps  other)  toxins,  notably  the  toxins  of 
staphylococci,  streptococci,  etc.  The  suppurative  processes  in  which 
amyloidosis  occurs  are  in  most  instances  examples  of  secondary  pyo- 
coccic  infections.  The  amyloid  material  is  deposited  in  the  outer  sur- 
face of  the  capillary  vessels,  and  in  the  intima  and  media  of  the  arteri- 
oles; the  adventitia  is  rarely,  and  the  endothelium  never,  affected.  In 
the  kidneys  the  ^Nlalpighian  tufts  are  especially  involved,  in  the  liver  the 
midzonal  region  of  the  lobules,  in  the  spleen  the  Malpighian  bodies,  and 
in  the  mucous  membranes  the  arterioles. 

Symptoms. — The  symptoms  are  largely  those  of  the  antecedent  dis- 
order, of  which  the  amyloidosis  is  the  end  result.  With  gradual  increase 
in  the  anemia,  cachexia,  and  weakness,  the  abdomen  is  observed  to 
enlarge,  or  polyuria,  diarrhoea,  or  oedema  may  develop.  The  abdominal 
enlargement  is  readily  found  to  be  due  to  enlargement  of  the  liver  or 
spleen  or  both ;  the  liver  may  become  enormous,  and  is  smooth,  hard, 
firm,  and  has  a  somewhat  sharp  or  rounded  edge;  the  spleen  is  enlarged 


INFANTILISM  335 

and  presents  a  firm,  resisting,  blunt  edge.  There  is  rarely  any  jaundice, 
and  ascites  develops  only  as  part  of  anasarca.  Involvement  of  the  kid- 
ney is  shown  in  oedema  and  increase  in  the  amount  of  the  urine,  which 
is  pale  in  color  and  of  very  low  specific  gravity;  it  contains  usually  a 
considerable  amount  (sometimes  very  little)  albumin,  and  hyaline  and 
waxy  casts  (which  may  give  the  amyloid  reaction).  In  the  event  of 
associated  nephritis  (which  is  common)  cellular  casts,  arterial  hyper- 
tension, arteriosclerosis,  hypertrophy  of  the  heart,  retinal  changes,  etc., 
may  be  found.  Involvement  of  the  intestine  may  be  symptomless,  but 
if  advanced,  the  lesions  are  likely  to  be  disclosed  by  more  or  less  intract- 
able and  painless  diarrhoea.  Changes  in  the  cutaneous  vessels,  and  a 
failing  heart,  are  often  in  part  answerable  for  the  oedema. 

Diagnosis. — The  diagnosis  is  readily  made,  the  combination  of  the 
etiological  factor,  progressive  increase  of  anemia,  cachexia,  and  weak- 
ness, enlargement  of  the  liver  and  the  spleen  polyuria,  albuminuria,  and 
diarrhoea  being  unmistakable. 

Prognosis. — The  prognosis  depends  chiefly  on  the  initiating  cause;  the 
advent  of  the  amyloidosis  only  makes  the  prognosis  hopeless. 

Treatment. — ^The  treatment  is  wholly  that  of  the  primary  disorder. 


INFANTILISM. 

Infantilism  is  a  condition  characterized  l)y  the  persistence  beyond  the 
ordinary  age  of  puberty  of  the  physical  and  mental  attributes  of  child- 
hood, including  hypoplasia  of , the  sexual  organs  and  absence  or  abeyance 
of  the  secondary  sexual  characteristics.  The  individual  remains  a  child 
in  body  and  in  mind  (emotions  and  intelligence),  the  adult  bodily  char- 
acteristics remain  in  abeyance  or  become  ill  developed,  the  union  of  the 
epiphyses  and  diaphyses  of  the  long  bones  fails  or  is  much  delayed.  In 
the  male,  the  facial,  axillary,  and  pubic  hair  does  not  grow,  nor  does  the 
larynx  enlarge  or  the  voice  deepen;  in  the  female,  the  axillary  and  pubic 
hair  does  not  grow,  the  breasts  do  not  develop,  the  hips  do  not  widen,  and 
there  is  little  indication  of  the  female  waist.  The  underlying  causes  may 
be  present  at  birth  (congenital  cases);  or  the  condition  may  be  due  to 
factors  that  become  operative  in  early  or  late  childhood.  The  ensuing 
phenomena  vary  accordingly:  in  some  the  infantilism  is  complete,  in 
some  incomplete,  whereas  in  other,  perhaps  related,  cases  the  onset  of 
puberty  is  merely  delayed — full  and  normal  development  ultimately 
ensuing.     Several  t}^es  may  be  distinguished: 

The  Loraix  Type. — In  this,  beyond  the  ordinary  age  of  puberty, 
the  figure  remains  small  and  childlike  as  regards  height,  but  the  general 
contour  is  that  of  approaching  puberty.  Although  there  is  no  growth  of 
the  facial,  pubic,  or  axillary  hair,  nor  of  the  breasts  in  die  female,  the  geni- 
tal organs  are  well  formed,  although  small;  the  head  is  relatively  small, 
the  shoulders  are  fairly  broad,  and  tlie  l)()ny  prominences  and  muscles  are 
clistinct — a  miniature  man  or  woman  who  has  retained  the  characteristics 


336  DISORDERS  OF  METABOLISM 

(mental  as  well  as  physical)  of  childhood.  The  cause  of  the  disease  is  not 
known:  indeed,  it  is  sometimes  referred  to  as  idiopathic;  but  syphilis,  alco- 
holism, and  consanguinity  in  the  parents  are  believed  to  be  of  etiological 
importance;  and  defective  development  of  the  cardiovascular  system  is 
believed  to  be  the  main  factor. 

The  Cardiac  Type. — Congenital  heart  disease,  and  also  heart  dis- 
ease beginning  early  in  life,  especially  pulmonary  or  aortic  stenosis,  may 
lead  to  infantilism.  In  some  otherwise  fairly  normal,  although  small 
adult  individuals  a  concealed  or  latent  mitral  stenosis  may  be  found. 

The  Metabolic  Type. — Disorders  of  internal  secretion  apparently 
may  give  rise  to  several  varieties  of  infantilism.  Thyroid  inadequacy, 
congenital  or  developing  early  in  life,  occasions  a  so-called  myxoedema- 
tous  infantilism  or  cretinism  (Brissaud's  type;  Hertoghe's  hypothyroid- 
ism), which  may  be  cured  by  thyroid  extract.  Another  form  occurs  in  con- 
nection with  disease  of  the  pituitary :  hyperpituitarism  originating  in  youth 
gives  rise  to  gigantism,  which  may  be  associated  with  infantile  proportion 
of  the  body,  infantile  genital  organs,  delayed  union  of  the  epiphyses  and 
diaphyses,  etc.  Hypopituitarism  originating  in  youth  gives  probably 
rise  to  infantilism  of  mind  as  well  as  body.  Gilford's  cases  of  dwarfs, 
micromegaly,  ateliosis  (continuous  youth  and  premature  old  age),  or 
progeria  perhaps  belong  to  this  category.  A  pancreatic  form,  sup- 
posedly due  to  deficient  pancreatic  secretion  and  associated  with  recur- 
ring attacks  of  severe  diarrhoea  in  children,  has  been  described  by  Byron 
Bramwell.    Improvement  has  followed  the  use  of  pancreatic  preparations. 

The  Intestinal  Type. — Herter  describes  as  intestinal  infantilism  a 
condition  occurring  in  childhood,  and  characterized  by  arrest  in  the 
development  of  the  body  (skeleton,  muscles,  and  organs),  maintenance 
of  good  mental  powers  and  fair  development  of  the  brain,  marked 
abdominal  distention,  slight,  moderate,  or  considerable  degree  of  simple 
anemia,  the  rapid  onset  of  physical  and  mental  fatigue,  irregularities  of 
intestinal  digestion  resulting  in  frequent  diarrhceal  discharges,  excessive 
appetite,  various  minor  signs  of  nervous  instability,  subnormal  tempera- 
ture, cold  hands  and  feet,  and  slight  signs  of  rickets.  Indol  and  phenol 
compounds  occur  in  the  urine;  fat  absorption  is  impaired;  and  the 
resorption  of  calcium  and  magnesium  is  deficient.  Herter  attributes  the 
condition  to  the  overgrowth  and  persistence  of  the  bacterial  flora  of  the 
intestine  belonging  normally  to  the  nursling  period  (Bacillus  bifidus  and 
Bacillus  infantilis).  The  condition  is  persistent,  and  relapses  are  com- 
mon; some  of  the  children  die  of  acute  intestinal  infections;  others  are 
likely  to  be  permanently  dwarfed;  but  normal  growth  may  follow 
careful  dietetic  regulations. 


SECTION   IV. 

DISEASES  OP  THE  DUCTLESS  GLANDS  AND 
OF  INTERNAL  SECRETION. 


Pathological  Physiology. — In  addition  to  the  several  organs,  such 
as  the  stomach,  the  liver,  the  pancreas,  the  kidneys,  the  testicle,  etc., 
which  produce  a  secretion  that  can  be  readily  procured  and  studied, 
other  organs  produce  a  secretion  not  so  open  to  investigation,  a  secretion 
which,  since  it  is  not  discharged  through  the  medium  of  a  duct  from  the 
organ  that  produces  it,  is  spoken  of  as  an  internal  secretion,  and  the 
organ  in  question  as  a  ductless  gland.  In  a  certain  sense  all  of  the  body 
cells  produce  an  internal  secretion — the  result  of  their  metabolic  activity 
— which  they  give  off  into  the  lymph  or  blood  stream.  Some  of  these  are 
the  end  results  of  destructive  metabolism  and  of  no  further  use  in  the 
economy — indeed,  they  may  be  distinctly  harmful  if  not  excreted  (cer- 
tain forms  of  auto-intoxication);  others  are  more  or  less  essential  to  the 
orderly  performance  of  the  functions  of  other  organs,  necessary  to  the 
preservation  of  life  and  the  maintenance  of  health ;  these  are  the  internal 
secretions  in  a  restricted  sense,  and  the  "glands"  that  produce  them  are 
the  "ductless  glands"  or  the  glands  with  an  internal  secretion.  They 
comprise  especially  the  thyroid,  the  parathyroids,  the  adrenals  (and  the 
chromaffin  system),  and  the  pituitary  body,  which  are  endowed  with 
specific  functions  that  will  be  discussed  under  the  respective  headings; 
perhaps  the  carotid  and  coccygeal  glands  also  should  be  here  included, 
but  nothing  is  known  of  their  function.  But  other  organs  produce 
internal  secretions:  some  of  these  also  are  "external  secretion;"  thus,  the 
pancreas  pours  into  the  duodenum  a  secretion  that  contains  trv])sinogen, 
which  hydrolyzes  protein,  diastase  (amylase),  which  hydrolyzes  carbo- 
hydrates, lipase  (steapsin),  which  saponifies  and  indirectly  enuilsifies 
fats,  and  perhaps  other  enzymes  (rennin,  lactase,  etc.);  but,  in  addition, 
the  islands  of  Langerlians  of  the  pancreas,  which  are  not  in  communica- 
tion with  tlie  pancreatic  duct,  produce  an  internal  secretion  tliat  finds 
its  way  directly  into  the  blood  and  controls  the  katabolism  of  the  dextrose 
of  the  bl(K)d,  muscles,  and  other  tissues — a  subject  discussed  under 
diabetes.  The  liver  and  the  kidneys,  in  a  certain  sense,  also  have  an 
internal  secretion  in  addition  to  the  niore  o])vioiis  external  secretion— 
22 


338  DISEASES  OF  THE  DUCTLESS  GLANDS 

the  bile  and  the  urine.  The  liver,  by  a  process  that  may  be  described  as 
internal  secretion,  produces  glycogen  and  an  enzyme  (urease)  that  leads 
to  formation  of  urea  from  protein  derivatives;  and  the  kidneys  appear  also 
to  produce  a  proteolytic  enzyme  subserving  the  same  purpose,  though 
probably  acting  in  the  liver  or  the  muscles  rather  than  in  the  kidney 
itself.  The  testicle  and  the  ovaries,  in  addition  to  their  specific  secretions 
which  are  discharged  externally,  produce  also  an  internal  secretion 
which  is  credited  with  the  production  of  the  secondary  male  and  female 
characteristics  respectively,  and  seems  to  exercise  some  tonic  influence 
on  the  neuromuscular  system.  Castration  in  either  sex  results  in  lessened 
oxidation,  accunuilation  of  fat,  and  in  more  or  less  loss  of  the  secondary 
sexual  characteristics,  which  loss  may  be  prevented  or  retarded  by  the 
use  of  testicular  or  ovarian  preparations  respectively.  The  duodenum 
produces  secretin  which  stimulates  the  pancreas  to  activity  and  entero- 
kinase  which  activates  the  proteolytic  ferment  of  the  pancreatic  juice 
(trypsinogen) ;  but  these  can  scarcely  be  called  internal  secretions  in  a 
restricted  sense.  Organic  substances  subserving  such  a  stimulating 
purpose  have  recently  been  spoken  of  as  kinases,  while  similar  inor- 
ganic substances  have  been  called  activators.  The  spleen,  the  lymph 
nodes,  the  hemolymph  nodes,  and  the  thymus  also,  perhaps,  produce  an 
internal  secretion,  but  there  is  no  conclusive  evidence  of  the  fact;  their 
diseases  are  discussed  under  diseases  of  the  blood  and  hemopoietic 
system. 

The  ductless  glands,  or  the  glands  with  an  internal  secretion  in  a 
restricted  sense,  are  subject  to  many  complicated  and  ill-understood 
relationships;  thus,  in  diseased  states  at  least,  there  is  a  more  or  less 
marked  relationship  between  the  thyroid  and  the  pituitary,  between  the 
thyroid  and  the  thymus,  between  the  pituitary  and  the  testicles  and  the 
ovaries,  and  between  the  thyroid,  the  pancreas,  and  the  adrenals.  The 
functional  harmony  of  these  organs  is  maintained  and  their  correlated 
interaction  is  effected  through  the  medium  of  chemical  substances,  so- 
called  hormones,  that  circulate  in  the  blood  and  other  fluids  of  the  body. 
Whereas,  the  pancreas  and  the  thyroid,  and  the  pancreas  and  the  adrenals 
(and  the  chromaffin  system)  each  inhibits  the  metabolic  activities  of  the 
other,  the  thyroid  and  the  adrenals  (and  the  chromaflSn  system)  seem 
the  one  to  augment  the  activities  of  the  other.  Experimental  removal 
of  one  of  these  glands  not  only  results  directly  in  a  loss  of  its  functional 
activities,  but  leads  also  indirectly,  since  restraint  is  removed,  to  an  in- 
creased or  diminished  functional  activity  of  the  correspondingly  related 
gland;  and  augmented  functional  activity  (such  as  may  be  attained  by 
feeding  experiments  or  the  injection  of  active  principles  or  extracts)  has 
a  contrary  eft'ect.  Thus,  for  instance,  loss  or  diminution  of  the  internal 
secretion  of  the  pancreas,  in  consequence  of  the  corresponding  loss  of 
inhibition,  is  associated  with  hyperfunction  of  the  thyroid  (increase  of 
protein  metabolism)  and  of  the  adrenals  and  the  chromaffin  system 
(adrenal  glycosuria).  Similar  phenomena  occur  also  in  human  subjects: 
thus,  hyperthyroidism  is  sometimes  associated  with  alimentary  glycosuria 


DISEASES   OE   THE   THYROID   GLAND  339 

or  diabetes.  The  pigmentation  of  Graves'  disease  (resembling  that  of 
Addison's  disease)  suggests  a  relationship  between  the  thyroid  and  the 
adrenals.  There  are  many  other  evidences  of  mutual  inter-relationship 
between  the  ductless  glands,  which,  however,  are  ill  understood. 


DISEASES   OF   THE  THYROID   GLAND. 

Pathological  Physiology.— The  normal  physiology  of  the  thyroid  is 
ill  understood.  In  consequence  of  the  activity  of  its  specific  principle 
iodothyrin  (a  constituent  of  colloid  and  not  found  elsewhere  in  the 
body),  and  perhaps  also  of  other  unknown  principles,  it  exercises  a 
profound  influence  on  metabolism.  It  detoxifies  intermediate  products 
of  metabolism  or  gives  over  into  the  circulation  an  internal  secretion 
essential  to  the  normal  functional  activity  of  other  organs,  acting,  there- 
fore, as  a  hormone  and  seeming  to  have  a  specific  action  on  the  central 
and  the  sympathetic  nervous  systems  and  on  the  skin  and  the  subcutane- 
ous tissues.  Injection  of  thyroid  preparations  increases  protein  and  fat 
katabolism.  An  influence  of  deficiency  of  secretion  on  carbohydrate 
metabolism  is  evident  in  the  fact  that  after  thyroidectomy  injections  of 
adrenalin  do  not  cause  glycosuria;  that  is,  the  limits  of  carbohydrate 
metabolism  are  increased.  Deficiency  of  secretion  also  exercises  a  restrain- 
ing influence  on  the  healing  of  fractures;  an  excess  seems  to  accelerate  the 
healing.  Destruction  or  loss  of  function  of  the  thyroid  (athyrea,  hypo- 
thyroidism) results  in  congenital  or  acquired  myxadema;  and  an  excess 
of  function  (hyperthyroidism),  or  perversion  of  function  (dysthyreosis), 
is  the  basis  of  Graves'  disease;  whence  the  two  diseases  represent  the 
one  the  antithesis  of  the  other.  In  the  one  the  gland  is  atrophic  or 
absent,  in  the  other  hyperplastic  and  hyperactive;  in  the  one  metabolism 
is  deficient  and  the  patient  increases  in  weight,  in  the  other  metabolism 
(especially  the  consumption  of  oxygen)  is  augmented  and  the  patient 
usually  emaciates;  in  the  one  the  patient  is  dull,  apathetic,  and  mentally 
deficient,  in  the  other  nervous  and  highly  excitable;  in  the  one  the  skin  is 
dry,  thick,  cool,  and  inactive,  in  the  other  moist,  warm,  and  active  (ery- 
thema, flushing,  sweating);  in  the  one  the  temperature  is  low,  the  pulse 
is  slow,  and  the  urine  lessened,  in  the  other  the  temperature  is  increased, 
the  pulse  is  rapid  (tachyflcardia),  and  the  urine  increased;  in  the  one 
(which  may  result  from  excision  of  the  thyroid)  t!ie  symptoms  may  be 
ameliorated  or  the  condition  entirely  cured  by  the  use  of  thyroid  extract,  in 
the  other,  symptoms  are  made  worse  by  thyroid  extract — which  may  also 
j)rovoke  similar  phenomena  in  normal  individuals — and  the  condition 
may  be  benefited  or  cured  by  partial  thyroidectomy. 

Thyroid  preparations  have  been  used  with  some  success  in  certain 
disorders  of  metabolism,  such  as  obesity,  arthritis  deformans,  etc. 
Their  use,  in  obesity,  for  instance,  in  which  they  seem  esjiecially  iiub'cated 
to  augment  the  kata})olisin  of  fat,  is  not  without  danger,  since  although 
they  have  a  much  gi-eater  accelerative  influence  on  protein  katabolism, 


340  DISEASES  OF  THE  THYROID  GLAND 

they  may  cause  glycosuria  or  diabetes  (which  is  often  latent  in  obese 
subjects),  and  a  fatty  heart  may  not  be  able  well  to  maintain  the  provoked 
increased  activity. 

ACUTE  THYROIDITIS. 

Etiology. — Acute  inflammation  of  the  thyroid  occasionally  occurs, 
usually  in  young  subjects,  in  consequence  of  trauma  or  of  bacterial 
infection.  The  infectious  cases  are  rarely  primary;  usually  they  are 
secondary,  occurring  in  the  course  of  typhoid  fever,  scarlatina,  diphtheria, 
measles,  influenza,  smallpox,  some  cases  of  recent  syphilis,  etc.  The 
lesions  may  be  simple  or  purulent. 

Symptoms. — The  symptoms  consist  of  local  pain  and  tenderness,  sen- 
sation of  fulness  in  the  neck,  perhaps  difficulty  in  swallowing,  and  an 
enlarged  and  more  or  less  tender  thyroid.  In  the  event  of  suppuration 
a  local  area  of  softening  or  fluctuation  may  be  detected.  The  general 
symptoms  are  those  of  the  primary  infection,  augmented  perhaps  by  the 
local  inflammation. 

Diagnosis. — In  the  diagnosis  one  must  exclude  simple  congestion, 
such  as  occurs  especially  in  women  from  emotional  excitement,  disturb- 
ance of  the  sexual  organs,  interference  with  the  circulation  (tight  collars), 
etc. 

Prognosis. — The  prognosis,  as  a  rule,  is  good  as  regards  the  thyroiditis 
itself,  but  modifications  in  the  gland  may  lead  later  to  Graves'  disease 
or  myxoedema. 

Treatment. — The  treatment  is  that  of  the  primary  disorder,  with  local 
antiphlogistic  measures  (especially  an  icebag),  and  incision  in  the  event 
of  suppuration. 

GOITRE. 

(Simple  Goitre;  Struma;  Bronchocele.) 

Goitre  is  a  term  indiscriminately  applied  to  any  enlargement  of  the 
thyroid  gland.  It  is  often  qualified  by  the  terms  benign  and  malignant 
(comprising  the  tumor  formations);  and  a  simple  goitre  is  differentiated 
from  the  so-called  exophthalnuc  goitre. 

Etiology. — Simple  goitre  occurs  as  a  sporadic,  an  endemic,  or  an  epi- 
demic disease.  The  sporadic  disease  occurs  in  all  parts  of  the  world. 
The  disease  is  endemic  especially  in  the  Swiss  and  Italian  Alps,  but  also 
in  certain  regions  of  France,  Spain,  Germany,  England,  Asia,  and  in  our 
own  country  in  the  region  of  the  great  lakes;  in  these  endemic  regions 
small  epidemics  sometimes  occur  from  time  to  time,  as  well  as  occasion- 
ally in  barracks,  schools,  etc.  The  disorder  is  more  common  in  women 
than  in  men  (six  or  more  to  one).  It  is  sometimes  congenital.  The 
goitre  begins  to  develop  usually  at  puberty  or  soon  thereafter,  and  may 
continue  to  increase  in  size  throughout  life,  although,  attaining  a  consid- 
erable size  by  the  time  adult  life  is  reached,  it  may  remain  stationary. 


aoiTRE  341 

The  cause  of  the  disease  is  not  known,  aUhouo-h  it  has  been  attributed  to 
the  water,  air,  and  soil  of  endemic  centres;  special  significance  has  been 
attributed  to  the  drinking-water — mineral,  radio-active,  and  bacterial 
constituents. 

Pathology.— The  thyroid  is  more  or  less  enlarged,  either  uniformly 
or  one  lobe  more  than  the  other;  the  shape  of  the  organ  is  generally 
more  or  less  preserved;  the  enlargement  is  often  nodular,  although  it 
may  be  smooth.  On  section  it  resembles  the  normal  gland,  although 
often  the  colloid  is  obviously  increased.  Parenchymatous  (or  colloid), 
cystic,  and  vascular  goitres  are  sometimes  distinguished.  Hyaline  degen- 
eration, calcareous  infiltration,  and  fibrosis  are  not  uncommon  in  ad- 
vanced cases.  MacCarthy  differentiates  the  following  types  or  stages 
of  goitre:  (1)  Cystic  goitre  (usually  spoken  of  as  simple  or  colloid 
goitre),  composed  of  many  small  and  large  cysts  with  colloid  contents;  it 
leads  to  enlargement,  but  no  symptoms  other  than  those  due  to  press- 
ure. (2)  Hypertrophic  parenchymatous  goitre — hypertrophy  of  the 
parenchyma  with  little  or  no  cyst  formation.  (3)  Papillary  cystic 
goitre — cyst  formations  with  colloid  contents,  papillary  ingrowths  into  the 
alveoli,  or  cysts  with  consequent  increased  secreting  surface.  Hj'per- 
thyroidism  may  occur  in  types  2  and  3.  (4)  Hypertrophic  foetal  thyroid 
—a  small  amount  of  epithelial  tissue  and  a  great  amount  of  inter- 
glandular  connective  tissue — the  goitre  of  the  cretin  with  tumor  formation 
and  hypothyroidism.  (5)  Foetal  adenoma  or  adenomatous  hypertrophy 
of  the  foetal  thyroid,  instead  of  connective  tissue  overgrowth;  it  may  occur 
as  an  encapsulated  tumor,  occasioning  inconvenience  only  by  pressure, 
or  degenerative  or  circulatory  changes  may  occur  and  lead  to  hyper- 
thyroidism. 

Symptoms. — The  chief  symptom  is  the  goitre  itself,  which  may  be 
very  small  or  very  large,  and  involve  the  entire  gland,  or  one  lobe  only 
or  disproportionately,  or  the  isthmus;  it  may  grow  larger  behind  the 
sternum  or  the  clavicles.  \\Qien  large  it  may  lead  to  inconvenience  on 
account  of  its  size  and  weight,  or  it  may  cause  compression  ])henomena 
— on  the  trachea,  oesophagus,  arteries,  veins,  and  nerves  of  the  neck. 
Sudden  death  occasionally  occurs  in  large  goitres  from  pressure  on 
the  vagus,  hemorrhage  and  compression  of  the  trachea,  oedema  of  the 
glottis,  etc. 

Diagnosis. — The  diagnosis,  as  a  rule,  is  obvious;  one  must  exclude 
tumors  and  exophthalmic  goitre. 

Prognosis. — The  condition  is  essentially  chronic,  although  some  cases, 
so-called  acute  goitres,  that  develop  in  newcomers  into  an  infected 
region,  often  disappear  if  the  subject  soon  leaves.  The  prognosis  is 
influenced  by  the  size  and  direction  of  growth  and  the  presence  or  absence 
of  compression  phenomena. 

Treatment. — Boiling  the  drinking-water  in  goitrous  regions  is  usually 
advised  as  a  prophylactic  measure.  Change  of  residence  to  a  non- 
goitrous  region  is  much  preferable.  Counterirritants,  iodine  externally, 
and  the  iodides  and  ergot  internallv,  and  the  ,r-rays  locally  arc  some- 


342  DISEASES  OF  THE  THYROID  GLAND 

times  of  service,  especially  if  the  goitre  be  small  and  of  recent  develop- 
ment. Large  and  growing  goitres  should  be  treated  surgically — removed 
in  part. 

HYPERTHYROIDISM  AND  EXOPHTHALMIC  GOITRE. 

{Graves'  Disease;  Basedoiv's  Disease;  Parry's  Disease;  Flajani's  Disease.) 

Exophthalmic  goitre  is  a  condition  of  aggravated  hyperthyroidism, 
characterized  by  enlargement  of  the  thyroid,  exophthalmos,  tachycardia, 
muscular  tremor,  and  vasomotor  disturbances;  it  takes  its  name  from 
the  two  obtrusive  manifestations  of  the  disorder,  but  there  are  many 
more  or  less  ill-developed  cases  that  present  neither  goitre  nor  exoph- 
thalmos and  are  preferably  spoken  of  as  hyperthyroidism. 

Etiology. — From  SO  to  95  per  cent,  of  the  cases  occur  in  women,  and 
most  frequently  between  the  ages  of  fifteen  and  thirty  years.  The 
disease  is  rare  during  childhood,  but  is  not  uncommon  in  the  fourth 
decade.  The  cause  is  not  known;  it  develops  not  uncommonly  at 
or  shortly  after  puberty;  its  onset  is  sometimes  attributed  to  fright, 
fear,  excitement,  worry,  anemia,  chlorosis,  gastro-intestinal  disturbances, 
infections,  etc.  Perhaps  these  factors,  if  at  all  operative,  are  to  be 
interpreted  as  furnishing  nervous,  toxic,  infectious,  or  metabolic  stimula- 
tion to  the  thyroid.  Etiological  significance  is  sometimes  attributed  to 
locality  and  climate,  but  the  nature  of  the  relationship,  if  any,  is  not 
understood. 

Pathology. — The  significant  lesion  consists  of  enlargement  of  the 
thyroid,  which  varies  considerably  in  different  cases;  it  may  be  very 
slight  or  very  great,  symmetrical  or  asymmetrical,  firm  or  soft  and 
elastic  (parenchymatous,  fibrous,  or  cystic).  The  characteristic  micro- 
scopic lesions  consist  of  changes  in  the  size  and  configuration  of  the 
alveoli,  due  especially  to  hyperplasia  and  infolding  of  the  epithelium; 
increase  in  the  size  of  the  epithelial  cells — the  normal  low  cuboidal 
cells  giving  way  to  high  cylindrical  cells;  and  gradual  disappearance  and 
absorption  of  the  colloid  material;  with  these  there  is  also  associated 
an  increase  in  the  bloodvessels  and  the  connective  tissue  stroma.  The 
symptoms  are  attributed  to  thyroid  toxemia  due  to  the  absorption  of 
the  products  of  a  hyperactive  (perhaps  perverted)  thyroid  (hyperthyroid- 
ism); this  consists  in  part  of  iodothyrin,  a  constitutent  of  the  colloid, 
which  is  usually  lessened  in  the  exophthalmic  goitres;  perhaps  also  to 
other  unknown  substances.  Sometimes  lesions  are  found  in  the  central 
nervous  system  (especially  the  restiform  bodies  of  the  medulla),  and  in 
the  sympathetic  nervous  system  (especially  the  cervical  sympathetic);  but 
they  are  inconstant  and  probably  not  significant.  The  muscles,  despite 
the  tremor,  show  no  noteworthy  lesions  aside  from  some  atrophy,  espe- 
cially of  the  muscles  of  the  neck,  hand,  arms,  and  peroneus;  in  advanced 
cases  the  heart  becomes  hypertrophied,  dilated,  and  degenerated. 

Symptoms.— The  onset,  as  a  rule,  is  insidious,  the  symptoms  mild, 
moderate,  or  severe,  and  the  course  protracted — chronic  cases;  occa- 


HYPERTHYROIDISM   AND   EXOPHTH ALMICjCrOITRE        343 

sionally  the  onset  is  abrupt — acute  cases,  wliich  also  may  he  mild, 
moderate,  or  severe;  the  severe  cases  may  run  a  rapid  course  and  soon 
lead  to  death.  In  some  cases  the  symptoms  of  hyperthyroidism  are 
present  from  the  beginning  (primary  cases),  \yhereas  in  others  they 
supervene  upon  a  goitre  already,  perhaps  for  a  long  time,  existent 
(secondary  cases).  In  some  cases  the  symptoms  are  many  and  obtru- 
sive (outspoken  or  complete  cases),  whereas  in  others  they  are  few, 
irregular,  atypical  (incomplete,  rudimentary  cases,  formes  frustes  of  the 
French).     Remissions  and  exacerbations  are  common. 

The  characteristic  features  of  the  disease  consist  of  enlargement 
of  the  thyroid,  exophthalmos  and  other  ocular  symptoms,  tachycardia, 
muscular  tremors,  and  various  vasomotor  disturbances.  The  goitre  is 
almost  invariably  present,  some  enlargement  being  present  in  many 
cases  in  which  it  is  not  suspected;  but  there  is  no  relationship  between 
the  size  of  the  goitre  and  the  severity  of  the  symptoms;  it  is  often 
present  from  the  beginning,  but  sometimes  it  develops  later,  at  least 
in  an  obtrusive  form.  It  may  be  slight,  moderate,  or  extreme,  and 
vary  in  size  from  time  to  time  (during  menstruation,  pregnancy,  times  of 
worry,  etc.);  it  may  be  unilateral,  bilateral,  symmetrical  or  asymmetrical; 
firm  or  soft,  elastic,  and  semifluctuating.  It  is  rarely  painful  except 
when  acutely  enlarged  (vascular  enlargement),  and  unless  very  large 
gives  rise  to  no  noteworthy  signs  of  compression  of  the  trachea  or 
adjacent  organs.  It  may  pulsate,  and  on  ausculation  reveal  a  systolic 
(arterial)  and  sometimes  also  a  diastolic  (venous)  murmur. 

Exophthalmos  is  present  in  from  75  to  90  per  cent,  of  the  cases,  and 
although  a  yery  obtrusive  symptom,  is  not,  as  a  rule,  an  early  symptom. 
It  varies  much  in  degree  (25  to  30  millimeters,  as  measured  by  the 
Hertel  exophthalmometer,  the  normal  being  about  20  millimeters  in 
adults,  and  less  in  children);  ordinarily  it  just  about  prevents  com- 
plete closure  of  the  eyelids,  but  rarely  the  eyeballs  may  be  advanced 
altogether  beyond  the  eyelids.  Usually  it  is  bilateral,  although  unequal; 
it  may  be  almost  if  not  completely  unilateral,  and  perhaps  associated 
\\ith  homolateral  goitre.  There  are  a  number  of  associated  ocular  phe- 
nomena :  A  peculiar  staring  expression  (widening  of  the  palpel  )ral  fissure), 
the  whites  of  the  sclerae  showing  all  around  the  cornea  (Dalrymple's 
sign),  associated  with  infrequent  and  incomplete  reflex  winking  (Stell- 
wag's  sign);  lagging  of  the  upper  eyelids  in  downward  movement  of 
the  eyeballs — incoordination  in  the  movements  of  the  eyelids  and  the 
eyeballs  (von  Graefe's  sign);  lack  of  the  power  of  binocular  convergence 
unassociated  with  diplopia  (Moebius'  sign);  difficulty  or  inability  to 
evert  the  upper  lid  (Gifl'ord's  sign);  tremor  of  the  upper  lid  when  it 
has  been  closed  gently  (Ilosenbach's  sign);  sudden  ele\ation  of  (he  upj)er 
lid,  exposing  the  sclera,  if  the  patient  looking  straight  forward  is  directed 
quickly  to  look  upward;  that  is,  the  lids  contract  spastically  in  advance 
of  the  elevating  eyeball  (Kocher's  sign).  All  of  these  eye  signs,  including 
the  exophthalmos,  are  due  to  toxic  contraction  of  the  unstriped  or!)ital 
muscle  arising   from   the  orbital   septum  anteriorly  and    inserted   just 


344  DISEASES  OF   THE  THYROID  GLAND 

posterior  to  the  equator  of  the  eyeball,  and  spasm  of  the  iinstrlped  superior 
and  inferior  tarsal  muscles  of  Miiller;  vascular  engorgement  and  oedema 
of  the  orbital  cavity  also  have  been  looked  upon  as  causes.  There  may 
also  be  absence  of  wrinkling  of  the  forehead  when  the  patient  looks 
upward  (Joffroy's  sign);  a  sensation  of  tension  or  strain  in  or  behind 
the  eyeballs;  tremor  of  the  eyeballs;  paralyses  of  the  ocular  muscles; 
excessive  dryness  or  epiphoria;  retinal,  pupillary,  or  corneal  (ulcerative) 
changes;  pigmentation  of  the  eyelids  (Tellais'  sign),  etc. 

Tachycardia  is  always  present,  and  is  commonly  the  earliest  note- 
worthy manifestation.  The  pulse  is  usually  above  100,  and  not  infre- 
quently 160  to  180  or  more.  There  is  associated  palpitation  and  over- 
action  of  the  heart,  throbbing  of  the  peripheral  arteries,  especially  of 
the  neck,  a  capillary  (and  perhaps  a  venous)  pulse,  early  a  functional 
systolic  murmur,  later  evidences  of  hj^ertrophy  and  dilatation  of  the 
heart  (especially  of  the  left  ventricle),  with  relative  mitral  insufficiency, 
arrhythmia,  etc.  Hemorrhages,  especially  epistaxis,  but  also  hemoptysis, 
hematemesis,  etc.,  sometimes  occur.  Muscular  tremors,  fine,  rhythmic, 
8  to  10  to  the  second,  are  present  in  almost  all  cases  and  are  noteworthy 
in  more  than  one-half  of  the  cases.  There  is  often  also  marked  mus- 
cular weakness;  sometimes  a  peculiar  giving  way  of  the  legs  (Charcot). 

There  are  many  vasomotor  symptoms,  such  as  subjective  complaint 
of  warmth,  and  itching,  dermographism,  erythema,  urticaria,  angio- 
neurotic oedema,  readily  provoked  and  excessive  flushing  and  sweating, 
diarrhoea,  sometimes  vomiting  and  abdominal  pain,  periodical  polyuria, 
cough,  dyspna^a,  intermittent  (sometimes  painful)  swelling  of  the  joints, 
etc.  Often  there  are  nervous  symptoms,  such  as  headache,  vertigo, 
insomnia,  different  forms  of  paralysis,  mental  irritability  or  depression; 
occasionally,  especially  in  the  acute  cases,  psychoses.  The  skin  reveals 
lessened  resistance  to  the  galvanic  current  (Chvostek);  it  may  become 
pigmented  or  reveal  spots  of  vitiligo;  the  hair  may  fall.  Attacks  of 
fever,  remittent  or  intermittent,  lasting  several  days  or  several  weelcs,  are 
not  uncommon.  The  metabolism  is  increased  (excessive  nitrogenous 
and  other  excretion). 

Eventually  emaciation,  cardiac  weakness  (myocardial  degeneration), 
low  blood  pressure,  and  more  or  less  secondary  anemia  supervene. 
There  may  be  a  relative  lymphocytosis  (usually  no  leukocytosis;  some- 
times leukopenia),  and  the  coagulability  of  the  blood  may  be  lessened. 
Unusual  and  rapid  loss  of  weight  often  attends  acute  exacerbations  of 
the  disease  (fever,  vomiting,  diarrhoea,  marked  vasomotor  disturbances, 
extreme  tachycardia,  arrhythmia,  perhaps  mania,  etc.) ;  the  loss  may  be 
partly  compensated  for  by  gain  during  a  succeeding  period  of  remission. 
Death  may  ensue  from  acute  thyroidism,  cardiac  weakness,  exhaustion 
from  vomiting  and  diarrhoea,  secondary  infection  (tuberculosis,  pneu- 
monia, etc.),  diabetes  (which  sometimes  ensues),  etc. 

Diagnosis.— The  fully  developed  disorder  presents  no  diagnostic 
difficulties,  but  incomplete  cases,  slight  or  moderate  hyperthyroidism, 
often  go  unrecognized.     Attention  to  other  than  the  three  (formerly) 


nVPERTFlYnOtDiSM  AND  EXOPI^THALMIC  GOITRE       345 

so-called  cardinal  symptoms  (goitre,  exophthalmos,  and  tachycardia) 
will  often  enahle  one  to  make  the  diagnosis  in  early  stages  and  in 
aberrant  cases.  Tachycardia  and  the  vasomotor  phenomena  (which 
determine  the  severity  of  the  disease)  with  or  without  slight  tur- 
gescence  of  the  tliyroid,  are  of  great  diagnostic  significance.  One 
must  not  mistalce  the  sliglit  and  temporary  enlargement  of  the 
thyroid  that  may  follow  shocks  and  emotional  disturbances,  or  occur 
at  puberty,  during  pregnancy,  and  the  climacteric,  for  Graves'  dis- 
ease, although  these  may  progress  to  the  most  serious  disorder,  and 
time  alone  may  be  required  for  demonstrative  differentiation.  Nor 
should  the  enlargement  of  anemic  states,  especially  chlorosis,  and  of 
some  forms  of  heart,  especially  mitral,  disease  be  mistaken.  The 
hyperthyroidism  of  early  tuberculosis  (sometimes  associated  with  tuber- 
culosis of  the  thyroid),  neurasthenic  states  in  which  transitory  thyroid 
enlargement  is  not  uncommon,  etc.,  must  also  be  excluded.  In  doubtful 
cases  recourse  may  be  had  to  the  use  of  iodine  internally  or  some 
thyroid  tablet:  in  the  event  of  hyperthyroidism  even  small  doses  readily 
provoke  tachycardia  and  other  characteristic  symptoms  (intolerance  of 
the  hyperthyroid  subject). 

Prognosis. — The  disease  usually  runs  a  protracted  course,  extending 
over  many  years — twenty  or  more.  Spontaneous  recovery  in  well- 
developed  cases  is  rare;  but  mild  cases  or  moderate  grades  of  hyper- 
thyroidism may  be  much  benefited,  if  not  completely  cured,  by  appro- 
priate treatment.  Marked  benefit,  if  not  cure,  may  be  expected  in  at 
least  half  of  the  cases.  Cases  that  develop  acutely,  or  acute  exacerbations 
of  chronic  cases,  may  lead  to  death  within  a  few  weeks  to  a  few  months. 

Treatment. — Rest  with  freedom  from  care,  worry,  and  excitement 
are  of  prime  importance;  in  severe  cases,  rest  in  bed  for  a  month  or  two 
is  essential;  and  in  all  cases  a  change  of  scene  and  air  is  beneficial.  Care- 
ful attention  must  be  directed  to  the  diet,  so  that  the  patient  may  be 
well  nourished.  Thomson  (who  believes  the  disease  to  be  a  toxemia 
originating  in  the  intestinal  tract)  urges  the  use  of  fermented  milk 
(keffir)  or  peptonized  milk  in  large  amounts,  vegetables  (except  peas, 
beans,  and  asparagus),  crusty  bread,  rice,  and  fruits  (except  uncooked 
apples  and  strawberries),  and  the  prohibition  of  butcher  meat,  oysters, 
clams,  and  lobsters;  one  egg  daily  may  be  permitted,  and  a  small 
amount  of  non-oily  fish,  poultry,  quail,  or  partridge  may  also  be 
taken.  The  bowels  must  be  opened  daily;  paroxysms  of  diarrhoea 
may  require  the  use  of  astringents,  which,  however,  are  rarely  very 
useful.  General  hydrotherapy,  as  well  as  cold  applications  to  the 
thyroid  and  the  heart  are  very  useful.  The  cardiovascular  and  vaso- 
motor phenomena  are  perhaps  best  controlled  with  belladonna  (or 
atropine)  given  to  the  point  of  toleration;  the  bromides  and  other 
nervines,  or  small  doses  of  opium  for  short  periods,  are  sometimes 
useful  adjuncts,  but  opium  should  be  given  with  the  greatest  circum- 
spection, or  not  at  all,  to  subjects  in  whom  the  prognosis  is  relatively 
good.    The  hyperactivity  of  the  heart  is  sometimes  benefited  by  aconite 


346  DISEASES  OF  THE  THYROID  GLAND 

or  veratrum  viride;  little  benefit  attends  the  use  of  digitalis,  strophanthus, 
convallaria,  etc.,  unless  there  is  actual  disease  of  the  heart;  otherwise 
arrhythmia,  etc.,  may  be  made  worse.  A  number  of  drugs  have  been 
more  or  less  highly  extolled  from  time  to  time.  Arsenic  is  believed 
to  exercise  a  modifying  influence  on  the  secretion  of  the  thyroid:  to 
secure  results  it  must  be  given  for  a  long  time;  phosphorus,  especially 
in  the  phosphates,  also  is  credited  with  some  action  on  the  thyroid  secre- 
tion, but  it  is  doubtful  if,  as  usually  given  (sodium  phosphate),  it  exercises 
any  virtues  other  than  those  attending  free  evacuation  of  the  bowels; 
quinine  hydrobromide  (the  neutral  salt)  to  the  point  of  toleration  for 
a  long  time  is  said  to  exert  beneficial,  even  curative,  properties.  In 
addition  to  sodium  phosphate  before  each  meal  and  a  blue  mass  pill 
twice  weekly,  Thomson  uses  intestinal  antiseptics,  such  as  sodium  sali- 
cylate and  sodium  benzoate,  of  each  10  grains  (0.6  gram)  one  hour  after 
each  meal,  and  a  capsule  of  naphthelene  3  grains  (0.2  gram)  and  sodium 
benzoate  6  grains  (0.4  gram)  at  bedtime;  phenol  bismuth  and  ammo- 
nium benzoate  also  are  used.  Iron  is  of  value  in  anemic  subjects.  Ergot, 
adrenalin,  electricity,  the  a^-rays,  etc.,  have  been  advocated  from  time  to 
time;  but  they  are  of  doubtful  value.  Iodine,  the  iodides,  and  thyroid 
extract  are,  as  a  rule,  harmful.  The  serum  of  thyroidectomized  dogs, 
sheep,  and  goats,  and  the  milk  of  thyroidectomized  goats,  and  extract  of 
the  thymus,  have  been  used  in  the  belief  that  they  contain  specific  anti- 
bodies; but  great  success  seems  not  to  have  attended  their  use.  The 
cytolytic  serum  of  Rogers  and  Beebe  seems  to  be  definitely  curative  in 
some  cases,  but  further  experience  in  its  use  is  desirable.  Surgical  treat- 
ment (resection  of  part  of  the  thyroid;  Hgation  of  the  superior  thyroid 
arteries)  is  indicated  in  patients  who  do  not  improve  under  well-directed 
medical  treatment,  including  rest,  in  from  three  to  six  months,  in  those 
who  become  progressively  worse  under  medical  treatment,  and  in  those 
with  signs  of  local  pressure. 


HYPOTHYROIDISM;    CRETINISM;    MYX OEDEMA. 

Deficiency  of  the  thyroid  secretion  (hypothyroidism,  athyrea),  may 
give  rise  to  one  of  three  conditions :  (1)  Cretinism;  congenital  or  acquired 
myxoedema  of  infants  and  children;  (2)  spontaneous  myxoedema  of 
adults;  and  (3)  postoperative  myxoedema. 

Cretinism. — Cretinism  is  a  disorder  due  to  lack  of  thyi-oid  secretion 
and  characterized  by  imperfect  development  of  the  body  and  the  mind. 
It  occurs  as  an  endemic  and  a  sporadic  aftection.  Endemic  cretinism 
is  common  in  endemic  goitrous  regions.  One  or  both  parents  may 
be  goitrous,  or  mildly  cretinoid;  although  if  both  parents  are  cretins 
the  marriage  is  usually  sterile.  The  thyroid  may  be  absent  or  small, 
sometimes  normal  in  size  or  enlarged;  the  epithelium  is  atrophic  and  the 
colloid  is  increased.  Sporadic  cretinism  occurs  in  non-goitrous  regions, 
and  may  result  from  aplasia  or  hypoplasia  of  the  thyroid,  thyroiditis  (infec- 


HYPOTHYROIDISM:   CRETINISM:   MYXCEDEMA  347 

tions  with  consecutive  sclerosis  or  destruction  of  the  thyroid  parenchyma). 
The  lesions  are  quite  the  same  as  those  of  endemic  goitre.  The  thymus 
often  persists. 

Symptoms. — Usually  toward  the  end  of  the  first  or  during  the  second 
year  arrest  of  bodily  and  mental  development  becomes  apparent  (in- 
fantile form);  occasionally  the  symptoms  are  delayed  for  several  years 
(juvenile  form),  although  they  always  appear  before  pul^erty;  but  the 
earlier  the  onset  the  more  marked  the  phenomena.  The  head  is  large, 
the  fontanelles  are  open,  the  forehead  is  low  and  broad,  the  nose  is 
flat,  the  mouth  is  usually  open,  the  lips  are  thick  and  through  them 
protrudes  a  thickened  tongue;  the  expression  is  stolid,  idiotic,  or  quite 
bestial.  The  body  is  stunted,  dwarfed,  the  limbs  and  the  neck  are  short 
and  thick,  the  skeletal  muscles  small  and  inefficient,  and  the  gait,  if  the 
child  walks  at  all,  weak  and  waddling;  and  the  abdomen  is  large  and  pro- 
tuberant. The  skin  is  pallid,  dry  (no  sweating),  thick,  inelastic,  and 
seemingly  edematous  (but  does  not  pit  on  pressure — myxoedematous) ; 
the  hair  is  thin  and  scanty,  the  nails  brittle,  and  the  teeth  carious.  The 
body  temperature  is  low,  the  pulse  infrequent,  and  metabolism  deficient. 
The  child  is  more  or  less  idiotic,  difficult  or  impossible  to  train;  speech 
is  often  limited  to  a  few  more  or  less  inarticulate  words;  deafness  may  be 
present;  the  genitals  are  retarded  or  do  not  develop  at  all.  Cretins 
may  live  forty,  fifty,  or  sixty  years. 

Diagnosis. — A  cretin  is  usually  recognizable  at  sight;  but  in  some 
cases  the  phenomena  are  not  marked  (semicretins;  moderate  hjqjo- 
thyroidism)  and  the  condition  may  be  overlooked.  Achondroplasia 
(foetal  rickets,  foetal  chondrodystrophy),  a  peculiar  form  of  dwarfism, 
may  be  distinguished  by  marked  shortening  of  the  extremities  (micro- 
melia),  great  enlargement  of  the  joints  (hyperplasia  of  the  cartilages), 
and  absence  of  myxoedema,  cretinoid  expression,  and  defective  mentality. 
Infantilism  is  characterized  by  an  infantile  condition  of  the  genitalia 
and  the  absence  of  secondary  sexual  characteristics,  but  there  is  no 
myxoedema  or  other  cretinoid  characteristics.  Idiocy,  hydrocephalus, 
etc.,  should  be  readily  distinguished. 

Prognosis. — The  disease  is  progressive  without  specific  treatment. 
Death  often  occurs  early  in  life,  but  if  the  subject  survives  a  few  years, 
life  may  be  prolonged  forty  or  more  years. 

Myxoedema  of  Adults. — Myxoedema  of  adults  is  a  disorder  occurring 
spontaneously  in  adults,  due  to  a  lack  of  thyroid  secretion,  and  character- 
ized by  myxoedema,  physical  weakness,  and  mental  deterioration.  The 
disorder  is  six  to  seven  times  as  common  in  women  as  in  men,  and  is 
most  common  in  adult  life  (thirtieth  to  the  fiftieth  year).  It  may  be 
hereditary  or  familial;  or  one  member  may  have  exophtlialmic  goitre 
and  another  myxoedema,  etc.  The  thyroid  is  usually  atro])liic  or  absent; 
if  of  normal  size  or  enlarged,  the  epithelium  is  atrophic  and  degenerated. 
The  thymus  and  the  pituitary  have  been  found  enlarged. 

Symptoms. — The  onset  is  usually  insidious.  The  patient  is  believed 
to])e  "taking  on  fiesh;"  but  the  skin  becomes  liarsli,  (h-y,  pale,  inelastic. 


348  DISEASES  OF  THE  THYROID  GLAHD 

thickened,  and  apparently  edematous  (but  does  not  pit  on  pressure 
— n'lyxoedema).  Thick  pads  of  such  tissue  may  develop  on  the  abdo- 
men, buttocks,  thighs,  supraclavicular  regions,  etc.  The  face  becomes 
broad,  swollen,  and  coarse,  the  lips,  nose,  and  tongue  thick,  and  the 
expression  dull  and  listless;  there  is  often  a  characteristic  flush  on  the 
cheeks.  The  gait  has  been  likened  to  that  of  a  hippopotamus.  Physical 
weakness  progresses  and  may  become  extreme;  and  to  this  is  joined 
mental  apathy,  slowness  of  thought  and  speech,  defective  memory, 
somnolence,  and  eventually  dementia  (which  may  be  preceded  by 
delirium,  mania,  etc.).  The  temperature  is  usually  subnormal.  There 
may  be  various  paresthetic  phenomena  or  actual  neuromuscular  pains 
(especially  in  the  calves);  undue  sensitiveness  to  cold;  arteriosclerosis 
with  hypertrophy  and  dilatation  of  the  heart;  indigestion  and  constipa- 
tion; albuminuria  or  glycosuria;  uterine  and  other  hemorrhages;  anemia, 
etc. 

Postoperative  Myxoedema.— Cachexia  strumipriva  is  a  myxoedema- 
tous  condition  with  the  attendant  physical  and  mental  deterioration  that 
develops  after  complete  and  sometimes  after  partial  removal  of  the 
thyroid  body.  The  amount  of  gland  necessary  to  prevent  this  form 
of  myxoedema  has  not  been  determined,  but  a  small  part,  less  than  one 
lobe,  usually  suffices.  The  symptoms  are  quite  the  same  as  those 
of  spontaneous  myxoedema  in  the  adult. 

Diagnosis. — Myxoedema  should  be  recognized  readily  by  attention  to 
all  the  phenomena,  cutaneous,  physical,  and  mental.  Obesity  should  be 
readily  excluded.  Bright's  disease,  suggested  by  the  pallor  and  sub- 
cutaneous swelling,  perhaps  albumin  and  casts,  should  be  readily  excluded 
by  the  absence  of  pitting  on  pressure,  and  by  the  thickness,  induration, 
and  dryness  of  the  skin,  loss  of  hair,  subnormal  temperature,  marked 
asthenia,  and  the  mental  phenomena.  Incomplete  or  mild  cases  are 
likely  to  be  overlooked,  being  mistaken  for  neurasthenia,  psychasthenia, 
senile  dementia,  etc. ;  but  careful  investigation  will  disclose  the  asthenia, 
the  mental  apathy,  the  myxoedematous  condition  of  the  skin,  the  small 
thyroid,  etc. 

Prognosis. — The  disease  is  steadily  progressive  in  the  absence  of 
specific  therapy. 

Treatment. — Deficiency  of  thyroid  secretion,  cretinism,  and  myxoedema 
are  imperative  indications  for  the  use  of  thyroid  preparations — a  specific 
treatment.  Usually  the  thyroid  of  sheep  is  used,  beginning  with  one 
grain  (0.06  gram)  thrice  daily  and  gradually  increasing  to  fifteen  grains 
(1  gram)  or  more  a  day  or  until  the  point  of  toleration  (thyroidism)  is 
reached  (nervousness,  cutaneous  flushing,  paresthesias,  muscular  twitch- 
ings  or  tremors,  tachycardia,  and  other  phenomena  suggesting  exoph- 
thalmic goitre).  The  eft'ects  are  inconceivable  to  those  unacquainted 
with  them.  After  cure  or  marked  improvement  has  been  effected  by 
large  doses,  smaller  doses  must  be  continued  to  insure  permanency  of 
results  and  prevent  relapse.  Good  food,  good  hygiene,  fresh  air,  hydro- 
therapy, and  tonics  (iron,  arsenic,  etc.)  are  useful  adjuvants. 


DISEASES  OF  THE  PARATHYROID  GLANDS  349 


TUMORS  AND  CYSTS  OP  THE  THYROID. 

Tumors  of  the  thyroid  may  be  benign  (?)  or  mahgnant — adenoma, 
carcinoma,  and  sarcoma.  An  adenoma  develops  as  a  solid,  encapsu- 
lated, usually  soft,  and  smooth,  growth  in  one  lobe  of  the  thyroid, 
compressing  the  normal  thyroid  tissue.  It  may  be  of  the  foetal  type — 
solid,  close  vesicles,  with  little  connective  tissue  stroma,  and  no  colloid; 
oi'  of  the  mixed  type — solid  vesicles  without,  and  large,  distended  vesicles, 
with  colloid;  or  of  the  papuliferous  cystic  type  —  cystic  vesicles  with 
papuliferous  ingrowths.  In  addition  to  cystic  formation  (softening)  these 
growths  are  prone  to  hemorrhage;  and  that  they  are  not  benign,  or  at 
least  do  not  remain  benign,  is  evident  in  the  fact  that  they  (especially 
the  papilliferous  cystadenoma)  may  give  metastases;  and  that  they  pro- 
ceed by  gradual  histological  variations  to  definite  carcinoma.  Sarcoma 
is  rare,  and  may  be  of  any  of  the  common  types.  As  a  rule,  tumors 
remain  for  a  considerable  time  unsuspected,  being  not  distinguished  (and 
often  indistinguishable)  from  simple  goitre  (hypertrophy);  but  malignant 
goitre  should  be  diagnosticated  in  unilateral  enlargements  in  adults, 
especially  if  the  growth  is  rapid  and  nodular.  The  diagnosis,  however, 
often  is  not  made  until  the  growth  has  penetrated  the  capsule,  formed 
adhesions  to  adjacent  tissue,  and  given  rise  to  metastases  to  the  regional 
lymph  nodes  or  to  distant  parts,  such  as  the  lungs  and  the  bones  (a 
solitary  bony  metastasis — inferior  maxilla,  skull,  sternum,  etc. — being 
quite  characteristic).  In  the  differential  diagnosis  one  must  exclude 
the  rare  large  solitary  tubercle  and  a  gumma. 

In  addition  to  the  softening  and  hemorrhagic  cysts  already  mentioned, 
the  thyroid  may  be  the  seat  of  echinococcus  cyst.  Aberrant  or  accessory 
thyroids  are  sometimes  encountered  at  the  base  of  the  tongue,  in  the 
mediastinum,  pleura,  etc.,  and  by  proliferation  may  give  rise  to  tumor 
formations. 


DISEASES  OF  l^HE  PAEATHYEOID  GLANDS. 

Pathological  Physiology. — The  parathyroid  glands  (or  bodies)  consist, 
as  a  rule,  of  two  pairs,  upper  and  lower  (four  glands,  sometimes  six  or 
eight),  somewhat  flattened  and  ovoid  in  shape,  from  6  to  S  mm.  long 
by  1  to  3  mm.  in  diameter,  situated  along  the  posterior  inner  edge  of  the 
lateral  lobes  of  the  thyroid.  The  physiological  activities  of  the  para- 
thyroids have  not  yet  been  completely  worked  out;  but  the  glands  seem 
to  be  essential  to  life  and  to  be  intimately  concerned  in  the  calcium  metab- 
olism. Operative  removal,  as  has  been  demonstrated  in  the  lower  animals, 
and  in  human  subjects  (unintentional  removal  or  deprivation  of  blood 
supply  when  removing  tlie  thyroid),  results  in  tetany— hypoparathyreosis 
or  cachexia  parastrumipriva  (Ilalsted).  The  phenomena  may  be  anieh- 
orated  by  feeding  parathyroid  preparations,  and  by  injections  of  calcium 


350      .  DISEASES  OF  THE  PARATHYROID  GLANDS 

salts;  and  they  may  be  prevented  by  autotransplantation  of  the  para- 
thyroids (Halsted).  The  parathyroids  are  doubtless  in  some  unknown 
way  related  to  the  other  ductless  glands  (through  the  medium  of 
hormones).  They  seem  also  to  exercise  some  influence  (antagonistic  to 
that  of  the  thyroid)  on  carbohydrate  metabolism:  following  extirpation 
of  the  parathyroids,  adrenalin  glycosuria  is  readily  produced,  that  is,  the 
limit  of  carbohydrate  metabolism  is  reduced. 

The  parathyroids  have  been  supposed  also  to  be  concerned  in  other 
convulsive  disorders,  such  as  epilepsy,  myoclonia,  myotonia,  paralysis 
agitans,  but  upon  insufficient  evidence.  Degeneration  and  sclerosis  of 
the  parathyroids  have  been  found  in  infantile  atrophy  (R.  L.  Thompson). 
Tumors  occasionally  occur.  Parathyroid  preparations  have  been  used 
with  success  in  parathyroid  insufficiency  (tetany);  and  without  success 
in  Graves'  disease,  mvx oedema,  convulsive  disorders,  etc. 


TETANY. 

Tetany  is  a  disorder  characterized  by  bilateral  tonic,  intermittent  or 
continuous  spasms  of  the  extremities,  and  increased  mechanical  and 
electrical  excitability  of  the  peripheral  nerves. 

Etiology. — Tetany  sometimes  occurs  endemically  or  epidemically 
in  certain  parts  of  Europe  (Berlin,  Vienna,  etc.),  but  it  is  rare  in  this 
country.  In  Europe  it  is  especially  common  in  young  men  of  the 
artisan  class,  such  as  shoemakers,  tailors,  etc.  It  sometimes  occurs 
in  infections,  such  as  typhoid  fever,  scarlatina,  measles,  cholera,  etc. ;  in 
intoxications,  such  as  chloroform,  lead,  and  ergotin  poisoning,  uremia, 
etc.;  in  gastro-intestinal  disorders,  such  as  dilatation  and  other  disorders 
of  the  stomach  with  retention;  and  in  pregnancy  and  during  lactation 
(nurse's  contracture.  Trousseau).  It  also  follows  operation  upon  and 
excision  of  the  thyroid  (removal  or  destruction  of  the  parathyroids). 
In  children  it  is  usually  associated  with  rickets,  but  sometimes  also  with 
acute  infections,  gastro-intestinal  disorders,  etc. 

The  nature  of  the  disorder  is  still  somewhat  imperfectly  understood, 
but  the  researches  of  McCallum  and  Voegtlin  and  others  suggest  that  it 
is  due  to  insufficiency  of  the  parathyroids  and  disturbance  of  the  calcium 
metabolism.  The  parathyroids  in  some  ill-understood  way  control 
the  calcium  exchanges  in  the  body,  and  the  absence  or  perversion  of 
the  parathyroid  secretion  leads  to  impoverishment  of  the  tissues  as 
regards  calcium,  perhaps  by  permitting  calcium  to  combine  with  other 
substances  and  thus  to  be  abstracted  from  the  tissues.  The  result  of  this 
calcium  impoverishment  is  h}^erexcitability  of  the  nerve  cells  and  tetany; 
so  that  tetany  may  be  regarded  as  a  state  of  hyperexcitability  of  the  nerve 
cells  due  to  calcium  impoverishment. 

Symptoms. — The  chief  symptom  consists  of  l)ilateral,  tonic,  painful, 
intermittent,  or  continuous  spasms  of  the  muscles  of  the  hands  (accou- 
cher's  hand),  and  less  frequendy  of  the  feet  (equinovarus  position); 


DISEASES  OF   THE  ADRENALS  351 

rarely  the  wrists,  arms,  face,  legs,  etc.,  may  be  involved.  There  is  also 
increased  mechanical  excitability  of  the  nerves:  tapping  the  facial, 
median,  ulnar,  perineal  nerves,  etc.,  serves  to  provoke  contracture 
(Chvostek's  sign);  and  compression  of  the  nerves  provokes  the  same 
result  (Trousseau's  sign).  The  attacks  continue  for  a  variable  time: 
in  children  often  only  an  hour  or  two,  in  adults  sometimes  for  a  week  or 
two — with  exacerbations  and  remissions.  There  is  also  increased 
electrical  excitability  of  the  nerves:  of  the  motor  nerves  to  the  galvanic 
current  (Erb's  sign),  of  the  sensory  nerves  (Hoffmann's  sign),  and  of  the 
nerves  of  special  sense  (F.  Chvostek's  sign).  The  sensorium,  as  a  rule, 
is  not  involved,  and  there  are  no  objective  sensory  changes.  In  severe, 
acute  cases  there  may  be  fever.  Laryngismus  stridulus  sometimes 
occurs  also  in  rickety  children. 

Diagnosis. — The  peculiar  bilateral  spasms  and  the  increased  mechan- 
ical and  electrical  excitability  of  the  nerves  are  quite  pathognomonic. 

Prognosis. — The  prognosis  varies  with  the  associated  conditions,  being 
serious  in  operative  tetany,  in  gastric  tetany,  and  in  laryngismus  stridulus. 

Treatment. — The  treatment  varies  with  the  etiological  factors.  In 
rickets,  infections,  and  intoxications,  the  treatment  is  that  of  the  imder- 
lying  cause.  Weaning  the  child  often  cures  the  cases  occurring  during 
lactation.  In  the  gastric  cases  lavage  with  saline  and  mild  antiseptic 
solutions  is  sometimes  efficacious.  In  operative  tetany  benefit  accrues 
from  the  use  of  parathyroid  preparations,  and  perhaps  also  from  the 
subcutaneous  transplantation  of  parathyroid  bodies.  The  acute  symp- 
toms are  effectively  controlled  by  the  intravenous  injection  (less  effec- 
tively by  the  subcutaneous  injection  or  ingestion)  of  5  per  cent,  solution 
of  calcium  lactate  (or  acetate),  in  physiological  saline  solution — 1000 
to  2000  c.c.  at  a  time;  magnesium  salts  also  may  be  used.  Chloral, 
bromides,  and  morphine  may  serve  as  useful  adjuvants. 


DISEASES   OF   THE    ADRENALS   AND    THE 
CHROMAFFIN  SYSTEM. 

Pathological  Physiology. — The  adrenals,  composed  of  readily  differen- 
tiated cortex  and  medulla,  are  partly  of  epithelial  and  partly  of  nervous 
origin.  The  cortex  in  all  probability  is  derived  from  the  coelum  epi- 
thelium; the  medulla  is  derived  from  the  sympathetic  nervous  system, 
and  consists  in  large  part  of  peculiar  polymorphous  cells,  wlu'ch  in  chromic 
acid  solutions  (chromic  acid  salts)  take  on  a  brownish  ])igmentation, 
and  are,  therefore,  spoken  of  as  chromaffin  cells.  Similar  cells  are  found 
elsewhere  in  the  sympathetic  nervous  system  and  its  derivatives — the 
ganglia  and  larger  nerve  trunks  of  the  symj)atheti(',  as  well  as  in  certain 
so-called  paraganglia,  especially  along  the  course  of  the  aorta  near  its 
bifurcation  (Zuckerkandl's  bodies),  the  carotid  glands,  the  coccygeal 
gland,  collection  of  cells  in  the  parovarium,  in  the  epididymis,  etc. — 


352  DISEASES  OF  THE  ADRENALS 

all  of  which  collectively  are  spoken  of  as  the  chromaffin  system.  Similar 
cells  have  been  found  also  in  aberrant  adrenal  rests  and  in  the  pituitary 
body. 

The  functions  of  the  adrenals  are  not  completely  known.  The  organ 
seems  to  be  essential  to  life;  removal  in  lower  animals  soon  leads  to  death 
in  the  picture  of  severe  intoxication.  The  cortex  is  believed  to  exercise 
a  detoxifying  function,  neutralizing  circulating  poisons  of  intermediate 
metabolism;  and  to  control,  at  least  in  part,  growth  and  development, 
especially  of  the  sexual  organs  (the  adrenals  of  animals  enlarge  during 
sexual  activity  and  pregnancy;  cortical  h^-perplasia  and  tumor  forma- 
tions are  sometimes  associated  with  precocious  sexual  development, 
and  h}'poplasia  with  retarded  sexual  development).  The  medulla 
and  the  chromaffin  system  throughout  the  body  contain  adrenalin, 
which  may  be  looked  upon  as  the  specific  product  of  the  chromaffin 
system.  Its  chief  function  is  the  maintenance  of  blood  pressure  (through 
its  stimulating  action  upon  the  vasoconstrictor  fibers  of  the  sympathetic) 
and  of  muscular  tone,  perhaps  by  furthering  oxidation  in  the  tissues. 
It  probably  exercises  some  influence  on  carbohydrate  metabolism,  since 
subcutaneous  or  intravenous  injections  give  rise  to  glycosuria.  The 
chief  evidence  of  disordered  function  is  cardiovascular  and  muscular 
asthenia  (adrenal  insufficiency),  which  is  most  marked  in  Addison's  dis- 
ease. Less  grades  of  such  asthenia  are  common  in  many  exhausting  and 
debilitating  diseases,  and  have  been  attributed  to  adrenal  insufficiency. 
Some  of  these,  such  as  pulmonary  tuberculosis,  gastric  carcinoma,  etc., 
may  be  associated  with  increased  cutaneous  pigmentation  (as  in  Addison's 
disease),  and  others,  such  as  neurasthenia,  etc.,  with  lov^'  blood  pressure. 
In  some  infections  (diphtheria)  and  other  disorders,  the  myasthenia 
may  come  on  suddenly  and  be  very  severe,  and  may  be  associated  with 
lessened  blood  pressure;  the  condition  may  be  relieved  by  adrenalin; 
in  some  fatal  cases  the  adrenals  have  been  found  lacking  in  adrenalin,  so 
that  a  condition  of  acute  adrenal  insufficiency  has  been  postulated. 
Less  severe  cases  are  spoken  of  as  subacute  and  chronic  adrenal  insuffi- 
ciency (incomplete  Addison's  disease).  ^Yhether  an  excess  of  adrenalin 
is  ever  formed  is  not  known,  but  the  well-known  fact  that  adrenalin 
provokes  arteriosclerosis  in  the  lower  animals  has  led  to  the  supposition 
that  it  may  be  active  in  the  causation  of  arteriosclerosis  in  man,  and  also 
to  the  suggestion  that  the  metabolic  products  retained  in  the  body  in 
renal  disease  stimulate  the  adrenal  medulla  to  increased  functional 
activity,  and  that  the  increased  adrenalin  thus  formed  is  the  cause  of 
the  excessive  blood  pressure.  Perhaps  through  some  other  influence 
an  excess  of  adrenalin  may  be  formed  (or  adrenalin  may  not  be 
excreted),  and  lead  not  only  to  the  heightened  blood  pressure,  but 
also  to  the  renal  and  cardiac  changes  of  chronic  cardiovascular-renal 
disease. 

Preparations  of  the  adrenal  (adrenalin)  injected  intravenously  or  sub- 
cutaneously  are  valuable  in  increasing  the  blood  pressure  in  shock  and 
conditions  of  low  vascular  tension  generally  (such  ^  infections,  intoxi- 


ADDISON'S  DISEASE  353 

cations,  etc.);  and  they  are  of  service  in  controlling  hemorrhages  from 
surfaces  to  which  they  can  be  applied  locally. 

Aside  from  Addison's  disease  and  tumor  formation,  the  adrenals  are 
rarely  the  seat  of  disease  of  clinical  interest.  Degenerative  changes 
(cloudy  swelling,  fatty  and  amyloid  degeneration)  accompany  similar 
conditions  in  other  organs.  Hemorrhages  occur  in  the  newborn  (espe- 
cially after  difficult  labors  and  still  births),  traumatisms,  toxic  and  infective 
processes.  They  may  give  rise  to  pain  in  the  upper  abdomen,  vomiting, 
collapse,  convulsions,  tympanites,  diarrhoea,  etc.,  and  death.  Tumors 
(hypernephromas)  partake  of  the  characteristics  of  retroperitoneal 
growths.  Tumors  of  adrenal  tissue  also  are  common  in  the  kidney 
(hypernephroma  being  the  most  common  tumor  of  the  kidney  in  the 
adult),  and  elsewhere  along  the  genito-urinary  (especially  the  female 
genital)  tract. 

ADDISON'S  DISEASE. 

Addison's  disease  is  a  disorder  due  to  adrenal  inadequacy  (hypo- 
epinephry)  characterized  anatomically,  as  a  rule,  by  tuberculosis  of  the 
adrenals  and  degenerative  lesions  in  the  chromaffin  system  elsewhere, 
and  clinically  by  muscular  and  vascular  asthenia,  gastro-intestinal 
irritability,  and  pigmentation  of  the  skin  and  mucous  membranes. 

Etiology. — The  disorder  is  most  common  in  young  adults  (before  the 
fortieth  year),  and  is  almost  twice  as  common  in  males  as  in  females. 
The  etiological  factors  are  those  of  tuberculosis  and  of  tumor  formation 
in  general,  and  are  as  ill  understood. 

Pathology. — -Usually  there  is  fibrocaseous  tuberculosis  of  the  adrenals 
— unilateral  or  bilateral;  less  commonly  there  is  simple  atrophy  with 
associated  fibrosis,  or  tumor  formation.  In  addition,  as  Wiesel  has 
pointed  out,  the  chromaffin  cells  of  the  sympathetic  nervous  system 
(adrenal  medulla,  abdominal  plexuses,  etc.)  disappear;  the  cortical 
substance  of  the  adrenals  may  be  preserved,  as  well  as  accessory 
adrenals,  if  any  be  found.  Many  of  the  ganglion  cells  exhibit  not 
only  the  lipochrome  pigmentation  (which  is  not  specific),  but  also 
the  specific  chromaffin  reaction  (characteristic  of  Addison's  disease). 
Wiesel  believes  Addison's  disease  to  be  a  specific  affection  of  the  chro- 
maffin system,  consisting  of  successive  atrophy  of  the  chromaffin  tissue, 
the  process  involving  the  adrenal  medulla  and  spreading  to  the  cortex; 
to  compensate  for  this  loss  of  chromaffin  tissue  some  of  the  ganglion  cells 
become  chromaffin.  The  cases  of  extensive  adrenal  tuberculosis  without 
clinical  signs  of  Addison's  di.'5ease  are  explained  on  the  basis  of  absence 
of  general  (listurl)ance  of  the  chromaffin  system;  and  the  cases  of  Addi- 
son's disease  without  disease  of  the  adrenal  are  believed  to  be  due 
probably  to  the  fact  that  lesions  of  the  chromaffin  system  outside  the 
adrenal  are  sufficient  to  produce  the  symptom-complex  of  the  disease. 

Symptoms. — The  following  is  adapted  from  Addison's  classical 
description:  The  patient  is  o})served  gradually  to  fall  off  in  general 
23 


354  DISEASES  OF  THE  ADRENALS 

health;  he  becomes  languid  and  weak,  indisposed  to  bodily  or  mental 
exertion;  the  appetite  becomes  impaired  or  entirely  lost;  the  whites  of  the 
eyes  become  pearly,  the  pulse  small  and  feeble,  or  perhaps  somewhat 
large,  but  excessively  soft  and  comprehensible;  the  body  wastes,  without, 
however,  presenting  the  dry  and  shrivelled  skin  and  extreme  emaciation 
usually  attendant  on  protracted  malignant  disease;  slight  pain  or  uneasi- 
ness is,  from  time  to  time,  referred  to  the  region  of  the  stomach,  and 
there  is  occasionally  actual  vomiting  which  may  be  both  urgent  and  dis- 
tressing; and  the  patient  may  manifest  indications  of  disturbed  cerebral 
circulation.  Gradually  a  characteristic  discoloration  of  the  skin  becomes 
apparent;  this  pervades  the  whole  surface  of  the  body,  but  is  commonly 
most  marked  on  the  face,  neck,  arms,  penis,  and  scrotum,  and  in  the 
flexures  of  the  axillae  and  around  the  navel;  it  presents  a  dingy  or  smoky 
appearance  or  various  tints  of  deep  amber  or  chestnut-brown;  it  may 
occur  in  patches,  or  certain  parts  may  be  so  much  darker  than  others  as 
to  impart  to  the  surface  a  mottled  appearance;  and  in  the  midst  of  this 
dark  mottling  certain  insular  portions  of  the  skin  may  present  a  blanched 
or  morbidly  white  appearance  (actual  defect  of  pigment),  contrasting 
strongly  with  the  surrounding  skin.  Similar  irregular  distribution  of 
pigmentation  may  occur  in  the  mucous  and  serous  membranes.  This 
singular  discoloration  usually  increases  with  the  advance  of  the  disease; 
the  anemia,  languor,  failure  of  appetite,  and  feebleness  of  the  heart 
become  aggravated;  the  body  wastes;  the  pulse  becomes  smaller  and 
weaker;  and  without  any  special  complaint  of  pain  or  uneasiness  the 
patient  gradually  sinks  and  expires. 

Diagnosis. — AJuscular,  vascular,  and  mental  asthenia,  pigmentation  of 
the  skin  and  \isible  mucous  membranes,  and  gastro-intestinal  symptoms 
(pain,  vomiting,  and  diarrhoea)  are  quite  diagnostic,  especially  when, 
as  stated  by  Addison,  "neither  the  most  diligent  inquiry  nor  the  most 
careful  physical  examination  tend  to  throw  the  slightest  gleam  of  light 
upon  the  precise  nature  of  the  patient's  malady."  The  maximum  blood 
pressure  may  be  100  mm.  Hg.  or  less.  The  blood  shows  the  ordinary 
changes  of  secondary  anemia  (which  excludes  pernicious  anemia).  Other 
sorts  of  pigmentation  must  be  excluded,  such  as  that  of  dark-skinned 
races;  pregnancy  and  disease  of  the  female  genitalia;  vagabond's  disease 
(pigmentation  of  exposed  parts;  rough  and  scratch-marked  skin;  often 
associated  pediculi);  pernicious  anemia;  Graves'  disease;  diseases  of 
the  stomach,  especially  carcinoma;  chronic  jaundice;  hemochromatosis 
(bronzed  diabetes);  chronic  malaria;  pellagra;  melanosarcoma  of 
the  skin;  chronic  poisoning  with  silver  nitrate  (argyria),  arsenic,  etc. 
It  is  wise  to  withhold  the  diagnosis  in  the  absence  of  asthenia.  In  case 
of  doubt  resort  may  be  had  to  tuberculin  tests,  but  positive  results  must 
be  interpreted  cautiously,  since  they  may  be  due  to  tuberculosis  else- 
where than  in  the  adrenals. 

Prognosis. — The  disease  is  doubtless  in\ariably  fatal.  The  common 
duration  is  about  three  or  four  years  from  the  onset  of  symptoms,  but 
this  may  be  influenced  by  tuberculosis  elsewhere  in  the  body.     Some- 


DISEASES   OF   THE   PITUITARY   BODY  355 

times  remissions  or  standstill  ensue  and  the  patient  may  live  ten  or 
more  years.  Rarely  there  are  what  are  called  acute  cases  (acute  adrenal 
inadequacy),  in  which,  with  marked  asthenia,  vomiting,  diarrhoea,  and 
the  p-eneral  evidences  of  severe  intoxication,  death  mav  ensue  within  a 
few  weeks. 

Treatment. — The  treatment  is  almost  wholly  symptomatic:  rest  in  bed 
on  account  of  the  astiienia  and  a  tendency  to  marked  and  perhaps  fatal 
syncope;  good  nutritious  diet — especially  milk;  strychnine  and  arsenic 
as  general  tonics;  bismuth,  creosote,  carbolic  acid,  cerium  oxalate,  dilute 
hydrocyanic  acid,  etc.,  for  the  gastro-intestinal  irritability.  The  use  of 
adrenal  preparations  by  the  mouth,  subcutaneously,  and  intravenously, 
is  indicated  theoretically;  practically  their  use  has  been  attended  by 
diverse  results :  they  seem  to  be  of  much  value  early,  in  doses  to  suit  the 
exigencies  of  individual  cases.  If  a  tumor  or  salivary  tubercle  of  the 
adrenal  can  be  diagnosticated  it  should  be  removed. 


DISEASES  OF  THE  PITUITAEY  BODY. 

Pathological  Physiology. — The  pituitary  body,  or  hypophysis  cerebri, 
is  composed  of  two  lobes — an  anterior,  the  larger,  of  epithelial  origin 
(a  diverticulum  of  the  buccal  epithelium),  and  a  posterior,  smaller, 
in  part  of  nervous  origin  (infundibular  pouch  of  the  thalamencephalon) 
and  in  part  of  epithelial  origin,  the  two  being  separated  by  a  persisting 
cleft.  The  physiological  properties  of  the  pituitary  body  have  not 
been  definitely  determined,  although  the  body  seems  to  be  essential 
to  the  maintenance  of  life.  The  posterior  lobe  (doubtless  the  nervous 
nucleus)  contains  a  blood-pressure-raising  substance  (pituitarin)  and 
a  diuresis-producing  substance  (increasing  the  blood  pressure  or 
acting  directly  on  the  renal  epithelium).  The  anterior  (perhaps  more 
important)  lobe  is  believed  to  exercise  some  influence  over  bodily  growth 
and  sexual  development.  Augmented  function  (hyperpituitarism),  such 
as  may  occur  in  hypertrophy  and  tumor  formations,  and  is  perhaps 
referable  to  increase  in  number  or  overactivity  of  the  chromophile  cells 
(less  likely  subactivity  of  the  chromophobe  cells),  seems  to  lead  to  gigant- 
ism if  it  occurs  during  early  life,  and  to  akromegaly  if  it  occurs  during 
adult  life.  Deficient  function  (hypopituitarism)  occurring  in  early  life 
seems  to  lead  to  certain  types  of  infuntilism  associated  with  excessive 
deposition  of  fat  and  imperfect  development  of  the  sexual  organs  and  of 
the  secondary  sexual  characteristics;  perhaps  the  loss  or  retrogression  of 
these  sexual  characteristics  in  adult  life  may  be  due  also  to  hypo-activity 
of  the  pituitary.  Removal  of  the  gland  in  lower  animals  has  led  to  the 
development  of  a  condition  comparable  to  that  believed  to  be  due  to 
hypopituitarism  in  man;  and  excision  of  the  enlarged  body  in  akro- 
megaly had  been  followed  by  notable  improvement  (Cushing).  The 
pituitary  also  bears  some  relationship  to  the  other  ductless  glands:  it 
has  been  found  enlarired  after  excision  or  disease  of  the  thvroid  and 


356  DISEASES  OF  THE  PITUITARY  BODY 

adrenal,  and  it  (especially  the  posterior  lobe)  is  said  to  contain  a  sub- 
stance (hormone)  that  stimulates  the  adrenal  and  inhibits  thyroid  activity, 
while  the  anterior  lobe  is  said  to  stimulate  thyroid  activity. 


AKROMEGALY. 

Akromegaly  is  a  disease,  probably  due  to  disordered  function  of  the 
pituitary  body,  and  characterized  by  abnormal  growth  especially  of  the 
face,  hands,  and  feet. 

Etiology. — Akromegaly  is  about  equally  common  in  the  two  sexes, 
and  is  most  common  in  the  third  decade  (75  per  cent,  of  the  cases);  it 
is  rare  before  the  twentieth  and  after  the  fortieth  year.  There  is  no 
known  cause,  ascribed  factors,  such  as  shock,  fright,  alcoholism,  syphilis, 
etc.,  being  of  more  than  doubtful  significance. 

Pathology. — ^The  majority  of  cases  exhibit  some  more  or  less  obvious 
disease  of  the  pituitary,  notably  tumor  formation  (adenoma,  carcinoma, 
sarcoma),  but  sometimes  softening,  hemorrhage,  and  fibrosis;  microscopic 
lesions  have  been  found  in  some  pituitary  bodies  normal  to  the  unaided 
eye.  The  bones  of  the  skull,  and  those  of  the  hands  and  feet,  especially, 
but  also  the  other  bones  of  the  body  to  a  greater  or  less  extent,  become 
enlarged,  thickened,  and  denser  than  normally.  The  enlargement  is 
due  to  periosteal  overgrowth,  and  involves  particularly  the  bony  promi- 
nences. The  soft  tissues  of  the  extremities  also  become  thickened — by 
connective  tissue  hyperplasia  and  fibrosis  (answerable  for  much  of  the 
enlargement).  The  other  ductless  gland  sometimes  shows  divers,  but 
no  constant,  changes.  The  viscera  (heart,  liver,  spleen,  kidneys,  etc.) 
are  sometimes  enlarged.  The  pancreas  may  be  fibrosed.  The  internal 
genitalia  may  be  enlarged,  but  the  testicles,  uterus,  and  ovaries,  usually 
are  atrophic  or  degenerated. 

Symptoms. — The  bony  enlargements  are  sometimes  the  earliest  symp- 
toms, but  in  the  majority  of  cases  antecedent  symptoms  referable  to  the 
overgrowth  of  the  pituitary  (brain  tumor)  may  be  elicited:  headache, 
vertigo,  vomiting,  mental  irritability  and  other  alterations,  disturbance 
of  the  special  senses  (sight,  hearing,  and  taste),  and  of  the  cranial  nerves 
(optic  neuritis,  oculomotor  and  other  paralyses).  These,  if  not  developed 
early,  are  likely  to  supen-ene  later.  In  addition  there  may  be  pares- 
thesias, more  or  less  severe  pains,  etc.,  in  the  extremities.  The  charac- 
teristic of  the  disease  is  abnormal  growth,  especially  of  the  face,  hands, 
and  feet — which,  although  much  enlarged,  are  not,  as  a  rule,  otherwise 
deformed.  The  head  increases  in  size,  but  less  so  than  the  face,  which 
in  consec[uence  of  marked  growth  of  the  superior  and  (especially)  the 
inferior  maxilla,  becomes  elongated.  The  teeth  become  separated,  from 
widening  of  the  alveolar  arches.  The  hands  and  feet  show  one  of  two 
types — the  long  or  the  thick  (spade-lilce,  sausage-like  fingers).  The 
hypertrophy  involves  also  the  soft  parts  of  the  hands  and  feet,  and  face 
(nostrils,  lips,  eyelids,  cheeks,  ear,  tongue,  etc.).    Later,  other  bones  (stev- 


AKROMEGALY  357 

num.  ribs,  vertebn^,  etc.)  may  become  involved,  and  kyphosis,  etc.,  may 
supervene.  The  skin,  in  general,  may  become  harsh,  dry,  and  thickened 
(perhaps  remotely  suggesting  myxuedema),  or  there  may  be  profuse 
sweats;  sometimes  also  the  mucous  membrane  of  the  mouth,  nose,  larynx, 
etc.,  becomes  thickened.  The  muscles  may  become  atrophic,  the  huge 
frame  and  bulk  of  the  subject  then  contrasting  markedly  with  the  general 
muscular  weakness.  Sexual  disorders  are  common — amenorrhoea  in 
women,  impotence  in  men.  Glycosuria  sometimes  supervenes.  Arterio- 
sclerosis and  hypertrophy  and  dilatation  of  the  heart  are  common. 
The  viscera  (liver,  spleen,  and  kidneys)  may  become  enlarged,  and 
the  lymph  nodes  and  the  thymus  may  become  palpable. 

Diagnosis. — The  disease  is  usually  recognized  on  sight.  Especial 
attention  should  be  paid  to  bitemporal  hemianopsia,  optic  neuritis  or 
atrophy,  oculomotor  paralyses,  and  other  symptoms  of  tumor  in  the 
sella  turcica,  as  early  signs.  Gigantism,  osteitis  deformans,  and  hyper- 
trophic pulmonary  osteo-arthropathy  must  be  differentiated. 

Prognosis. — The  disorder  is  progressive,  but  often  lasts  for  many 
(twenty  or  more)  years.  Death  results  from  general  asthenia,  secondary 
infection,  brain  tumor,  cardiac  weakness,  diabetes,  etc. 

Treatment.— There  is  no  known  efficacious  medical  treatment.  Oper- 
ative removal  of  at  least  a  part  of  the  enlarged  pituitary  appears  to  be 
the  treatment  of  the  future;  it  has  already  been  successfully  done  with 
benefit  by  Gushing. 


SECTION  V. 

DISEASES  OF  THE  BLOOD  AND  HEMOPOIETIC 

SYSTEM. 


Pathological  Physiology. — ^The  blood  is  a  tissue  as  well  as  a  fluid — a 
tissue  reflecting  the  state  and  condition  of  the  so-called  hemopoietic 
organs,  of  which  it  is  the  circulating  portion;  and  a  fluid  containing  the 
soluble  products  of  the  metabolic  activities  of  all  the  component  parts  of 
the  body.  Morphologically  it  is  of  comparatively  simple  constitution,  con- 
sisting of  erythrocytes,  leukocytes,  platelets,  and  plasma;  but  chemically 
it  is  of  exceedingly  complex  composition.  It  subserves  primarily  the  func- 
tion of  conveying  to  the  body-cells  oxygen  and  absorbed  food  products, 
essential  to  their  life  and  well  being,  and  of  receiving  and  disposing  of  the 
products  of  cellular  activity,  whether  these  be  refuse  or  of  further  use  in 
the  economy;  but,  in  addition,  the  blood  is  charged  with  another  most 
important  function — that  of  defense  against  divers  infectious  and  toxic 
processes  to  which  the  body  is  constantly  exposed.  Thus,  it  represents 
the  sum  total  of  the  activity  and  inactivity,  the  anabolism  and  katabolism, 
and  normal  and  perverted  function  of  all  the  tissues  and  organs  of  the 
body,  of  which  it  is  the  connecting  link. 

So  subject  is  the  composition  of  the  blood  to  the  influences  of  extra- 
circulatory  conditions  that  disorders  of  the  blood  must  be  largely,  if  not 
wholly,  merely  a  reflection  of  diseased  processes  elsewhere.  Is  the  body 
anywhere  diseased,  so  also  is  the  blood;  divers  toxic  processes,  such  as 
accompany  infections,  intoxications,  and  disorders  of  metabolism,  like 
diabetes,  gout,  uremia,  etc.,  are  in  a  sense  disorders  of  the  blood:  so 
that  one  may  well  doubt  whether  the  blood  is  ever  primarily  diseased. 
In  a  general  sense  also  one  may  say  that  the  hemopoietic  system  com- 
prises all  the  tissues  and  organs  of  the  body,  since  each  contributes  its 
moiety  to  the  composition  of  the  whole.  But  since  custom  and  con- 
venience sanction  a  separate  discussion  of  disorders  in  which  changes 
in  the  blood  are  noteworthy,  so  also  they  sanction  restriction  of  the 
term  hemopoietic  organs  to  those  concerned  in  the  ])r()(hicti()n  of  (lie 
formed  elements  of  the  blood. 

In  the  foetus  this  hemopoietic  system  consists  of  the  bone  marrow,  the 
lymph  nodes,  the  spleen,  and  the  liver,  and  there  is  no  sharj)  line  of 


360  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

differentiation  between  the  tissues  producing  erythrocytes,  on  the  one 
hand,  and  leukocytes,  on  the  other.  At  birth  the  Hver  has  lost  its  blood- 
forming  function;  and  as  growth  continues  the  other  hemopoietic  organs 
gradually  become  specialized,  so  that  in  adult  life  the  erythroblastic 
and  the  leukoblastic  tissues  are  sharply  differentiated,  although  under 
the  stress  of  circumstance  they  may  revert  to  the  foetal  type.  In  adult 
life  the  erythrocytes  are  formed  in  the  red  marrow  of  the  bones  by  divi- 
sion or  loss  of  the  nuclei  of  the  erythroblasts,  which  in  turn,  perhaps,  are 
derived  from  colorless,  mononuclear,  non-granular  mother  cells  that 
take  on  hemoglobin;  it  is  believed  that  in  some  diseased  states  the  hemo- 
lymph  nodes  also  may  form  erythrocytes.  The  granular  leukocytes  are 
formed  in  the  bone  marrow,  being  derived  from  certain  mononuclear 
neutrophilic,  eosinophilic,  or  basophilic  cells,  which  in  the  course  of  time, 
and  usually  before  they  enter  the  circulation,  develop  polymorphous 
nuclei,  and  give  rise  to  the  polynuclear  neutrophiles,  eosinophiles,  and 
basophiles  (so-called  mast-cells)  of  the  circtilating  blood.  The  origin 
of  the  so-called  mononuclear  leukocytes  is  still  in  dispute,  although  the 
weight  of  evidence  assigns  them  to  the  bone  marrow;  perhaps  they  are 
mother  cells.  The  lymphocytes  are  formed  in  the  lymph  nodes,  thymus, 
tonsils,  and  lymphoid  tissues  generally  throughout  the  body.  In  the 
central  portions  of  the  so-called  germ  centres,  where  proliferation  is  active, 
the  cells  are  large  and  correspond  with  the  large  lymphocytes  of  the  cir- 
culating blood,  but  toward  the  periphery  of  the  germ  centres,  the  cells 
are  smaller  and  correspond  with  the  ordinary  small  lymphocytes  of  the 
circulating  blood.  Wliether  any  circulating  lymphocytes  are  formed  in 
the  bone  marrow  in  health  is  not  definitely  known,  although  it  seems 
likely;  but  in  diseased  states,  such  as  leukemia,  the  marrow  contributes 
large  numbers  of  so-called  lymphocytes — probably  not  identical  with  the 
circulating  lymphocytes  of  health.  There  is  considerable  evidence  that 
both  the  red  and  the  white  cells  are  derived  from  a  common  ancestor — a 
large  mononuclear,  non-granular,  somewhat  basophilic  marrow  cell; 
but  when  once  started  on  their  life  journey,  cells  of  the  one  series  cannot 
become  converted  into  the  other.  The  blood  platelets,  according  to 
the  studies  of  J.  H.  Wright,  are  formed  by  detachment  of  the  pseudo- 
pod-like  processes  of  the  giant  cells  (megakaryocytes)  of  the  bone  marrow. 
The  erythrocytes  are  designed  to  absorb  and  diffuse  oxygen  and  per- 
haps carbon  dioxide — their  sole  known  function — which  they  effect  by 
reason  of  their  contained  hemoglobin,  and  for  which  their  flexibility 
and  biconcave  surface  admirably  adapts  them.  The  functions  of  the 
leukocytes  are  ill  understood:  endowed  with  independent  motility, 
they  appear  to  be  concerned  in  the  absorption  of  fat  and  protein  from 
the  intestine  and  in  other  nutritive  (cellular)  processes;  they  contribute 
to  the  clotting  of  blood  by  producing  fibrin  ferment,  thrombokinase;  they 
produce  also  apparently  a  fat-splitting  and  a  tryptic  ferment;  they 
facilitate  the  repair  of  injuries;  they  are  especially  concerned  in  various 
defensive  processes  (phagocytosis)  whereby  the  body  is  enabled  to  resist 
bacterial  invasion;  and  they  act  as  scavengers  in  removing  animate  and 


ANEMIA  361 

inanimate  foreign  substances  that  act  as  sources  of  irritation.  But  their 
function  is  doubtless  more  comprehensive.  Tlie  polynuclear  leukocytes 
are  those  especially  concerned  in  phagocytosis;  the  eosinophiles,  while 
non-phagocytic  are  especially  concerned  in  parasitic  infections;  the 
mast-cells  and  the  lymphocytes  also  doubtless  have  specific  functions, 
although  they  are  unknown.  The  blood  platelets  are  much  concerned  in 
coagulation  of  the  blood  (whence  they  have  been  termed  thrombocytes) ; 
they  are  diminished  in  conditions,  such  as  pernicious  anemia,  purpura, 
typhoid  fever,  etc.,  in  which  clotting  is  poor  and  the  bone  marrow 
deficient  in  megakaryocytes. 

The  blood  doubtless  varies  considerably  in  composition  from  time  to 
time  under  various  influences,  but  the  remarkable  fact  is  its  tendency 
to  maintain  a  uniform  composition  under  many  and  varied  conditions. 
Normally  the  erythrocytes  number  about  5,000,000  to  the  cubic  milli- 
meter in  man,  and  4,500,000  in  women;  the  leukocytes,  6000  to  10,000 
(averaging  about  7500);  and  the  platelets,  200,000  to  700,000.  The 
plasma  also  tends  to  maintain  a  uniform  composition  by  the  excretion 
of  deleterious  substances  through  the  kidney,  skin,  and  lungs,  and,  as 
occasion  demands,  absorbing  from  or  discharging  into  the  lymph 
channels  some  of  its  substance. 

The  circulating  blood  corpuscles  are  believed  to  enjoy  only  a  brief  life 
career.  The  erythrocytes  are  credited  with  an  average  life  of  three  or 
four  weeks,  but  this^  is  not  susceptible  of  proof.  They  probably  gradu- 
ally succumb  to  the  stress  of  a  strenuous  existence,  and  are  finally  com- 
pletely destroyed  in  the  spleen  and  liver,  perhaps  even  in  the  vascular 
channels,  and  at  least  in  certain  diseased  states  in  the  hemolymph 
nodes.  The  life  span  of  the  leukocytes  is  not  known;  they  are  believed 
to  succumb  even  earlier  in  circulatory  life  than  the  erythrocytes,  and 
to  find  their  campo  santo  in  the  spleen. 

Anemia. — What  otherwise  would  be  an  early  dearth  of  blood  corpuscles 
is  prevented  by  continued  new  formation.  This,  which  suffices  in  health 
to  maintain  a  uniform  standard,  may  prove  insufficient  in  disease,  or  it 
may  fail  entirely.  The  ensuing  corpuscular  deficiency  is  spoken  of  as 
anemia,  a  term  that  properly  comprises  a  lessening  of  the  total  volume 
of  the  blood  or  a  deficiency  of  any  one  of  its  constituent  elements, 
corpuscles,  hemoglobin,  or  albuminous  and  other  constituents  of  the 
plasma.  Changes  in  the  plasma,  however,  are  ill  understood,  and  while 
in  some  cases  they  probably  are  of  prime  importance,  clinically  our 
attention  is  practically  always  directed  to  the  corpuscles  and  the 
hemoglobin. 

Anemias  are  commonly  divided  into  the  primary  and  the  secondary 
anemias.  Strictly  speaking  all  anemias  are  secondary,  that  is,  the  con- 
sequence of  some  underlying,  though  often  overlooked,  or  unknown, 
cause.  Since,  however,  the  cause  of  some  anemias  cannot  be  ascer- 
tained, we  may  continue  provisionally  the  designation  primary,  essential, 
or  idiopathic  anemia.  These  comprise  chlorosis  and  pernicious  anemia. 
Splenic    anemia,   leukemia,   and    Hodgkin's   disease,    sometimes  here 


362  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

included,  are  not  in  any  sense  primary  anemias.  Secondary  or  symp- 
tomatic anemias,  those  due  to  obvious  causes,  are  further  divided, 
according  to  their  course,  into  acute  and  chronic. 

Anemia  may  be  brought  about  by:  (1)  Hemorrhage;  (2)  lessened 
corpuscular  production  (deficient  hemogenesis)  ;  or  (3)  increased  destruc- 
tion (increased  hemolysis);  that  is,  by  the  loss  of  a  considerable  volume 
of  blood  or  by  causes  that  injure  either  the  hemopoietic  tissues  or 
the  corpuscles  after  they  have  been  formed.  Although  deficient  hemo- 
genesis is  perhaps  at  the  basis  of  chlorosis,  the  majority  of  cases  of 
anemia  result  from  increased  hemolysis,  to  which,  in  cases  of  long-con- 
tinued or  very  severe  anemia,  defective  and  deficient  hemogenesis  may 
be  added.  The  hemolysis  may  be  induced  by:  (1)  Bacterial  toxins;  (2) 
chemical  poisons;  (3)  cellular  and  other  hemolysins;  (4)  the  action  of 
heat  (burns)  and  of  cold  (paroxysmal  hemoglobinemia) — which  either 
kill  the  erythrocytes  outright  or  injure  the  enveloping  elastic  membrane 
and  permit  the  diffusion  of  the  contained  hemoglobin  into  the  plasma 
(hemoglobinemia).  Similar  results  may  ensue  from  changes  in  the  pro- 
tein composition  of  the  plasma,  and  from  changes  in  the  molecular  con- 
centration (electrolytic  conductivity  by  means  of  ions)  of  the  plasma 
and  consequent  changes  in  osmotic  tension.  A  plasma  too  rich  or  too  poor 
in  salts  (ions)  leads  to  shrinkage  or  swelling  of  the  erythrocytes  and  loss 
of  hemoglobin.  The  hemoglobin  set  free  in  the  plasma  is,  as  a  rule, 
speedily  removed  by  the  spleen  and  liver,  but  in  some  cases  (occasionally 
in  malaria,  paroxysmal  hemoglobinemia,  etc.),  the  hemolysis  occurs  so 
rapidly  and  to  such  an  excessive  degree  that  the  liver,  spleen,  bone 
marrow,  etc.,  are  unable  successfully  to  cope  with  it  and  hemoglobinuria 
results.  The  hemoglobin  may  become  converted  into  methemoglobin, 
either  in  the  cells  or  in  the  plasma.  The  consequences  of  anemia  are 
obvious — reduction  in  the  oxygen-carrying  capacity  of  the  blood  and 
insufficient  nutritive  supply  to  the  organs,  particularly  the  brain  and 
the  heart.  The  factors  inducing  the  anemia  may  or  may  not  implicate 
the  leukoblastic  tissues,  so  that  the  white  corpuscles  may  remain  normal, 
or  they  may  become  increased  (leukocytosis),  or  diminished  (leukopenia). 

Following  anemia — ^whatever  its  cause — regeneration  of  the  corpuscles 
usually  begins  immediately,  and  it  proceeds,  sometimes  slowly,  some- 
times remarkably  rapidly — the  rate  depending  apparently  upon  the 
nature  of  the  stimulus  and  the  vitality  of  the  erythroblastic  and  leuko- 
blastic tissues.  Whatever  the  nature  of  the  stimulus  (infectious,  toxic, 
chemotactic),  it  results  at  first  in  the  discharge  into  the  circulation  of  the 
already  formed  and  warehoused  mature  cells — normal  erythrocytes, 
polynuclear  leukocytes,  etc.  Should  these  not  suffice  to  restore  and 
maintain  the  normal  balance,  more  or  less  immature  cells  appear  in  the 
circulation — erythrocytes  variable  but  rather  small  in  size,  distorted  in 
shape,  poor  in  hemoglobin,  some,  perhaps,  nucleated  and  exhibiting 
polychromatophilia  (evidence  likely  of  immaturity  rather  than  senility), 
and  leukocytic  antecedents  of  the  polynuclear  neutrophiles.  The  appear- 
ance of  such  cells  in  the  circulating  blood,  then,  is  to  be  interpreted  as  an 


PLETHORA   AND  POLYCYTHEMIA  363 

effort  on  the  part  of  the  bone  marrow  to  supply  a  deficiency.  Under  tliese 
circumstances  the  erythroblastic  (red)  centers  in  the  bone  marrow  have 
become  hyperplastic,  have  encroached  upon  and  replaced  more  or  less  of 
the  fatty  (yellow)  marrow  of  the  long  bones.  In  the  more  severe  tvpes 
of  anemia,  represented  by  the  several  varieties  of  pernicious  anemia,  in 
addition,  to  the  foregoing,  megalocytes  and  megaloblasts  appear  in  the 
circulation  in  considerable  number,  and  the  bone  marrow  reverts  to  the 
foetal  or  juvenile  type  (megaloblastic  degeneration,  Ehrlich);  that  is, 
although  red,  as  in  milder  anemias,  it  contains  many  large  cells — meg- 
alocytes and  megaloblasts.  This  is  interpreted  as  evidence  of  overstrain 
and  consequent  inefficient  effort  to  replace  lost  cells — the  production  of 
cells  of  the  foetal  life  (metaplasia  of  the  erythroblastic  tissue) .  In  some 
cases  the  bone  marrow  ultimately  becomes  incapable  of  supplying  the 
demand;  it  may  become  exhausted,  or  its  activity  may  be  inhibited  by 
the  initiating  infectious,  toxic,  or  other  cause,  and  complete  cessation  of 
its  function  may  ensue  (aplastic  anemia) :  the  bone  marrow  becomes  pale, 
yellowish,  or  fatty  throughout.  In  some  cases  the  stimulus  to  activity 
involves  the  leukoblastic  rather  than  the  erythroblastic  tissues,  and 
leukocytosis,  leukemia,  etc.,  result.  In  other  cases  inhibition  of  leuko- 
blastic activity  and  leukopenia  ensue,  as  in  some  anemias,  typhoid  fever, 
cachexias,  intoxications,  etc.  In  leukemia  and  occasionally  in  other 
conditions  (infections),  the  entire  hemopoietic  system  (bone  marrow, 
spleen,  lymph  nodes,  even  the  liver)  may  revert  to  the  foetal  type,  and 
cells  indistinguishable  from  bone-marrow  cells  may  be  formed  in  the 
spleen,  lymph  nodes,  etc.  Many  of  these  cells  partake  of  the  undif- 
ferentiated, perhaps  ancestral  type.  In  lymphatic  leukemia  the  normal 
granular  series  of  bone-marrow  cells  may  entirely  disappear.  In  some 
cases  the  stimulus  to  activity  is  not  specific,  at  least,  not  in  its  entirety, 
and  both  the  erythroblastic  and  the  leukoblastic  tissues  may  be 
involved,  as  is  exemplified  in  the  occurrence  of  cells  of  the  leuko- 
blastic series  in  some  cases  of  severe  anemia  (ordinary  pernicious 
anemia,  leukanemia),  and  the  marked  reduction,  if  not  total  absence, 
of  the  leukocytic  (granular,  bone-marrow)  cells  in  cases  of  aplastic 
anemia,  etc. 

Plethora  and  Polycythemia. — An  increase  in  the  total  volume  of  blood 
(so-called  plethora)  was  formerly  much  believed  in,  but  its  existence  is, 
at  least,  doubtful.  One  may  suspect  such  a  condition  in  a  person,  u.'iually 
a  man,  who  eats  too  much  and  drinks  too  much  (especially  alcohol),  who 
is  large  in  muscle  and  round  in  fat,  who  exhibits  general  cutaneous 
hyperemia  and  dilated  venules  of  the  face,  and  whose  heart  perhaps  is 
large  and  arteries  full  and  bounding.  A  serous  plethora  lias  l)een  found 
to  be  common  in  chlorosis.  More  commonly  there  is  an  increased 
number  of  erythrocytes  in  a  measured  amount  of  blood  (polycythemia) : 
physiologically  in  the  newborn,  and  at  high  altitudes  in  conse(iuence  of 
lowered  atmospheric  pressure  and  consequent  increased  peripheral  dis- 
tribution; ayd  pathologically,  in  congenital  heart  disease,  in  ac(|uired 
heart  and  pulmonary  disease  attended  with  blood  stasis,  in  erythremia 


364  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

with  splenomegaly,  and  in  cholera  and  odier  diseases  in  which  the  blood 
may  become  inspissated. 

Leukocytosis. — ^At  birth  the  number  of  leukocytes  varies  from  about 
14,000  to  19,000  per  cubic  millimeter;  gradually  the  number  diminishes, 
so  that  in  adult  life  they  average  about  7500,  the  normal  limit  being 
usually  set  down  as  from  6000  to  10,000.  They  vary  somewhat  in  the 
same  individual  from  time  to  time.  Under  divers  circumstances  the  num- 
ber may  be  increased  beyond  the  normal  limits,  a  condition  spoken  of  as 
leukocytosis — which  usually  is  temporary,  but  may  last  for  some  con- 
siderable time  (subacute  or  clironic  leukocytosis).  In  the  short-duration 
cases  the  increased  niunber  of  leukocytes  is  derived  mainly  from  already 
formed  cells  resting  or  awaiting  a  summons  in  the  sinuses  of  the  bone 
marrow  and  the  capillaries  of  the  liver  and  lung;  but  in  the  long-duration 
cases  new  formation  occurs  and  the  bone  marrow  exhibits  leukoblastic 
changes.    Leukocytosis  may  be  physiological  or  pathological. 

Physiological  Leukocytosis. — An  increased  number  of  leukocytes  is 
normal — at  and  for  some  time  after  birth;  during  the  latter  part  of 
pregnancy  and  parturition;  after  a  cold  bath,  exercise,  and  massage; 
and  during  digestion,  particularly  of  a  meal  rich  in  protein.  It  is  doubt- 
ful whether  under  any  of  these  circumstances  any  new  formation  occurs ; 
probably  there  is  only  a  redistribution  of  leukocytes  already  formed. 
The  increase  is  scarcely  if  ever  more  than  one-third  of  the  normal,,  and 
the  relative  proportion  of  the  different  varieties  of  leukocytes  remains 
unchanged. 

Pathological  leukocytosis  may  be  due  to:  (1)  Infections,  especially 
those  associated  with  an  inflammatory,  purulent  exudation.  In  these 
cases  it  is  attributed  to  chemotactic  influences,  and  there  is  probably  a 
new  formation  of  leukocytes.  The  absence  of  leukocytosis  in  some  infec- 
tions is  notable — typhoid  fever,  malaria,  measles,  rotheln,  influenza, 
mumps,  early  stages  of  tuberculosis  (except  meningeal  form),  and  leprosy. 
(2)  Zooparasitic  invasions,  especially  trichinosis,  uncinariasis,  filariasis, 
echinococcosis,  etc.  (3)  Intoxications,  such  as  illuminating  gas  pois- 
oning, uremia,  etc.  (4)  The  cachexias  of  malignant  disease  and  other 
marantic  states.  (5)  Hemorrhage.  (6)  Terminal  or  preagonal  states,  (7) 
Certain  drugs.  The  number  of  leukocytes  usually  varies  between  15,000 
and  30,000;  occasionally  it  may  reach  upward  of  50,000,  and  very  rarely 
even  upward  of  100,000.  Although  usually  there  is  an  increase  of  all  forms 
of  leukocytes,  there  is,  in  contrast  to  physiological  leukocytosis,  usually 
also  a  disproportionate  or  so-called  relative  increase  in  some  one  of  the 
types,  so  that  one  speaks  of  polynuclear  leukocytosis,  large  mononuclear 
leukocytosis,  lymphocytosis  (lymphemia),  eosinophilia,  basophilia,  and 
myelocytosis  (myelemia).  Myelocytosis  aside  from  myeloid  leukemia  is 
a  rare  occurrence;  but  a  small  percentage  of  myelocytes  is  occasionally 
seen  in  certain  infections  and  more  or  less  severe  anemias,  especially  in 
children.  Basophilia  also  is  a  rare  and  ill-understood  condition;  it  occurs 
in  myeloid  leukemia  and  rarely  in  certain  parasitic  infections.  Eosino- 
philia (5  to  30  per  cent,  of  the  total  number  of  leukocytes)  is  a  significant 


ACUTE  SECONDARY  ANEMIA  365 

diagnostic  sign  of  parasitic  infections  (trichinosis,  uncinariasis,  filariasis, 
ecchinococcosis,  bilharziosis,  etc.);  it  occurs  also  in  certain  skin  disorders 
(urticaria,  pemphigus,  psoriasis,  pellagra,  purpura,  etc.),  in  bronchial 
asthma,  in  myelocytic  leukemia,  in  certain  inflammatory  exudates,  etc. 
Lymphocytosis  (a  relative  and  absolute  increase  in  the  number  of  circu- 
lating lymphocytes)  is  normal  in  the  infant;  it  is  especially  conspicuous 
in  pertussis,  and  sometimes  occurs  in  syphilis  and  certain  forms  of 
septicopyemia  attended  with  lymph-node  involvement;  and  it  is  the 
characteristic  feature  of  lymphocytic  leukemia.  A  large  mononuclear 
leukocytosis  (relative)  sometimes  occurs  in  malaria.  The  polynuclear 
neutrophilic  leukocytosis  is  the  most  common  and  most  important  form ; 
it  occurs  especially  in  infectious  inflammations  with  or  without  suppura- 
tion. Significance  attaches  not  only  to  an  increase  in  the  total  number  of 
leukocytes,  but  also  to  a  relative  increase  (80  to  95  per  cent.)  of  the  poly- 
nuclear neutrophiles,  even  when  the  total  number  of  leukocytes  is  only 
slightly  above  the  normal.  The  following  opinions  seem  warranted: 
(1)  An  early  and  marked  polynuclear  leukocytosis  is  usually  significant 
of  good  resistance  to  a  more  or  less  severe  infection;  (2)  persistence  or 
increase  in  the  leukocytosis  is  significant  of  continued  good  resistance; 
(3)  a  slight  total  leukocytosis,  or  a  relative  polynuclear  neutrophilic 
leukocytosis,  may  mean  only  a  minor  infection,  or  a  severe,  perhaps 
fulminating  infection,  against  which  the  forces  of  resistance  are  more  or 
less  incapable  of  contending;  (4)  a  delayed  and  then,  perhaps,  only 
moderate  leukocytosis  usually  means  a  more  or  less  severe  infection 
and  deficient  resistance;  (5)  a  high  leukocytosis  with  increasing  toxic 
manifestations,  while  signifying  good  resistance,  does  not  preclude  the 
possibility  of  ultimate  exhaustion  of  all  the  body  forces,  including  the 
powers  of  resistance  as  represented  in  part  by  the  leukocytosis;  (6)  a 
moderate  or  high  relative  (as  well  as  absolute)  polynuclear  leukocytosis, 
while  often  significant  of  suppuration,  is  more  properly  indicative  of 
severity  of  infection  which  may  or  may  not  lead  to  suppurative  exudation, 
depending  upon  the  associated  phenomena;  the  diagnosis  of  suppuration 
should  be  made  upon  all  the  clinical  evidence,  and  not  upon  one  sign 
(the  leukocytosis)  alone. 


ACUTE  SECONDARY  ANEMIA. 

Etiology. — ^Acute  secondary  anemia  is  almost  always  due  to  hemor- 
rhage, either  external  or  internal,  spontaneous  or  traumatic;  in  degree 
it  usually  corresponds  with  the  rapidity  and  the  total  volume  of  blood 
lost.  In  rare  cases  acute  anemia  results  from  bacterial  infection  or 
intoxication,  though  these  usually  lead  to  subacute  or  chronic  anemia. 
Infectious  diseases,  such  as  typhus,  malaria,  and  typhoid  fevers,  and 
certain  forms  of  sepsis,  especially  puerperal  sepsis,  and  poisoning  by 
nitrobenzol  and  other  substances  that  rapidly  destroy  the  blood  (hemo- 
lysis), sometimes  result  in  very  acute  anemia. 


366  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

Pathology. — After  death  from  very  severe  hemorrhages  one  usually 
finds  fatty  degeneration  of  the  viscera,  especially  the  heart  muscle,  the 
liver,  the  kidneys,  and  the  stomach,  and  sometimes  hyperplasia  of  the 
erythroblastic  tissue  of  the  bone  marrow^. 

Symptoms. — The  symptoms  of  acute  anemia  consist  of  pallor  of  the 
skin  and  visible  mucous  membranes;  increased  frequency  of  the  heart 
beat,  anemic  murmurs,  and  smallness  and  emptiness  of  the  pulse;  cool- 
ness of  the  extremities,  and  generally  low  body  temperature;  marked 
dyspnoea  in  consequence  of  the  marked  diminution  in  the  oxygen- 
carrying  constituent  of  the  blood;  thirst;  evidences  of  cerebral  anemia, 
such  as  faintness,  spots  before  the  eyes,  noises  in  the  ears,  vertigo,  nausea, 
vomiting,  fibrillary  tremors,  and  perhaps  convulsions  (in  extreme  cases). 
The  amount  of  blood  lost  in  some  cases  is  extreme  (rupture  of  an  aneu- 
rysm, ectopic  pregnancy,  etc.),  and  may  lead  immediately  to  death 
from  acute  asphyxia  and  anemia  of  the  brain ;  but  many  patients  survive 
very  great  and  sudden  losses — perhaps  one-half  of  the  total  volume  of 
blood.  If  not  sudden,  the  loss  of  blood  may  be  even  greater,  and  the 
patient  survive — repeated  hematemesis,  hemorrhages  from  duodenal  or 
typhoid  ulceration,  etc. 

Examination  of  the  blood  reveals  oligocythemia,  and  usually  a  dis- 
proportionate oligochromemia,  so  that  the  color  index  is  usually  low^^ — ^0.8 
or  lower.  The  oligocythemia  rarely  reaches  the  high  grade  observed  in 
pernicious  anemia;  thus,  after  repeated  hemorrhages  from  gastric  ulcer, 
the  count  may  be  scarcely  less  than  2,000,000  or  1,800,000.  Regenera- 
tion of  the  blood  begins  almost  immediately,  and  continues  apace,  so 
that  in  some  cases  of  severe  heinorrhage  restitution  is  almost  complete 
at  the  end  of  ten  to  fourteen  days;  usually,  however,  the  normal  condi- 
tion is  not  reached  for  several  weeks  or  months.  The  hemoglobin  value 
is  restored  less  rapidly  than  the  corpuscles,  and  may  remain  relatively 
low  (low  color  index)  for  a  considerable  time.  The  total  volume  of  the 
blood  is  usually  soon  restored  by  absorption  of  fluids  (as  well  as  salts) 
from  the  lymphatics  and  elsewhere. 

Microscopically,  anisocytosis  may  be  observed,  and  while  a  few  ery- 
throcytes may  be  undersized,  the  majority  appear  swollen  after  severe 
hemorrhages;  poikilocytosis  is  usually  slight;  polychromatophiha  is 
often  present  early,  but  soon  disappears;  nucleated  corpuscles  (mostly 
normoblasts)  appear  early,  sometimes  in  large  numbers  and  inter- 
mittently, and  may  be  found  until  restitution  of  the  blood  is  complete. 
Significant  of  regeneration,  the  absence  of  erythroblasts  augurs  ill. 
The  leukocytes  are  often  slightly  increased — poly  nuclear  neutrophilic 
leukocytosis,  which  usually  disappears  with  convalescence.  Rarely 
slight  lymphocytosis  or  myelocytosis  has  been  observed.  In  severe  cases 
the  blood  approaches  that  of  pernicious  anemia — marked  oligocythemia, 
high  color  index,  marked  poikilocytosis,  megalocytes,  etc. 

Prognosis. — The  prognosis  varies  with  the  amount  of  blood  lost,  the 
rapidity  of  the  loss,  the  general  condition  of  the  patient  at  the  time  of  the 
hemorrhage,  and  the  evidences  of  regeneration. 


CHRONIC  SECONDARY   ANEMIA  367 

Treatment. — ^The  treatment  should  consist  of  rest  in  bed,  with  depres- 
sion of  the  head;  hgation  of  the  bleeding  vessel,  if  possible;  and  the  injec- 
tion into  the  veins  of  a  volume  of  physiological  saline  solution  sufficient 
to  maintain  the  circulation  (500  to  2000  c.c).  Sterile  0.9  per  cent, 
sodium  chloride  solution  is  commonly  used,  but  a  preferable  solution 
(which  must  be  sterilized)  is  the  following: 

J^ — Sodium  chloride 9  0 

Potassium  chloride 0  1 

Calcium  cliloride 0  25 

Water 1000  0 

— Hare. 

In  sudden  severe  hemorrhages  likely  to  prove  immediately  fatal,  Crile 
advises  resort  to  rapid  rhythmic  pressure  upon  the  chest  with  a  view  to 
produce  artificial  respiration  and  a  moderate  artificial  circulation;  at 
the  same  time,  by  means  of  a  cannula  inserted  in  a  large  artery  near  the 
heart,  he  injects  some  physiological  saline  (or  Ringer's  or  Locke's)  solu- 
tion, and  as  soon  as  the  fiuid  has  begun  to  flow,  by  means  of  a  hypo- 
dermic needle  inserted  into  the  rubber  tubing  near  the  cannula,  he 
injects  15  to  30  minims  (1  to  2  c.c.)  of  adrenalin  chloride,  1  to  1000;  the 
injection  may  be  repeated  in  a  minute,  if  required.  This  brings  about 
a  rising  arterial  and  coronary  pressure,  and  stimulates  the  heart  to 
renewed  activity.  Crile  believes  this  treatment  more  effective  than  the 
use  of  stimulants,  nitroglycerin,  intravenous  infusions,  electricity,  need- 
ling of  the  heart,  or  direct  cardiac  massage.  The  later  treatment  is  that 
of  the  primary  disease;  and  in  addition,  measures,  to  be  mentioned  under 
chronic  anemia,  designed  to  restore  the  blood  to  the  normal. 


CHRONIC  SECONDARY  ANEMIA. 

Etiology. — Chronic  secondary  anemia  may  be  due  to:  (1)  Bacterial 
infections,  whence  it  is  a  concomitant  of  all  infectious  diseases,  especially 
typhoid  fever,  acute  rheumatic  fever,  septicemia,  diphtheria,  syphilis, 
tuberculosis,  etc.  The  anemia  of  the  acute  infectious  diseases,  however, 
is  often  subacute  rather  than  chronic,  and,  as  a  rule,  responds  promptly 
to  treatment.  (2)  Zooparasitic  infections,  such  as  malaria  and  the 
dift'erent  worms  (Uncinaria  americana,  Dibothriocephalus  latus,  Filaria 
bancrofti.  Schistosoma  htiematobium  or  japonicum),  which  often  pro- 
duce an  anemia  scarcely  distinguishable  clinically  from  progressive 
pernicious  anemia.  (3)  Intoxications,  (a)  biological  (not  separable  from 
the  infectious  diseases);  (/;)  inorganic,  such  as  lead,  arsenic,  mercury, 
phosphorus,  potassium,  certain  coal  tar  derivatives,  etc.;  (/■)  autogenic 
poisons,  such  as  occur  in  disorders  of  the  gastro-intestinal  tract, 
nephritis,  carcinoma,  so-called  cholemia,  pregnancy,  etc.  (4)  Prolonged 
drains  upon  the  system,  with  loss  of  the  albuminous  constituents  of  the 
blood,  such  as  occur  in  prolonged  supj)uratioii,  ne})liritis,  prolonged 
lactation,    dysentery,    etc.      (5)  Repeated    hemorrhages — gastric    and 


368  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

duodenal  ulcer,  liver  cirrhosis  with  hemorrhages,  hemorrhoids,  menor- 
rhagia,  metrorrhagia,  hemophilia,  etc.  (6)  Inanition  and  starvation, 
due  to  deficient  food  or  inability  to  swallow  food,  such  as  occur  in  oeso- 
phageal carcinoma  and  somewhat  similarly  in  obstruction  of  the  thoracic 
duct.  (7)  Insanity.  In  these  latter  cases  the  plasma  often  suffers  much, 
and  on  account  of  inspissation  the  blood  corpuscles  may  be  relatively 
numerous  (5,000,000  or  more  to  the  cubic  millimeter). 

Symptoms. — ^In  many  cases  the  symptoms  due  to  the  anemia  are  inti- 
mately bound  up  with  those  due  to  the  primary  disorder,  and  it  is  difficult 
to  separate  the  one  from  the  other.  In  general,  however,  the  symptoms 
of  the  anemia  are  those  of  general  nervous  and  muscular  irritability  and 
weakness.  The  patient  is  readily  fatigued  by  bodily  or  mental  exertion, 
he  is  incapable  of  concentrated  or  continued  mental  effort,  and  headache, 
vertigo,  syncopal  attacks,  tinnitus,  dimness  of  vision,  insomnia  (or 
somnolence),  are  common,  and  occasionally  nausea  and  vomiting  may 
be  present.  The  appetite  is  poor,  the  digestion  often  imperfect  (vari- 
ability of  HCl)  and  often  painful  (hyperesthesia  of  the  gastric  mucosa), 
and  constipation  is  the  rule  (defective  intestinal  peristalsis).  The  heart's 
action  is  weak,  though  readily  excited — whence  palpitation  and  arrhyth- 
mia, as  well  as  dyspnoea,  are  common;  a  systolic  murmur  is  usually 
present,  and  a  venous  hum  (bruit  de  diable)  may  be  heard  in  the  neck; 
the  second  pulmonary  sound  is  accentuated;  from  dilatation,  a  relative 
mitral  insufficiency  may  occur;  the  pulse  is  small,  weak,  and  compres- 
sible, and  the  extremities  are  usually  cool.  Slight  oedema,  due  to  increased 
permeability  of  the  vessels,  occurs  in  some  cases,  and  hemorrhages  into 
the  mucous  membranes,  under  the  skin,  and  in  the  retina  and  cerebral 
meninges  are  not  uncommon.  The  urine  is  often  increased  in  amount. 
Occasionally  there  is  slight  fever  (anemic  fever).  There  may  be  amenor- 
rhoea  or  menorrhagia;  and  perhaps  impotence. 

The  blood  reveals  oligocythemia  (4,000,000  to  2,000,000),  and  dis- 
proportionate oligochromemia  (65  to  30  per  cent.);  therefore  a  low  color 
index  (0.8  to  0.6).  In  some  cases,  however,  these  figures  are  exceeded, 
and  approach  those  of  pernicious  anemia.  Microscopically,  the  cor- 
puscles are  pale,  and  reveal  anisocytosis,  poikilocytosis,  and  polychroma- 
tophilia;  nucleated  corpuscles  (usually  normoblasts)  may  be  present. 
There  is  little,  if  any,  leukocytosis  due  to  the  anemia  as  such,  but  leu- 
kocytosis as  a  manifestation  of  the  primary  disorder  is  not  uncommon. 

Diagnosis. — The  diagnosis  has  to  do  not  only  with  the  recognition  of 
the  anemia,  but  also  with  its  degree,  and  largely  with  its  underlying  dis- 
order. Cases  of  so-called  simple  anemia  are  usually  chlorosis,  pernicious 
anemia,  tuberculosis,  gastric  carcinoma,  neurasthenia,  etc.,  and  an  effort 
should  be  made  to  differentiate  these. 

Prognosis. — The  prognosis  is  that  of  the  primary  causative  factor. 

Treatment. — The  treatment  is  primarily  concerned  with  the  detection 
and  removal  of  the  underlying  cause.  In  addition,  however,  the  patient's 
recovery  may  be  materially  aided  by  attention  to  the  diet,  and  by  suit- 
able medicines.    The  diet  should  be  varied  and  nutritious,  and  should 


CHLOROSIS  369 

comprise  a  generous  amount  of  red  meats,  milk,  eggs,  as  well  as  other 
iron-containing  articles,  especially  vegetables.  Of  medicaments,  iron  is 
of  prime  importance,  and  should  be  given  in  all  cases.  As  a  ride,  no 
preparation  is  better  than  Blaud's  pills,  which  should  be  given  in  generous 
doses  (10  to  15  grains,  0.65  to  1  gram,  three  times  a  day);  in  some 
cases  reduced  iron,  the  dried  sulphate  or  the  citrate  of  iron,  or  Basham's 
mixture  render  excellent  service,  x^rsenic  is  often  a  useful  adjuvant,  and 
may  be  given  as  Fowler's  solution,  2  minims  (0.12  c.c),  three  times  a 
day.  Occasionally  bitter  tonics  and  hydrochloric  acid  are  indicated  to 
improve  the  appetite,  but  hydrochloric  acid  had  better  be  withheld  unless 
we  are  certain  that  there  is  a  deficiency  of  hydrochloric  acid  in  the  gastric 
juice.     The  following  is  often  productive  of  excellent  results : 

I^ — Reduced  iron 80  grains  5;2 

Quinine  sulphate 20  grains  1  3 

Strychnine  sulphate 2  grains  0  13 

Ai'senous  acid 1  grain  0  06 

Mix  and  make  40  pills. 

S. — One  pill  three  times  daily. 

Minute  doses  of  mercuric  bichloride  are  sometimes  serviceable,  even  in 
non-syphilitic  cases.  The  debility  of  exhausting  disorders,  such  as 
typhoid  fever,  prolonged  lactation,  neurasthenia,  etc.,  is  often  much 
improved  by  the  lactophosphates,  the  hypophosphites,  cod  liver  oil,  etc. 
In  cases  that  do  not  respond  promptly  iron  may  be  given  hypodermicly, 
the  citrate  in  doses  of  h  grain  (0.03  gram)  to  children,  2  grains  (0. 13  gram) 
to  adults,  every  other  day.  The  bowels  should  be  kept  open  once  daily. 
Other  suitable  measures  consist  of  medicated  baths,  massage,  and  change 
of  climate  —  high  altitudes  being  of  undoubted  service  in  some  cases, 
since  it  seems  that  the  increase  in  the  corpuscular  count  obtained  at 
high  altitudes  does  not  always  disappear  upon  return  to  lower  levels. 


CHLOROSIS. 

(Chloranemia;  Green  Sickiiess.) 

Chlorosis  is  a  form  of  anemia  occurring  in  young  girls  about  the  time 
of  puberty,  and  characterized  by  marked  oligochromemia  and  sometimes 
by  a  peculiar  greenish  tint  of  the  skin. 

Etiology. — Chlorosis  is  peculiarly  a  disease  of  the  female  sex,  occurring 
in  blondes  more  frequently  than  in  brunettes,  and  about  the  age  of  pu- 
berty, that  is,  from  the  fourteenth  to  the  seventeenth  year,  but  recurrences 
up  to  and  probably  beyond  the  twenty-fifth  year  are  common.  True 
chlorosis  never  occurs  in  males.  It  is  most  common  among  domestic 
servants  and  immigrants,  particularly  Irish;  but  if  many  chlorotic  girls 
are  underfed  and  overworked,  have  insufficient  exercise  and  fresh  air, 
many  have  been  reared  under  the  most  favorable  circumstances  and  do 
no  work;  if  many  have  been  subject  to  distressing  emotional  disturbances, 
such  as  worry,  youthful  love  affairs,  etc.,  others  are  unrestrainefl  and 
24 


370  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

free  from  care.  The  mothers  of  some  chl orotic  girls  themselves  were 
chlorotic  about  the  age  of  puberty. 

The  exciting  cause  of  the  disease  is  unknown- — despite  many  hypoth- 
eses. Virchow  attributed  it  to  hypoplasia  of  the  cardiovascular  system, 
especially  the  aorta,  and  the  genitalia;  but  these,  though  sometimes 
observed,  can  scarcely  cause  the  disorder,  since  it  is  difficult  to  compre- 
hend the  relationship  between  hypoplasia  of  the  aorta  and  oligochrome- 
mia,  since  such  hypoplasia  does  not  cause  chlorosis  in  boys,  and  whereas 
iron  may  cure  chlorosis,  it  must  be  powerless  to  correct  the  hypoplasia. 
Sir  Andrew  Clark  believed  the  disease  to  be  a  manifestation  of  intes- 
tinal auto-intoxication  due  to  coprostasis — -a  view  with  little  foundation 
in  fact,  since  otherwise  most  girls  and  women  would  be  chlorotic,  and 
because  evidences  of  intestinal  putrefaction  have  not  been  found  con- 
stantly in  the  urine  of  chlorotics.  The  occurrence  of  chlorosis  in  girls 
about  the  time  of  puberty  suggests  an  intimate  relationship  between  the 
series  of  changes  then  taking  place  and  the  alterations  in  the  blood; 
possibly  time  may  show  that  some  derangement  in  the  internal  secretion 
of  the  ovary  developing  at  the  time  the  ovary  begins  to  functionate 
actively,  may  be  answerable  for  the  disease.  The  majority  of  cases  can- 
not be  incipient  pulmonary  tuberculosis,  as  has  been  suggested,  since 
they  are  readily  cured  with  iron ;  nor  is  it  likely  that  they  are  cases  of 
more  or  less  ill-declared  hyperthyroidism,  associated  or  not  with  tuber- 
culous lesions  in  the  thyroid.  Unquestionably  chlorosis  seems  to  be 
much  less  common  than  it  was  years  ago,  which  is  due  to  the  fact  that 
the  causes  of  many  chloranemic  conditions  are  more  commonly  recog- 
nized ;  this  suggests  the  additional  fact  that  chlorosis  in  reality  is  a  sec- 
ondary anemia,  of  which  the  cause  is  not  always  demonstrable.  The 
common  absence  of  marked  changes  in  the  erythrocytes,  the  deficiency  of 
pigments  in  the  urine  and  feces,  and  the  non-occurrence  of  even  slight 
jaundice,  suggest  that  the  disease  is  due  to  defective  hemogenesis  rather 
than  augmented  hemolysis. 

Symptoms. — The  symptoms,  for  the  most  part,  are  those  of  the  con- 
comitant anemia,  and  as  such  do  not  differ  from  those  described  in  con- 
nection with  chronic  secondary  anemia.  The  early  symptoms  are  usually 
breathlessness,  palpitation  of  the  heart  (which  too  often  suggests  heart 
disease),  vertigo,  faintness,  weariness  of  the  mind  and  body  without 
obvious  cause,  and  indisposition  to  exertion.  In  marked  contrast  with 
the  subjective  complaints,  the  girl  often  presents  a  much  prized  though 
deceptive  peach  complexion  (chlorosis  rubra),  especially  upon  exertion  or 
excitement,  and  she  is  more  likely  to  be  fat  and  round  than  thin  and  angu- 
lar. In  marked  cases,  however,  the  skin  exhibits  the  ordinary  pallor  of 
any  secondary  anemia;  occasionally  it  presents  a  peculiar  yellow-greenish 
color,  most  notable  on  the  face,  ears,  dorsal  surface  of  the  hands,  and  the 
chest;  pigment  spots  especially  about  the  joints  are  often  present;  the 
eyes  are  bright,  the  conjunctivae  transparent,  and  the  sclerotics  bluish. 
Indeed,  the  observing  physician  may  usually  make  the  diagnosis  from 
mere  inspection,  and  yet  the  disease  is  frequently  overlooked.     The 


CHLOROSIS  371 

appetite  is  often  characteristically  capricious,  the  patient  evincing  a  liking 
for  most  extraordinary  articles,  such  as  chalk,  paper,  pickles,  etc.  (pica 
chlorotica) ;  epigastric  distress  is  common  after  eating,  and  constipation 
is  the  rule.  Appropriate  examination  often  reveals  gastric  hyperacidity, 
frequently  gastroptosis  and  even  gastrectasis  (especially  if  the  patient 
has  succumbed  to  the  vanity  of  tight  lacing).  Examination  of  the  heart, 
suggested  by  the  palpitation,  usually  reveals  excited  action;  a  systolic 
murmur,  commonly  with  its  point  of  maximum  intensity  toward  the  pul- 
monary area,  though  frequently  audible  over  the  entire  precordium;  a 
venous. hum  in  the  neck  (bruit  de  diahle);  and  often  percussion  evidence 
of  enlargement  (dilatation)  of  the  heart.  The  murmur  is  usually 
attributed  to  anemia  (and  partakes  of  the  characteristics  of  so-called 
anemic,  functional,  murmurs);  in  some  cases,  however,  it  is  probably  due 
to  dilatation  of  the  root  of  the  pulmonary  artery,  and  in  some  cases  to 
relative  mitral  insufficiency  (irregular  action  of  the  papillary  muscles); 
Venous  thrombosis  (femoral,  cerebral  sinuses)  is  by  no  means  uncom- 
mon (2  per  cent,  or  more  of  the  cases).  The  extremities  are  often  cold 
(defective  circulation).  Qidema  or  puffiness  of  the  feet  and  ankles  is 
sometimes  present,  and  has  been  mistaken  for  evidence  of  nephritis  or 
heart  disease.  Divers  nervous  manifestations  are  common — headache, 
neuralgic  pains  in  the  neck  and  the  back,  and  reflected  elsewhere, 
general  irritability  and  capriciousness,  vulgar  "hysterics,"  dermograph- 
ism and  other  evidences  of  vasomotor  instability  (or  ataxia),  etc.  Slight 
fever  occurs  occasionally. 

The  total  volume  of  the  blood  is  increased,  due  to  increase  of  the  plasma 
(serous  plethora;  polyplasmia),  in  consequence  of  which  the  vascular 
system  is  overdistended.  The  blood  as  it  flows  from  the  puncture  is 
pale,  but  the  characteristic  feature  is  the  marked  reduction  in  the  hemo- 
globin. The  erythrocytes  are  often  normal  in  number;  they  are  usually 
over  4,000,000,  that  is,  about  80  per  cent,  of  the  normal,  whereas  the 
hemoglobin  varies  from  35  to  65  per  cent,  in  different  cases,  averaging 
about  40  per  cent.  The  color  index  thus  approaches  0.5.  In  some  cases, 
however,  there  is  quite  a  reduction  in  the  erythrocytes — to  3,000,000  or 
2,500,000,  or  even  less;  but  the  disproportionate  reduction  of  the  hemo- 
globin (the  low  color  index)  is  a  constant  feature.  Microscopically  the 
individual  erythrocytes  are  pale  (low  color  index,  deficiency  of  hemo- 
globin), and  anisocytosis  (small  cells)  and  poikilocytosis  may  be  present 
and  sometimes  are  marked  (severe  cases);  large  erythrocytes  (mega- 
locytes),  however,  are  rarely  if  ever  seen;  nucleated  red  cells  are  some- 
times present;  polychromatophilia  is  rare.  The  leukocytes  are  usually 
normal  in  number,  but  a  slight  increase  especially  of  the  lymphocytes  is 
by  no  means  unknown. 

Diagnosis. — As  already  stated,  the  diagnosis  is  often  suggested  by 
mere  ins])ection  of  the  patient,  but  the  frecjuency  widi  which  the  disease 
is  overlooked  and  mistaken  for  something  else  is  deplorable.  If  a  hemo- 
globinometer  is  not  at  hand,  recourse  may  be  had  to  the  simple  device 
of  comparing  a  drop  of  the  patient's  blood  with  a  drop  of  presumably 


372  DISEASES  OF   THE   HEMOPOIETIC  SYSTEM 

normal  blood,  whereupon  the  deficiency  of  hemoglobin  is  immediately 
apparent.  Care  should  be  taken  not  to  mistake  beginning  pulmonary 
tuberculosis  for  chlorosis,  nor  chlorosis  for  nephritis  (on  account  of 
slight  oedema),  or  heart  disease  (on  account  of  palpitation  and  a  murmur), 
or  hyperthyroidism,  or  neurasthenia.  The  examination  of  the  blood  is 
usually  conclusive,  but  one  must  bear  in  mind  that  a  chloranemic  con- 
dition of  the  blood  is  the  unusual  condition  in  secondary  anemias. 

Prognosis. — The  prognosis  is  good.  Recovery,  under  proper  treat- 
ment, ensues  in  from  two  to  four  or  six  months,  but  relapses  are  not 
uncommon,  largely  because  of  too  early  discontinuance  of  treatment. 

Treatment. — Rest  in  bed  with  an  abundance  of  fresh  air  and  sunlio;ht, 
for  a  time  at  least,  is  advisable  in  all  but  the  mildest  cases.  The  food 
should  be  nutritious  and  generous  in  amount — milk,  eggs,  meats,  fish, 
stewed  fruits,  green  vegetables,  etc. ;  but  it  is  sometimes  a  tax  on  the 
patience  of  the  physician  to  convince  a  chlorotic  girl  that  she  can  digest 
food  other  than  chalk  and  pickles,  and  that  meat  in  particular  will  agree 
with  her  delicate  stomach.  Iron  is  a  specific  remedy.  It  is  a  matter  of 
comparative  indiflFerence  which  preparation  is  given,  provided  the  iron 
is  given  in  generous  amount.  Xo  preparation  is  better  than  Blaud's 
pills : 

IJ — Dried  iron  sulphate. 

Potassium  carbonate,  of  each 100  grains.      6  6 

Mix  and  make  40  pills. 
S. — One  pill  three  times  a  day  for  the  first  week,  two  pOls  three  times  a  day  for  the  second 
week,  and  three  pills  three  times  a  day  thereafter. 

The  treatment  must  be  persisted  in  for  at  least  three  months,  despite  the 
conviction  of  the  patient  that  she  is  cured  earlier,  since  otherwise  recur- 
rence is  almost  inevitable.  Under  the  influence  of  iron  the  erythrocytes 
soon  reach  the  normal  num})er,  and  while  the  hemoglobin  value  increases, 
considerable  time  is  often  required  to  attain  the  normal  percentage.  Ex- 
actly how  the  iron  acts  is  a  matter  of  speculation,  and  the  theoretical 
objection  to  large  doses,  whereby  more  iron  is  given  within  a  few  days 
than  is  contained  normally  in  the  entire  body,  is  not  sustained  by  any 
clinical  or  experimental  facts.  Indeed,  a  markedly  chlorotic  patient, 
despite  the  evident  need  of  iron  in  her  blood,  excretes  iron  in  her  feces, 
even  before  the  administration  of  iron  is  commenced.  Those  who  prefer 
them  may  use  reduced  iron,  the  citrate  of  iron  and  potassium,  or  the  citrate, 
the  dried  sulphate,  the  pyrophosphate,  the  lactate,  or  the  succinate  of  iron 
or  the  tincture  of  the  chloride;  one  or  the  other  of  these  may  be  given 
from  time  to  time  should  convalescence  prove  tedious,  in  which  case  also 
minute  doses  of  arsenic  or  of  manganese  may  prove  serviceable.  The  so- 
called  organic  preparations  of  iron,  said  to  reproduce  the  normal  iron  of 
the  body,  are  in  no  way  superior,  and  in  many  ways  inferior,  to  the 
preparations  mentioned. 

In  addition  to  the  foregoing,  the  patient's  bowels  should  be  kept  open 
dailv — for  which  purpose,  as  a  rule,  nothing  is  better  than  the  compound 
rhuWb^pill  (U.  S.  P.): 


PERNICIOUS  ANEMIA  373 

I^— Rhubarb 48  grains  3  20 

Purified  aloes 36  grains  2140 

Myrrh       .       . 12  grains  0  80 

Oil  of  peppermint 4  minims  0  25 

Mix  and  make  48  pilLs. 

S. — One  or  two  pills  niglit  and  morning. 

Cascara  sagrada,  saline  cathartics,  phenolphthalein  (1  to  2  grains,  0.06 
to  0.13  gram),  etc.,  are  also  efficacious.  Cleansing  of  the  bowel  should 
precede  the  beginning  of  the  iron  treatment.  To  patients  with  evident 
intestinal  fermentation,  it  is  wise  to  give  for  a  time  .so-called  intestinal 
antiseptics,  especially  bismuth  salicylate,  /S-naphthol,  thymol,  aspirin, 
preparations  of  the  lactic  acid  bacillus,  etc.  In  other  patients  with  imper- 
fect digestion,  hydrochloric  acid,  nux  vomica,  and  the  bitter  tonics  prove 
efficacious;  but  one  must  remember  that  hyperchlorhydria  is  common  in 
chlorosis. 


PERNICIOUS  ANEMIA. 

Pernicious  anemia  is  a  chronic  disease  of  the  hemopoietic  tissues 
characterized  by  hemolysis  of  unknown  cause,  abnormal  hemogenesis, 
and  alternating  periods  of  remission  and  relapse. 

There  has  been  and  there  still  is  much  discussion  as  to  what  is  and 
what  is  not  properly  pernicious  anemia.  There  are  several  disorders 
that  m?y  give  rise  to  clinical  and  blood  pictures  resembling,  if  not  quite 
identical  with,  pernicious  anemia  that  should  be  excluded,  since  they  are 
obviously  secondary  anemias  of  severe  (perhaps  one  might  say  also 
pernicious)  and  even  fatal  type.  These  include:  (1)  Some  ca.ses  due  to 
severe  and  frequently  repeated  hemorrhages;  (2)  certain  cases  of  severe 
malarial,  syphilitic,  and  other  infections;  (3)  Dibothriocephalus  latus  and 
other  zooparasitic  infections,  in  which  the  blood  picture  may  be  quite 
identical  with  that  of  pernicious  anemia  and  the  termination  fatal; 
(4)  cases  of  severe  and  fatal  anemia  occurring  during  pregnancy  or  soon 
after  parturition,  and  due  presumably,  as  is  the  vomiting,  nephritis,  and 
eclampsia  of  pregnancy,  to  some  auto-intoxication,  or  to  puerperal 
hemorrhage  or  infection;  these  occur,  as  a  rule,  in  young  subjects  (thirty 
to  thirty-five  years),  do  not  show  the  remissions  characteristic  of  per- 
nicious anemia,  and  are  often  curable  upon  removal  of  the  initiating  cause; 
(5j  ca.ses  due  to  primary  changes  in  the  bone  marrow,  such  as  primary 
or  secondary  tumor  formation,  or  leukemia  (.so-called  myelophthisic 
anemia).  There  remains  a  series  of  cases  of  unknown  cause  to  which 
the  term  pernicious,  i(li(jj)athic,  essential,  Addison's,  or  Bienncr's  anemia 
may  l)e  applied. 

Etiology. — Pernicious  anemia  is  especially  common  in  adult  life:  more 
than  half  the  cases  occur  after  the  fortieth  year;  it  is  rare  in  childhood. 
It  is  more  than  twice  as  common  in  men  as  in  women  (eliminating  the 
cases  occurring  in  pregnancy).  The  cause  of  the  disea.se  is  not  known. 
It  has  been  variously  attributed  to  nervous  shock;  to  repeated  or  long- 


S74  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

continued,  perhaps  concealed,  gastro-intestinal  hemorrhages  (which  are 
more  likely  a  result  than  a  cause  of  the  disease);  to  atrophy  of  the 
gastro-intestinal  mucosa  (which,  however,  is  not  always  present,  and  if 
present  may  as  well  be  a  result  as  a  cause,  or  a  manifestation  of  the 
same  cause);  to  subinfection  with  intestinal  bacteria;  and,  especially 
by  Hunter,  to  oral  and  gastro-intestinal  sepsis.  Hunter  states  that  the 
disease  is  a  well  characterized  specific  infective  disease  of  hemolytic 
nature  localized  in  the  alimentary  tract;  that  in  its  etiology  long-standing 
sepsis,  oral  and  gastric,  plays  an  essential  and  important  antecedent 
and  concurrent  part;  that  anemia  is  but  one  of  the  symptoms,  of  which 
there  are  three  others:  (1)  Glossitic  and  gastro-intestinal;  (2)  hemo- 
lytic; and  (3)  febrile  and  nervous — far  more  characteristic  and  due  not 
to  the  anemia,  but  to  the  infective  agencies  underlying  the  disease.  Dis- 
approving of  the  term  pernicious,  he  separates  this  so-called  Addisonian 
(primary  cryptogenetic)  anemia,  a  specific  infective  disease,  sharply  from 
other  types  of  severe  or  pernicious  (Biermer's)  anemia,  which  he  believes 
may  be  due  to  other  types  of  general  sepsis;  and  all  these  types,  which  he 
characterizes  as  infective  anemias,  he  differentiates  from  so-called  non- 
infective  anemias — that  is,  chlorosis  and  all  the  ordinary  posthemorrhagic 
and  other  types  of  secondary  anemia. 

Pathology. — The  conspicuous  lesions  consist  of  pallor,  a  lemon  tint, 
or  even  slight  jaundice  of  the  skin;  pallor  of  all  the  viscera;  a  peculiar 
bright  red  color  of  the  muscles  and  light  yellowish  fat;  fatty  degeneration 
of  the  liver,  heart,  and  kidneys  (toxic,  perhaps,  rather  than  anemic  degen- 
eration); petechial  hemorrhages  in  the  subcutaneous,  submucous,  and 
subserous  tissues;  effusions  in  the  serous  sacs;  systemic  or  disseminated 
degeneration  of  the  posterior  columns,  and  sometimes  of  the  lateral 
columns  and  of  the  gray  matter  of  the  spinal  cord  (perhaps  also  toxic 
rather  than  anemic).  Hunter  emphasizes  the  importance  of  certain 
so-called  infectious  lesions;  a  peculiar  glossitis,  gastritis  or  gastric 
atrophy,  and  patchy  enteritis,  which  he  believes  to  be  insufficient  in 
themselves  to  originate  the  intense  anemia  by  an  interference  with  nutri- 
tion. The  liver,  spleen,  lymph  nodes,  and  hemolymph  nodes  usually 
show  considerable  deposit  of  blood  pigment  and  large  numbers  of 
phagocytes  (macrophages)  containing  more  or  less  completely  destroyed 
erythrocytes — all  evidences  of  excessive  hemolysis.  The  fatty  portions 
of  the  bone  marrow  are  usually  more  or  less  replaced  by  red  marrow 
resembling  the. foetal  or  juvenile  type  (megaloblastic  degeneration  or 
metaplasia),  interpretable  as  an  effort  to  compensate  for  the  excessive 
hemolysis;  there  may  be  also  some  evidences  of  leukoblastic  hyperplasia. 
In  some  cases  the  bone  marrow  is  either  incapable  of  responding  or 
ultimately  becomes  exhausted,  whereupon  it  may  be  more  or  less  com- 
pletely yellow  (fatty)  throughout  (aplastic  anemia). 

Symptoms. — The  disease,  as  a  rule,  is  exceedingly  insidious  in  onset, 
and  it  often  has  made  considerable  progress,  that  is,  the  blood  is  remark- 
ably bad,  when  the  patient  first  seeks  medical  advice.  The  initial  mani- 
festations are  variable  and  permit  of  some  grouping  of  the  cases:  (1) 


PERNICIOUS  ANEMIA  375 

Gradually  increasing  weakness,  especially  upon  exertion,  with  dyspnoea 
and  palpitation  of  the  heart;  (2)  gastro-intestinal  derangements — sore 
mouth,  anorexia,  nausea,  vomiting,  diarrhoea,  or  perhaps  constipation; 
(3)  general  nervous  irritability  or  inadequacy,  lost  power  of  mental 
effort  or  concentration,  headache,  vertigo,  tinnitus,  fainting,  somnolence, 
cutaneous  parasthesias  and  ataxia,  spasticity  of  the  muscles  of  the  legs, 
etc.  In  the  course  of  time  the  symptoms  become  aggravated.  The 
weakness  and  weariness  increase;  mental  effort  and  concentration  are 
even  less  well  sustained  than  previously;  and  dyspnoea  and  palpita- 
tion of  the  heart  become  more  marked.  Hemorrhages  (usually  pete- 
chial) may  occur  into  the  skin,  visible  mucous  membranes,  retina,  etc.; 
nausea  and  vomiting  may  become  aggravated,  and  are  often  associated 
with  paroxysmal  attacks  of  epigastric  pain  and  diarrhoea.  In  a  majority 
of  the  cases  nervous  phenomena  become  more  or  less  obtrusive,  such  as 
various  paresthesias,  numbness,  tingling,  etc.  (even  in  the  absence  of 
demonstrable  changes  in  the  spinal  cord);  in  other  cases  symptoms 
suggestive  of  tabes  dorsalis  (severe  pains,  absent  knee-jerks,  etc.)  occur; 
they  may  even  precede  and  ultimately  become  more  marked  than  symp- 
toms referable  directly  to  the  anemia;  in  other  cases,  spasticity  of  the 
muscles  of  the  legs  and  increased  knee-jerks,  associated  late,  perhaps,  with 
incontinence  of  urine  and  feces,  supervene.  To  a  not  uncommon  mental 
apathy  a  depressive  psychosis  (melancholia)  sometimes  succeeds. 

On  examination  the  patient  may  present  a  general  cutaneous  pallor, 
such  as  might  be  encountered  in  any  severe  anemia;  in  other  cases  there 
is  a  characteristic  waxy,  lemon-yellow  color  of  the  skin;  in  some  cases 
there  is  even  slight  jaundice  (not  as  frequent  as  is  often  diagnosticated); 
and  rarely  there  is  more  or  less  pigmentation  (and  perhaps  associated 
leukoderma),  suggesting  Addison's  disease.  The  subcutaneous  fat  is 
usually  well  preserved,  and  there  is  often  comparatively  little  loss  of 
weight.  As  a  rule,  there  is  a  notable  absence  of  abnormal  physical  signs. 
The  heart  is  usually  somewhat  dilated;  there  may  be  hemic  murmurs 
over  the  heart  and  in  the  cervical  veins,  or  a  murmur  of  relative  mitral 
insufficiency;  the  pulse  may  be  full  but  not  well  sustained;  the  blood 
pressure  is  usually  low  (often  less  than  100  mm.  Hg., systolic  or  maximum) ; 
and  a  capillary  pulse  may  be  visible.  (Edema  of  the  legs  and  hands  is 
common,  and  transudations  may  occur  into  the  pleura,  peritoneum, 
etc.  The  spleen  and  liver  may  be  slightly  enlarged;  occasionally  also 
the  palpable  lymph  nodes.  Hydrochloric  acid  and  the  digestive  ferments 
are  usually  absent  or  greatly  diminished;  there  is  rarely  any  marked 
dilatation  of  the  stomach  or  motor  insufficiency  except  perhaps  at  the 
time  of  the  paroxysmal  pains.  The  urine  is  usually  pale  and  of  low 
specific  gravity;  in  from  one-fourth  to  one-half  of  the  cases  it  contains  a 
small  amount  of  albumin  and  perhaps  a  few  casts;  occasionally  it  is  dark 
in  color,  due  usually  to  an  excess  of  urobilin.  Fever  occurs  in  about  three- 
fourths  of  the  cases — often  (100°  to  102°)  for  a  week  or  two  at  a  time. 

The  blood  is  abnormally-  fluid,  and  the  total  volume  is  lessened.  The 
red  cells  are  remarkably  reduced,  numbering  often  2,000,000  or  less 


376  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

when  the  patient  first  consuUs  a  physician — which  in  itself  suggests  the 
disease;  later  they  may  fall  to  1,000,000  or  less  (even  143,000,  Quincke). 
The  color  index  is  high,  1.0  to  1.5  or  more  (often  increasing  with  the 
progress  of  the  disease  and  lessening  during  the  periods  of  remission); 
this  is  characteristic  of  the  disease,  and  attributable  not  to  hemoglo- 
binemia  (which,  however,  is  occasionally  present),  but  to  the  large  number 
of  macrocytes  rich  in  hemoglobin.  Poikilocytosis  is  usually  extreme; 
there  is  marked  anisocytosis,  megalocytes  being  present  usually  in  such 
size  and  numbers  as  to  increase  the  average  diameter  of  the  erythro- 
cytes (offsetting  the  lessened  diameter  of  the  microcytes);  polychroma- 
tophilia  (diffuse  and  granular)  is  exceedingly  common  (more  so  than  in 
any  disease  other  than  lead  poisoning) ;  and  nucleated  red  corpuscles,  espe- 
cially megaloblasts,  are  present  in  more  than  90  per  cent,  of  the  cases.  The 
leukocytes  are  usually  diminished  (5000  or  less) — usually  a  polynuclear 
deficit;  there  may  be  a  relative,  sometimes  an  absolute,  lymphocytosis. 
Sometimes  the  leukocyte  count  is  normal,  especially  during  the  remis- 
sions; rarely  there  is  a  slight  leukocytosis  (blood  crisis;  complicating, 
perhaps,  terminal  infection).  A  few  myelocytes  are  often  encountered. 
The  blood  platelets  are  lessened.  Often  what  are  spoken  of  as  blood 
crises  occur — sudden  increase  of  the  erythrocytes  (50  or  more  per  1000 
leukocytes),  and  of  the  leukocytes  (especially  the  eosinophiles).  The  crises 
may  be  spoken  of  a  normoblastic  or  megaloblastic,  depending  upon  the 
predominating  type  of  nucleated  cell.  These  often  are  favorable  signs 
of  bone-marrow  activity  and  are  followed  by  general  and  blood  improve- 
ment; but  sometimes  they  represent  the  final  effort  of  an  exhausted 
marrow  and  may  portend  an  early  fatal  issue. 

A  characteristic  of  the  disease  is  alternating  periods  of  remission  and 
relapse — which  often  succeed  each  other  with  considerable  regularity. 
As  a  matter  of  fact,  when  the  blood  is  poor  it  is  remarkably  inconstant, 
the  erythrocyte  count  either  increasing  or  diminishing.  A  total  count  of 
over  4,000,000  is  rarely  attained;  but  the  blood  may  remain  stationary 
at  a  good,  rather  high  level  for  from  two  to  six,  sometimes  six  to  twelve, 
months  or  more.  Considerable  improvement  as  well  as  deterioration  of 
the  blood  not  infrequently  occurs  without  noteworthy  change  in  the 
general  subjective  complaints  of  the  patient;  these  (as  well  as  the  fatty 
degeneration  of  the  viscera  and  the  lesions  in  the  spinal  cord)  likely  are 
due  in  part  only  to  the  anemia  as  such,  and  in  part  to  the  underlying 
(toxic?)  factor. 

Diagnosis. — The  diagnosis  should  be  made  more  frequently  than  it  is, 
and  might  readily  be  made  by  attention  to  Addison's  statement  that  it  is 
a  disease  "occurring  without  any  recognizable  cause  whatever;  where 
there  has  been  no  previous  loss  of  blood,  no  exhausting  diarrhoea,  no 
chlorosis,  no  purpura,  no  renal,  splenic,  glandular,  strumous,  or  malig- 
nant disease,  .  .  .  and  without  any  organic  lesion  that  could 
properly  or  reasonably  be  assigned  as  an  adequate  cause  of  any  serious 
consequences."  In  addition  to  the  phenomena  common  to  any  severe 
anemia,  the  following  are  significant  of  pernicious  anemia:  Severe  cause- 


PERNICIOUS  ANEMIA  377 

less  anemia  in  a  middle-aged  or  elderly  male  subject;  generally  well-pre- 
served panniculus  adiposis  with  little  loss  of  weight;  sore  mouth;  par- 
oxysmal attacks  of  epigastric  pain  often  attended  with  diarrhoea;  retinal 
and'  other  hemorrhages;  extraordinarily  low  erythrocyte  count  at  the 
first  examination,  that  is,  the  patient's  general  good  appearance  is  in 
notable  contrast  to  the  condition  of  his  blood,  and  he  is  often  able  to 
continue  at  his  work  with  an  erythrocyte  count  approaching  1,000,000; 
high  color  index;  normal  leukocyte  count  or  leukopenia;  an  unusually 
large  number  of  megalocytes  (over  30  per  cent,  of  the  total  erythrocyte 
count  being  quite  diagnostic),  megaloblasts,  and  poikilocytes;  poly- 
chromatophilia;  and  alternating  periods  of  remission  and  relapse.  All 
types  of  severe  secondary  anemia  may  be  excluded  by  the  detection  of  a 
causative  factor,  especially  severe  and  frequently  repeated  hemorrhages, 
pregnancy,  severe  infections,  intestinal  parasitism  (ova  in  the  stools), 
etc.  Gastric  carcinoma,  myxoedema,  etc.,  sometimes  bear  a  more  or  less 
superficial  resemblance  to  pernicious  anemia,  but  with  ordinary  care  they 
should  be  readily  excluded. 

Aplastic  anemia  virtually  is  only  an  extremely  severe  and  rapidly 
fatal  form  of  pernicious  anemia,  characterized  by  slight  if  any  response 
on  the  part  of  the  bone  marrow  to  the  demand  for  erythrocytes.  The 
marrow  of  the  long  bones  is  yellow  throughout — aplastic  (rather  than 
hyperplastic  or  metaplastic)  as  contrasted  with  the  ordinary  type  of 
pernicious  anemia.  It  is  a  disease  that  especially  affects  young  women 
before  the  thirty-fifth  year;  subcutaneous  and  submucous  hemorrhages 
are  more  common;  it  is  steadily  progressive,  showing  none  of  the  char- 
acteristic remissions;  and  it  usually  leads  to  death  wnthin  a  few  months 
(three  or  thereabouts).  The  blood  is  characterized  by  the  common 
extraordinary  oligocytosis,  but  the  color  index  is  likely  to  be  low  (0.8); 
erythroblasts  are  usually  absent  and  so-called  erythroblastic  crises  do  not 
occur;  poikilocytosis,  anisocytosis,  and  polychromatophilia  are  less 
marked  than  in  the  ordinary  type  of  pernicious  anemia;  there  is  marked 
leukopenia,  due  largely  to  a  loss  of  granular  leukocytes,  so  that  most 
(75  to  90  per  cent.)  of  the  white  cells  are  lymphocytes;  and  the  blood 
platelets  are  markedly  lessened. 

Leukanemia  is  a  term  given  by  Leube  to  a  blood  state  that  combines 
some  of  the  features  of  pernicious  anemia  and  of  leukemia,  especially 
megaloblasts,  myelocytes,  and  lymphocytes.  The  majority  of  the  cases 
can,  with  little  difficulty,  l)e  classified  as  pernicious  anemia,  on  the  one 
hand,  or  leukemia,  on  the  other;  in  the  terminal  stages  of  both  of  these 
diseases  blood  findings  significant  of  the  other  are  not  rare. 

Prognosis. — The  disease  usually,  if  not  invariably,  runs  a  fatal  course  in 
from  one  to  three  years;  occasionally,  as  in  aplastic  anemia,  within  a  few- 
months;  perhaps  rarely  it  continues  for  five  or  more  years  with  vmcom- 
monly  long  periods  of  remission.  Death  usually  ensues  from  progres- 
sively increasing  weakness,  oedema  of  the  lungs,  or  terminal  infections. 

Treatment. — The  essentials  of  treatment  comprise  prolonged  rest 
(mental  and  physical),  an  abundance  of  fresh  air,  and  good,  nulrilious, 


378  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

readily  digestible  food  (especially  milk  and  vegetables,  but  not  too  much 
nitrogenous  food);  and  the  administration  of  arsenic  and  hydrochloric 
acid.  Arsenic  seems  to  act  by  stimulating  the  erythroblastic  centres  in  the 
bone  marrow.  It  should  be  given  cautiously,  in  gradually  increasing  doses, 
to  the  point  of  toleration  (epigastric  pain,  nausea,  vomiting,  diarrhoea, 
puffiness  and  itching  or  burning  of  the  eyelids,  etc.).  Arsenous  acid, 
Fowler's  solution,  or  sodium  cacodylate,  may  be  given.  In  some  cases 
good  results  follow  hypodermic  administration :  sodium  cacodylate,  |  grain 
(0.008  gram),  iron  citrate,  2  grains  (0.13  gram),  daily  or  every  second  day. 
Hydrochloric  acid  is  indicated  on  account  of  the  gastric  achylia,  but  it  is 
said  to  have  also  other  beneficial  effects.  Particular  attention  should  be 
paid  to  the  teeth  and  mouth.  The  services  of  a  dentist  are  often  of  the 
greatest  utility.  Antiseptic  mouth  washes  should  be  used.  Lavage  of  the 
colon  also  is  serviceable,  especially  in  the  event  of  indicanuria  and  other 
evidences  of  supposed  intestinal  decomposition.  Hypodermoclysis  with 
physiological  saline  solution  also  has  been  commended.  Cholesterin  (3  per 
cent,  solution  in  hot  olive  oil,  100  c.c.  daily)  has  been  recommended  with  a 
view  to  combining  a  hemolysin  in  the  blood,  which  is  believed  to  rob  the 
erythrocytes  of  their  cholesterin  and  lead  to  hemolysis,  analogous  to  the 
action  of  cobralecithin.  Large  amounts  of  milk,  cream,  and  butter  tend 
to  achieve  the  same  object.  Red  bone  marrow  has  fallen  into  disuse;  by 
some  its  occasional  good  results  have  been  attributed  to  the  glycerin 
contained  in  the  commonly  used  preparation — the  glycerin  extract. 


LEUKEMIA. 

(Leukocythemia.) 

Leukemia  is  a  disease  of  the  hemopoietic  system,  characterized  by 
hyperplasia  of  the  leukoblastic  tissues  and  by  marked  and  usually  per- 
manent increase  in  the  number  of  circulating  leukocytes. 

The  older  writers  described  three  types  of  leukemia — the  splenic,  the 
lymphatic,  and  the  medullary;  but  under  the  influences  of  Ehrlich  these 
became  merged  into  two,  the  splenomedullary  and  the  lymphatic — 
which  were  held  to  be  sharply  differentiated  the  one  from  the  other. 
The  one,  the  lymphatic  type  (lymphemia),  was  believed  to  be  due  to 
primary  disease  of  the  lymph  nodes;  the  other,  the  splenomedullary 
or  myelogenous  type  (myelemia)  was  believed  to  be  due  to  primary 
disease  of  the  bone  marrow.  But  with  the  determination  of  the  fact  that 
a  number  of  cases  of  lymphatic  leukemia  occur  with  slight  or  no  note- 
worthy changes  in  the  lymph  nodes,  and  that  in  all  cases  of  leukemia 
more  or  less  conspicuous  changes  occur  in  the  bone  marrow,  the  possi- 
bility of  all  cases  of  leukemia  being  myelogenous  seemed  proved. 

The  data  now  at  hand  warrant  the  opinion  that  leukemia  is  a  disease 
of  the  leukoblastic  tissues  throughout  the  body — the  bone  marrow,  the 
spleen,  and  the  lymph  nodes;  that  the  process  may  begin  in  either  the 
bone  marrow  or  the  lymph  nodes  (it  is  not  likely  that  it  ever  begins  in  the 


LEUKEMIA  370 

spleen);  that  in  some  cases  the  lesions  are  most  marked  in  the  bone 
marrow,  in  others  in  the  lymph  nodes,  but  that  changes  are  always 
present  in  the  bone  marrow;  that,  depending  perhaps  upon  the  nature 
of  the  initiating  (chemotactic  ?)  factor,  the  leukoblastic  proliferation  in 
one  series  of  the  cases  is  of  the  lymphocytic  or  lymphoid  type,  and  gives 
rise  to  a  large  number  of  circulating  lymphocytes,  whereas  in  another  series 
of  cases  it  is  of  the  myelocytic  or  myeloid  type,  and  gives  rise  to  a  large 
number  of  circulating  myelocytes ;  and  that  the  essence  of  the  process  is 
a  reversion  to  the  more  or  less  undifferentiated  leukoblastic  tissue  of 
foetal  life.  This  is  suggested  by  the  fact  that  the  circulating  lymphocytes 
and  myelocytes  of  leukemia  differ  materially  from  the  normal  circulating 
lymphocytes  and  bone-marrow  myelocytes  (reversion  to  a  common 
ancestral  type?),  and  by  the  fact  that  the  process,  whether  myeloid  or 
lymphoid,  soon  involves  in  similar  metaplasia  tissues  other  than  that 
where  it  originated;  that  is,  the  bone  marrow  may  become  converted 
into  lymphoid  tissue,  or  the  lymph  nodes  and  the  spleen  may  become 
converted  into  myeloid  tissue — these  respective  changes  being  metaplasias 
rather  than  the  result  of  the  proliferation  of  so-called  metastases. 

The  foregoing  facts  permit  of  the  differentiation  of  the  cases  into  two 
main  types:  (1)  Myelocytic  or  myeloid  (splenomedullary),  and  (2) 
lymphocytic  or  lymphoid.  In  some  respects  these  represent  extremes  of  ^ 
type  rather  than  distinct  diseases;  some  cases  do  not  fit  well  into  either 
group,  and  may  be  spoken  of  as  atypical  (transitional,  intermediate,  or 
mLxed)  forms. 

Etiology. — The  cause  and  the  nature  of  the  disease  are  not  known. 
Many,  especially  the  acute,  cases  run  a  course  strongly  suggesting  an 
infection,  but  no  infectious  agent  has  yet  been  discovered,  if  one  excepts 
Spirochseta  lymphatica  (Wliite  and  Proescher),  which  still  awaits  con- 
firmation. Warthin  and  others  are  inclined  to  look  upon  the  disease  as 
allied  to  the  tumor  formations,  believing  that  transitions  occur  from  leu- 
kemia through  myeloma  to  ordinary  sarcoma.  In  some  cases  there  is  a 
history  of  antecedent  infections,  such  as  malaria,  syphilis,  typhoid 
fever,  tonsillitis,  puerperal  and  other  types  of  septicopyemia,  etc. ;  but  in 
most  of  the  cases  the  supposed  infection  is  in  reality  the  declared,  although 
not  diagnosticated,  leukemia. 

Myelocytic  or  Myeloid  Leukemia. — Myelocytic  or  myeloid  leu- 
kemia, the  most  common  form,  occurs  especially  in  males  (two-thirds  of 
the  cases),  and  is  most  common  in  the  fourth  and  fifth  decades  (GO  per 
cent,  of  the  cases). 

Pathology. — The  lesions  consist  of  myelocytic  hyperplasia  of  the  leu- 
koblastic tissues  of  the  bone  marrow  and  of  myelocytic  (or  myeloid) 
metaplasia  of  the  spleen  and  perhaps  also  of  the  lymph  nodes.  The 
marrow,  especially  of  the  long  bones,  but  also  of  the  ribs,  vertebra', 
sternum,  etc.,  becomes  converted  into  a  reddish  or  grayish-red  tissue, 
and  the  fatty  marrow  of  the  long  bones  gradually  (lisaj)j)ears.  The 
spleen  becomes  enlarged,  and  may  weigh  4()()()  to  (iOOO  grams  or  more; 
its  shape  is  preserved;  it  varies  in  consistency  with  the  amount  of  sclerosis; 


380  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

on  section  it  usually  much  resembles  the  associated  bone  marrow,  but 
it  may  show  areas  of  infarction,  hemorrhage,  or  sclerosis.  The  liver  also 
becomes  enlarged,  and  may  weigh  as  much  as  the  enlarged  spleen,  or 
more.  The  lymph  nodes  throughout  the  body  (the  superficial  and  deep 
chains,  the  hemolymph  nodes,  the  tonsils,  etc.)  also  may  be,  but  are  not 
always,  enlarged.  Microscopically  the  bone  marrow  and  the  spleen 
exhibit  myeloid  transformation — myelocytes  and  cells  derived  therefrom 
(all  the  granular  leukocytes),  mononuclear  cells  (perhaps  ancestors  of  the 
myelocytes),  megakaryocytes  (with  divers  sorts  of  inclusions),  erythro- 
cytes and  erythroblasts  in  various  and  atypical  stages  of  development, 
etc.  Similar  changes  may  be  found  also  in  the  lymph  nodes.  The 
capillaries  of  the  liver,  kidneys,  lungs,  etc.,  are  overfilled  with  similar 
cells,  and  there  are  sometimes  extra-capillary  collections,  and  degenera- 
tion of  the  parenchymatous  cells. 

Symptoms. — The  onset  of  the  disease  is  insidious:  the  patient  may 
seek  advice  on  account  of  progressive  loss  of  flesh  and  strength,  the  dis- 
comfort occasioned  by  a  large  mass  in  the  region  of  the  spleen,  various 
gastro-intestinal  disturbances,  dyspnoea  and  palpitation  of  the  heart, 
especially  on  exertion  (and  other  evidences  of  anemia),  or  a  sudden, 
perhaps  serious  hemorrhage.  Anemia  is  not  an  early  symptom,  but 
jbecomes  marked  as  the  disease  advances,  and  is  attended  by  the  usual 
symptoms.  Hemorrhages  occur  in  80  per  cent,  of  the  cases:  epistaxis 
is  the  most  common;  but  frequently  there  is  bleeding  from  the  gums, 
the  stomach,  the  intestine,  the  uterus,  etc.;  into  the  skin  (purpuric  and 
ecchymotic  spots),  in  the  retina  (blindness),  into  the  brain  (hemiplegia, 
etc.),  and  into  the  serous  cavities.  The  first  hemorrhage  is  sometimes 
severe  and  fatal.  Gastro-intestinal  disturbances  (anorexia,  nausea, 
vomiting,  diarrhoea,  etc.)  are  sometimes  marked,  and  have  been  found 
with  unusual  (sometimes  ulcerated)  lesions  in  the  intestines.  Occa- 
sionally there  is  more  or  less  marked  dyspnoea,  due  in  part,  perhaps  to 
myeloid  deposits  in  the  lungs  and  the  respiratory  mucosa.  Hemorrhage 
or  myeloid  nodes  may  cause  dimness  of  vision  or  blindness  if  they  occur  in 
the  retina  or  optic  nerve  or  disk;  exophthalmos,  if  in  the  orbit;  deafness,  or 
Meniere's  disease,  if  in  the  semicircular  canal,  etc.  Priapism  is  occasion- 
ally a  distressing  symptom.  Fever  (102°  to  104°)  occurs  from  time  to  time 
in  almost  if  not  quite  all  cases.  Toward  the  end  evidences  of  anemia  often 
become  ascendant — dyspnoea,  palpitation,  oedema,  and  other  evidences  of 
cardiac  weakness  and  dilatation. 

Examination  reveals  a  greatly  enlarged  spleen — which  may  reach  far 
beyond  the  median  line  and  into  the  pelvis;  it  is  usually  hard,  but  some- 
times painful  and  tender;  it  reveals  distinct  notching;  often  it  progres- 
sively increases  in  size,  but  when  very  large  it  may  remain  stationary, 
and  it  may  become  smaller  after  a  severe  gastro-intestinal  hemorrhage  or 
diarrhoea,  or  in  consequence  of  progressive  sclerosis.  The  liver  also  is 
usually  enlarged;  and  the  superficial  lymph  nodes  may  be  palpably 
enlarged.  The  bones  may  be  tender  to  percussion.  The  urine  contains 
a  great  excess  of  uric  acid  (more  than  in  any  other  disease),  due  to 


LEUKEMIA  •  381 

destructive  katabolism  of  nucleins  (of  the  leukocytes).  In  a  majority  of 
the  cases  it  contains  also  at  least  a  small  amount  of  albumin  and  perhaps 
a  few  casts. 

The  conspicuous  feature  of  the  disease  is  the  great  increase  in  the 
number  of  circulating  leukocytes.  They  usually  vary  from  100,000  to 
500,000  when  the  patient  first  seeks  advice;  commonly  there  is  a  pro- 
gressive, though  not  steady,  increase  in  their  number,  so  that  counts  of 
1,000,000  or  more  are  not  rare.  This  increase  is  due  to  an  absolute 
increase  of  all  the  normal  circulating  leukocytes  (including  lymphocytes) 
and  to  a  large  number  of  myelocytes.  The  myelocytes  and  the  poly  nuclear 
neutrophiles  each  vary,  as  a  rule,  between  30  and  60  per  cent,  of  the  total 
leukocytes,  the  poly  nuclear  neutrophiles  being  usually  in  excess  of  the 
myelocytes;  the  eosinophiles  and  the  basophiles  (mast  cells)  also  show 
a  percentage  as  well  as  an  absolute  increase;  the  lymphocytes  and  the 
so-called  large  mononuclear  leukocytes  (variously  named),  as  a  rule, 
show  no  percentage  increase  (usually  a  percentage  decrease),  but  a  great 
absolute  increase.  All  of  the  leukocytes  (including  the  myelocytes) 
exhibit  various  deviations  from  the  normal  in  size,  shape,  character  of 
the  nucleus,  and  staining  affinities  of  the  protoplasm  and  of  the  granules. 

The  red  cells  may  not  be  much  reduced  until  the  disease  has  made 
considerable  progress,  when  marked  oligocythemia  may  occur — 2,000,000 
or  less;  so  that  in  advanced  cases  the  ratio  of  leukocytes  to  erythrocytes 
may  be  1  to  2,  even  1  to  1.  The  color  index  is  usually  low  (0.8  or  less), 
as  in  any  secondary  anemia.  Normoblasts  and  megaloblasts  are  always 
present;  they  are  often  polychromatophilic,  and  may  exhibit  mitosis. 
The  blood  platelets  are  increased.  Charcot-Leyden  crystals  often  sepa- 
rate out  from  the  clotted  blood. 

Lymphocytic  or  Lymphoid  Leukemia. — Lymphocytic  or  lymphoid 
leukemia  (lymphemia)  is  relatively  uncommon,  and  occurs  mostly  in 
males  (two-thirds  of  the  cases).  The  acute  cases  are  most  common 
before  the  thirtieth  year,  many  occurring  before  the  twentieth  year; 
the  chronic  cases  are  most  common  after  the  thirtieth,  especially  after 
the  fiftieth  year  (80  per  cent,  of  the  cases). 

Pathology. — The  lesions  consist  of  lymphocytic  or  lymphoid  hyper- 
plasia of  the  leukoblastic  tissues — the  lymph  nodes,  the  spleen,  and 
the  bone  marrow.  The  changes  likely  may  begin  anywhere  in  the  leuko- 
blastic tissues,  but  the  bone  marrow  apparently  is  always  involved;  in 
some  cases  the  lymph  nodes  show  no  changes  whatever.  The  naked  eye 
appearances  are  not  notably  different  from  those  seen  in  myelocytic 
leukemia;  but  microscopically  the  cellular  infiltrations  and  nodule 
formations  are  of  the  lymphoid  type  (large  or  small  cell,  depending 
largely  upon  the  acuteness  or  chronicity  of  tlie  process). 

Symptoms. — The  onset  may  be  abrupt  or  insidious.  The  acute  cases 
exhibit  the  common  phenomena  of  an  acute  infection,  with  fever  (104°  to 
107°),  and  its  common  concomitants,  weakness,  progressive  emaciation, 
etc.  Often  the  cases  are  mistaken  for  typhoid  fever,  puerperal  infection, 
other  types  of  septicopyemia,  etc.     Usually  there  is  moderate  enlarge- 


382  ■  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

ment  of  the  palpable  lymph  nodes,  but  this  may  be  totally  wanting,  or 
it  may  supervene  late  in  the  course  of  the  disease.  In  some  cases  the 
early  complaint  is  of  enlarged  tonsils,  which  is  usually  misinterpreted 
as  tonsillitis  (confirmation  of  this  supposition  being  sometimes  found 
in  enlargement  and  tenderness  of  the  adjacent  cervical  lymph  nodes,  the 
fever,  and  leukocytosis — without  a  differential  count).  Hemorrhages  are 
quite  characteristic,  and  with  the  other  phenomena  suggest  the  disease 
even  without  a  blood  examination.  The  hemorrhages  occur  into  the  skin 
(petechise,  ecchymoses),  in  the  mucous  membranes,  especially  the  mouth, 
gastro-intestinal  tract,  genito-urinary  tract,  etc.;  in  the  serous  mem- 
branes, the  retina,  the  viscera,  etc.;  often,  especially  in  the  mouth  and 
the  gastro-intestinal  tract  they  are  attended  by  much  ulceration  and 
sloughing.  The  chronic  cases  usually  begin  with  increasing  weakness 
and  enlargement  of  the  lymph  nodes — the  cervical,  the  axillary,  the 
inguinal,  etc.  In  some  cases  there  is  at  first  marked  enlargement  which 
has  developed  rapidly,  but  this  gradually  subsides  and  the  disorder  then 
goes  on  chronically;  but  in  some  cases,  in  the  absence  of  glandular  enlarge- 
ment, the  diagnosis  is  first  disclosed  by  an  examination  of  the  blood. 
Hemorrhages  are  uncommon  in  the  chronic  cases.  Attacks  of  fever 
may  occur  from  time  to  time. 

Examination  discloses  much  the  same  abnormal  physical  conditions 
as  are  encountered  in  myelocytic  leukemia.  The  palpable  lymph  nodes, 
as  a  rule,  are  more  or  less,  sometimes  enormously,  enlarged  (in  contrast 
to  the  usual  slight  enlargement  in  myelocytic  leukemia) ;  the  mesen- 
teric and  retroperitoneal  nodes  may  be  palpable;  the  spleen  and  the 
liver,  however,  are  rarely  as  enlarged  as  in  myelocytic  leukemia.  The 
skin,  in  addition  to  hemorrhages,  may  disclose  urticarial  swellings, 
lymphomatous  nodules,  etc. 

The  diagnostic  feature  of  the  disease  is  the  great  increase  of  circu- 
culating  lymphocytes.  The  total  leukocyte  count  varies  from  normal  to 
500,000  or  more;  usually  at  the  first  count  it  varies  between  20,000  and 
60,000;  the  average  is  less  than  in  myeloid  leukemia  (about  150,000  as 
compared  to  about  400,000),  but  rarely  in  very  acute  cases  the  count 
may  exceed  that  of  the  myelocytic  variety.  The  increase  consists  exclu- 
sively of  lymphocytes,  which  may  constitute  99  per  cent,  or  more  of  the 
total  count.  The  acute  cases  usually  reveal  a  very  high  total  leukocytic 
count,  high  percentage  of  lymphdcytes  (90  to  99  per  cent.),  and  pre- 
ponderance of  large  lymphocytes;  the  chronic  cases,  less  high  total 
count,  less  percentage  of  lymphocytes  (50  to  80  per  cent,  or  more),  and 
preponderance  of  small  lymphocytes.  The  small  lymphocytes  doubtless 
are  derived  in  large  measure  from  the  lymph  nodes ;  but  the  large  lympho- 
cytes of  leukemia  seem  to  be  unquestionably  bone-marrow  cells,  since 
they  differ  materially  from  the  normal  large  lymphocytes  of  the  cir- 
culating blood,  and  much  resemble,  if  they  are  not  identical  with,  cells 
variously  described  as  Grawitz's  unripe  or  immature  leukocytes,  indif- 
ferent lymphoid  cells  (Pappenheim  and  Wolff),  Naegeli's  myeloblasts, 
Turk's  stimulation  cells,  etc.;  perhaps  they  are  in  reality  mother  cells, 


LEUKEMIA  383 

and  to  be  interpreted  as  manifestations  of  reversion  to  an  ancestral  type. 
Some  of  the  small  lymphocytes  also  are  distinctly  of  this  type,  and 
often  there  is  no  sharp  line  of  distinction  between  the  so-called  large 
and  the  small  lymphocytes.  The  lymphocytes  occasionally  exhibit  mitotic 
figures;  commonly  they  show  divers  retrograde  changes.  The  granidar 
leukocytes  are  relatively  and  absolutely  reduced;  one  or  the  other  type 
may  be  entirely  absent  from  time  to  time.  Occasionally  a  few  myelo- 
cytes may  be  seen  (stimulation  myelocytosis).  The  erythrocytes  usually 
are  reduced  to  between  3,000,000  and  4,000,000  when  the  patient  is 
first  seen;  the  color  index  is  low,  and  there  are  the  other  evidences  of 
secondary  anemia — which  increase  with  the  progress  of  the  disease. 
Erythroblasts  are  usually  present,  especially  in  the  acute  cases. 

Atypical  Leukemia. — The  term  atypical  leukemia  finds  some,  but 
incomplete,  justification  in  certain  deviations  from  the  common  types 
exhibited  by  the  two  varieties  of  leukemia  and  in  the  occurrence  of  cer- 
tain disorders  more  or  less  resembling  leukemia,  or  out  of  which  leu- 
kemia may  develop.  In  otherwise  typical  leukemia,  the  blood  picture 
is  sometimes  atypical ;  thus,  the  typical  picture  of  lymphocytic  leukemia 
may  be  present  with  a  total  leukocyte  count  of  7500  or  less;  in  myelo- 
cytic leukemia  the  eosinophiles  or  mast  cells  may  be  absent  or  unusually 
numerous,  and  the  percentage  of  polynuclear  neutrophiles  may  be  very 
high  or  very  low;  and  under  the  influence  of  infections,  such  as  influenza, 
miliary  tuberculosis,  etc.,  the  leukemic  blood  picture  may  become 
remarkably  altered,  or  it  may  disappear  entirely  temporarily.  The  blood 
picture  often  becomes  atypical  shortly  before  death.  In  some  cases 
leukemic  or  leukemic-like  changes  occur  in  the  hemopoietic  tissues 
without  leukemic  changes  appearing  in  the  circulating  blood  (discussed 
under  tumors  and  tumor-like  formations  of  the  lymph  nodes);  in  some 
of  these  cases  true  leukemia  with  the  characteristic  blood  picture  may 
subsecjuently  develop.  Rarely  leukemic  changes  have  been  found  in 
the  blood  without  leukemic  changes  in  the  hemopoietic  tissues  (doubt- 
less due  to  imperfect  examination).  The  supposed  association  of  some 
features  of  leukemia  with  some  features  of  pernicious  anemia  (leukanemia, 
Leube)  has  already  been  mentioned.  Only  rarely,  and  then  doubtfully, 
do  any  of  these  conditions  justify  the  term  atypical  leukemia. 

Chloroma.- — Chloroma  is  an  atypical  form  of  lymphocytic  leukemia  in 
which  the  leukol)lastic  hyperplasias  take  on  a  greenish  tint  and  in  which 
some  of  those  growing  in  the  bone  marrow  penetrate  the  bone  and  give 
rise  to  veritable  tumor  formations  that  invade  the  surrounding;  tissues. 
The  tumor-like  growths  are  found  most  commonly  in  the  skull,  prbit, 
ribs,  sternum,  vertebrae,  etc.,  but  also  in  the  long  bones  and  in  the 
lymph  nodes,  the  viscera  (kidneys,  liver,  spleen),  the  skin,  etc.  They  give 
rise  to  local  pain  (headache,  pains  in  the  legs,  etc.),  regional  swellings 
(especially  in  the  temporal  region,  the  orbit,  etc.),  deafness,  exophthal- 
mos, blindness,  etc.  The  general  manifestation,  such  as  weakness, 
emaciation,  hemorrhages,  anemia,  enlargement  of  the  lyinj)li  nodes,  tlic 
spleen,  and  the  liver,  and  the  blood  picture  are  (piite  like  (liose  of  lynipho- 


384  DISEASES  OF   THE   HEMOPOIETIC  SYSTEM 

cytic  leukemia;  rarely  they  have  been  said  to  resemble  myelocytic 
leukemia.  The  disorder  is  usually  fatal  within  four  or  six  months; 
occasionally  it  has  been  protracted  to  a  year  or  more. 

Diagnosis. — ^The  diagnosis  of  leukemia  is  often  suggested  by  enlarge- 
ment of  the  spleen  or  the  lymph  nodes  (especially  significant  if  associated 
with  hemorrhages),  but  certainty  is  obtained  only  by  an  examination  of 
the  blood.  One  should  distinguish  between  acute  and  chronic  cases: 
myelocytic  leukemia  is  almost  always  chronic;  lymphocytic  leukemia 
may  be  acute  (large  cell  variety)  or  chronic  (small  cell  variety).  Acute 
cases  are  also  characterized  by  fever,  hemorrhages,  and  marked  fluctu- 
ation in  the  number  of  circulating  leukocytes  and  in  the  size  of  the 
enlarged  lymph  nodes  and  the  liver  and  the  spleen.  One  must  exclude 
typhoid  fever,  which  the  acute  cases  resemble  in  the  fever,  typhoid  state, 
enlarged  spleen,  perhaps  intestinal  hemorrhages  (and  the  ulceration  of 
Peyer's  patches  that  may  be  found  after  death).  Different  types  of 
septicopyemia  (acute  endocarditis,  puerperal  infection,  liver  abscess, 
etc.),  scurvy,  hemorrhagic  purpura,  etc.,  also  must  be  excluded;  in 
many  cases  the  diagnosis  is  not  possible  without  an  examination  of  the 
blood.  The  lymphocytosis  that  sometimes  occurs  in  certain  infectious 
diseases,  notably  pertussis,  but  also  syphilis,  malaria,  etc.,  and  the 
myelocytosis  that  may  occur  in  infections,  such  as  diphtheria,  scarlatina, 
etc.,  and  in  certain  forms  of  secondary  anemia  (notably  von  Jaksch's 
disease),  should  not  be  confused  with  leukemia.  Care  should  be  taken 
also  not  to  overlook  the  disease  in  the  beginning  when  the  leukocytosis 
may  be  very  slight,  or  later,  during  a  period  of  remission,  when  there 
may  be  a  fall  to  almost,  if  not  quite,  the  normal  number  of  leuko- 
cytes; a  differential  count  will  furnish  the  clue  to  the  correct  diagnosis. 
The  differentiation  from  Hodgkin's  disease  and  other  disorders  attended 
with  enlarged  lymph  nodes  is  discussed  under  tumors  and  tumor-like 
formation  of  the  lymph  nodes. 

Prognosis. — The  disease  is  always  fatal — within  a  week  to  two  or  three 
months  in  the  acute  cases;  within  from  six  months  to  three  or  more 
years  in  the  chronic  cases.  In  the  acute  cases  death  usually  ensues  in 
consequence  of  fever,  hemorrhages,  anemia,  and  exhaustion.  In  the 
chronic  cases,  remissions  for  weeks  or  months  are  not  uncommon  (spon- 
taneous or  due  to  intercurrent  infection,  treatment,  etc.).  Death  may 
result  from  the  ordinary  progress  of  the  disease,  which  toward  the  end  is 
likely  to  be  rapid,  or  from  an  intercurrent  infection,  such  as  tuberculosis, 
pyococcic  infection,  influenza,  pneumonia,  etc. 

Treatment. — The  nature  of  the  disease,  so  far  as  we  know,  seems  to 
preclude  effective  treatment.  The  acute  cases  pursue,  as  a  rule,  a  steadily 
progressive  course  to  the  fatal  issue,  although  rarely  a  case  beginning 
apparently  acutely  becomes  stayed  and  goes  into  the  chronic  stage.  In 
the  chronic  cases  arsenic  and  the  .r-rays  are  often  of  much  benefit — 
arsenic  in  both  varieties  of  the  disease,  the  a;-rays  especially  in  the  myelo- 
cytic variety.  The  arsenic  should  be  given  in  gradually  ascending  doses 
to  the  point  of  toleration;  sometimes  benefit  is  not  apparent  until  the 


ERYTHREMIA  385 

dose  reaches  a  dram  of  Fowler's  solution  daily.  The  a;-ray  treatment 
should  be  carried  out  as  recommended  by  Stengel  and  Pancoast  systemati- 
cally :  the  bone  marrow  in  different  regions  in  succession  should  be  sub- 
jected to  the  action  of  the  x-rays  for  periods  averaging  fifteen  minutes 
daily;  the  spleen  should  not  be  subjected  to  the  direct  action  of  the 
.r-rays  until  it  has  become  reduced  in  size  and  the  total  leukocyte  count 
has  diminished ;  special  care  must  be  exercised  to  avoid  even  the  slight- 
est toxic  reaction.  The  treatment  should  be  continued  until  the  spleen 
and  the  leukocyte  count  are  normal;  discontinuance  of  the  treatment 
should  be  gradual,  and  the  period  of  cessation  should  not  be  too  pro- 
tracted. The  .T-rays  exert  a  specific  leukolytic  action,  especially  on  the 
young  cells — the  non-granular  mononuclear  leukocytes  and  the  myelo- 
cytes; and  the  serum  of  a  leukemic  subject  tljat  has  improved  under 
a;-ray  treatment  contains  a  substance  which  injected  into  lower  animals 
produces  leukopenia,  disintegrating,  first,  the  mononuclear  cells;  perhaps 
the  future  will  furnish  us  a  leukolytic  serum  efficient  in  human  subjects. 
Splenectomy  in  leukemia,  of  course,  is  an  irrational  measure. 


ERYTHREMIA. 

{Erythrocytosis;  Megalosplenic  Polycythemia  or  E rythrocythemia ;  Polycythemia  uith 
Cyanosis  and  Enlarged  Spleen;  Yaquez's  Disease.) 

Erythremia  is  a  disease  of  the  hemopoietic  tissues,  characterized  by 
hyperactivity  of  the  erythroblastic  tissues  of  the  bone  marrow,  and  by 
polycythemia,  chronic  cyanosis,  and  enlarged  spleen. 

Etiology. — The  disease  occurs  with  about  equal  frequency  in  the  two 
sexes,  and  especially  after  the  thirty-fifth  year.  The  cause  is  not  known. 
Some  of  the  early  cases  were  attributed  to  tuberculosis  of  the  spleen,  but 
doubt  has  been  thrown  upon  the  accuracy  of  the  observation.  Hyp^'- 
activity  of  the  erythroblastic  tissues  of  the  bone  is  believed  to  be  the 
basis  of  the  disorder,  but  the  initiating  cause  is  unknown. 

Pathology. — The  noteworthy  changes  consist  of  a  purplish-red  bone 
marrow  (myelomatosis  rubra)  due  to  extraordinary  hyperplasia  of  the 
erythroblastic  tissues;  and  enlargement  of  the  spleen  due  to  hyperplasia 
of  all  the  constituent  elements,  and  some  evidences  of  chronic  passive 
congestion.  The  changes  in  the  spleen  are  believed  by  some  observers 
(Osier,  etc.)  to  be  active  rather  than  passive;  perhaps  a  reversion  to 
the  foetal  condition  of  erythrocytogenesis;  others  (Widal,  Weintraud,  etc.) 
suggest  that  the  spleen  loses  its  function  of  hemolysis,  in  consequence  of 
which  erythrocytes  accumulate  and  the  erythroblastic  tissues  of  the  bone 
marrow  l)ecome  abiionnally  stimulated.  The  disease  has  been  attril)uted 
also  to  diminished  oxygen  absorption  by  tlie  erythrocytes  and  consc(|Ucnt 
hyperplasia  of  the  erythroblastic  tissues. 

Symptoms. — The  symptoms  begin  gradually,  as  a  rule,  in  middle  life 
or  later;  they  consist  of  grarhially  increasing  weakness,  headache,  ver- 
tigo, hebetude,  and  other  symptoms'attributable  to  cerebral  congestion; 
25 


386  DISEASES  OF  THE  HEMOPOIETIC  SYSTEM 

chronic  cyanosis;  and  enlargement  and  fulness  of  the  abdomen,  with 
a  sense  of  weight,  especially  in  the  region  of  the  spleen.  The  skin  in 
general,  but  especially  of  the  face,  hands,  and  feet,  and  the  visible  mucous 
membranes  take  on  a  peculiar,  mottled,  purplish-red  color;  the  lips,  ears, 
and  finger  tips  become  even  darker,  more  dusky.  The  color,  especially 
of  the  limbs,  becomes  darker  under  the  influence  of  cold  (varying  thus 
with  the  seasons)  and  of  gravity;  and  it  lessens  if  the  arms  or  legs  be 
held  upright  (vasomotor  instability).  The  cyanosis  is  attributable  to  the 
polycythemia  and  increased  volume  of  blood,  increased  viscosity  of  the 
blood,  slow  circulation,  and  distended  venules  and  capillaries  (loss  of 
tonicity).  In  long-standing  cases  pigmentation  of  the  skin  and  mucous 
membranes  ensues.  Hemorrhages  from  the  mucous  membranes  (nose, 
mouth,  lungs,  stomach,  etc.)  are  not  uncommon  (stasis  and  impaired 
nutrition) ;  occasionally  they  occur  in  the  viscera,  notably  the  brain,  where 
they  give  rise  to  the  ordinary  phenomena  and  sequels  of  apoplexy.  The 
fulness  in  the  abdomen  is  due  to  an  enlarged  spleen,  which  is  present  in 
at  least  four-fifths  of  the  cases.  The  liver  also  may  be  somewhat  enlarged. 
The  heart  may  become  hypertrophied.  The  blood  pressure  is  usually 
normal.  Examination  of  the  blood  reveals  increased  (in  some  cases 
doubled)  total  volume,  increased  specific  gravity  (up  to  1077),  and  in- 
creased viscosity  (3  to  4  times  the  normal);  the  erythrocytes  are  increased 
up  to  9,000,000  to  13,000,000  per  cubic  millimeter,  the  hemoglobin  to 
120,  150,  even  200  per  cent.,  and  the  leukocytes  to  10,000  or  20,000  or 
more.  In  a  majority  of  the  cases  there  is  a  relative  increase  of  the 
polynuclear  neutrophiles  (75  to  90  per  cent.),  and  sometimes  of  the  large 
mononuclear  leukocytes;  occasionally  myelocytes  are  seen;  the  erythro- 
cytes, as  a  rule,  are  normal  in  size,  but  there  are  some  poikilocytes  and 
many  erythroblasts  (normoblasts  and  megaloblasts).  The  blood  changes 
together  indicate  hyperactivity  of  the  bone  marrow. 

Diagnosis. — Chronic  cyanosis,  enlarged  spleen,  and  erythrocythemia 
constitute  a  triad  of  symptoms  that  is  almost  pathognomonic.  One 
must  eliminate  other  causes  of  chronic  cyanosis,  such  as  chronic  cardiac 
and  pulmonary  disease,  the  methemoglobinemia  of  poisoning  by  coal 
tar  products,  so-called  enterogenous  cyanosis,  local  asphyxias  (Raynaud's 
disease  and  allied  conditions),  etc. 

Prognosis. — So  far  as  is  known  the  disorder  is  ultimately  fatal.  It 
usually  pursues  a  chronic  course,  upward  of  six  to  eight  years  or  more. 

Treatment. — No  really  effective  treatment  is  known.  Removal  of  the 
spleen  seems  contra-indicated  from  the  nature  of  the  disease  and  the 
tendency  to  hemorrhage.  Venesection  is  of  value  in  relieving  temporarily 
the  headache,  vertigo,  etc. ;  it  may  be  repeated  from  time  to  time.  Potas- 
sium iodide  has  been  advocated,  and  oxygen  by  inhalation  has  been  used 
with  a  view  to  relieve  the  cyanosis,  but  both  are  of  at  least  doubtful 
utility.  The  x-rays,  as  in  leukemia,  constitute  perhaps  the  best  treatment, 
but  the  data  at  hand  are  not  yet  sufficient  to  warrant  a  positive  opinion. 


PURPURA  387 

THE   HEMOKRHAGIC  DISEASES. 

HEMORRHAGE  IN  THE  NEWBORN. 

Hemorrhage  occasionally  occurs  in  the  newborn,  and  usually  from 
the  umbilicus,  the  gastro-intestinal  tract,  the  rectum,  the  mouth,  the 
nose,  the  bladder,  etc.  It  is  commonly  associated  with  jaundice.  It 
may  be  due  to:  (1)  Injuries  received  during  birth.  (2)  Septicopyemia 
acquired  during  or  after  birth.  (3)  Syphilis  (syphilitic  arteriocapillary 
disease),  in  which  event  it  may  be  present  even  at  birth,  and  may  be 
associated  with  visceral  hemorrhages.  (4)  Epidemic  hemoglobinuria 
(Winckel's  disease),  a  disorder  of  unknown,  though  probably  infectious, 
nature  (hospital  epidemics),  developing  usually  within  the  first  four 
to  ten  days  of  life,  and  characterized  by  fever,  jaundice,  punctiform 
hemorrhages  in  the  tissues  and  organs,  dyspnoea,  cyanosis,  gastro- 
intestinal derangements  (diarrhoea),  enlarged  spleen,  albuminuria, 
hematuria  or  methemoglobinuria,  etc.,  and  soon  leading  to  death.  In 
some  cases  there  is  marked  fatty  degeneration  of  the  viscera  (Buhl's 
disease).  (5)  Morbus  maculosus  neonatorum,  a  disorder  clinically 
akin  to  morbus  maculosus  of  the  adult,  and  as  ill  understood  etiologi- 
cally,  although  it  is  perhaps  infectious  (sometimes  attended  by  fever, 
occurs  especially  in  hospitals,  and  sometimes  appears  to  be  self-limited). 
The  bleeding  is  perhaps  most  common  from  the  bowel  (melena — which 
should  not  be  confounded  with  blood  sucked  from  the  breast);  it  may 
also  occur  from  the  stomach,  mouth,  nose,  umbilicus,  etc.  Death  occurs 
in  50  per  cent,  or  more  of  the  cases.  The  treatment  of  these  disorders  is 
that  of  syphilis  or  septicopyemia,  to  which  may  be  added  the  subcu- 
taneous injection  of  normal  human  or  other  blood  serum  and  such  local 
measures  (mentioned  under  hemophilia)  as  may  tend  to  control  the 
bleeding. 

PURPURA. 

The  term  purpura  comprises  a  series  of  disorders  characterized  by 
the  occurrence  of  hemorrhages  into  the  skin  and  mucous  membranes. 
Commonly,  like  anemia,  it  is  symptomatic  of  some  more  or  less  obvious 
disorder,  but  often  it  partakes  of  the  nature  of  an  independent  disease 
of  unknown  cause.  One  may  distinguish,  therefore,  two  types — the 
secondary  or  symptomatic,  and  the  primary  or  idiopathic. 

The  hemorrhages,  so-called  purpuric  spots,  vary  in  size — from  small 
roundish  petechise,  1  to  3  mm.  or  more  in  diameter,  to  larger  ecchymoses, 
often  irregular  in  outline  and  perhaps  due  to  confluence  of  several  small 
areas.  Occasionally  the  hemorrhages  are  linear  (vibices).  \Vlien  fresh 
they  are  bright  red  in  color,  and  being  extravasations  they  do  not  dis- 
appear on  pressure;  soon  they  become  dark  or  purplish,  and  gradually 
transformed  into  reddish-brown  or  yellowish  areas,  so  that  at  the  end  of 
a  week,  as  a  rule,  only  more  or  less  faintly  pigmented  spots  remain. 


388  THE  HEMORRHAGIC  DISEASES 

Successive  crops  occasion  considerable  color  variation  of  adjacent  spots. 
Most  frequently  the  legs  are  involved,  and  then  in  order  of  frequency  the 
arms,  the  trunk,  the  face,  and  the  accessible  mucous  membranes. 

Secondary  (symptomatic)  purpura  occurs  in:  (1)  Infections,  such  as 
typhus  fever,  cerebrospinal  fever,  and  acute  endocarditis — all  three  of 
which  are  especially  characterized  by  a  purpuric  eruption;  it  may  occur 
also  in  septicopyemia  (pyococcic  infections),  smallpox,  typhoid  fever, 
scarlatina,  measles,  syphilis,  cholera,  etc.  (2)  Intoxications,  such  as 
snake  bite;  drug  poisonings,  especially  with  the  iodides,  but  also  bro- 
mides, quinine,  salicylic  acid,  belladonna,  copaiba,  ergot,  mercury, 
arsenic,  etc.;  and  autogenic  poisonings,  such  as  may  attend  nephritis, 
jaundice,  etc.  (3)  Cachectic  states  or  nutritional  disorders,  such  as  are 
associated  with  the  marasmus  of  old  age  (senile  purpura),  general 
inanition,  carcinoma,  sarcoma,  pernicious  anemia,  leukemia,  Hodgkin's 
disease,  etc.  (4)  Nervous  disorders  (myelopathic  purpura),  such  as 
myelitis,  tabes  dorsalis  (in  which  it  may  follow  and  be  confined  to  the 
area  of  the  lightning  pains),  hysteria  (hemorrhagic  stigmas),  neuralgias, 
such  as  trifacial  neuralgia  and  sciatica  (in  which  the  purpura  may  be 
limited  to  the  painful  area),  etc.  (5)  Mechanical  disorders,  such  as 
marked  venous  stasis  (as  in  heart  disease,  following  the  application  of 
a  tight  bandage,  etc.),  embolism,  epileptic  seizures,  whooping-cough 
paroxysms,  local  injuries,  etc.  Mechanical  factors  seem  operative  in 
other  types  of  the  disorder,  and  perhaps  explain  the  frequency  of  the 
petechise  on  the  legs. 

Primary  (idiopathic)  purpura  comprises  several  disorders,  variously 
described  as  simple  purpura,  arthritic  (rheumatic)  purpura,  hemorrhagic 
purpura,  abdominal  (Henoch's)  purpura,  etc.  These  differ  perhaps  in 
grade,  intensity,  or  localization  of  the  process  rather  than  in  nature.  In 
the  present  state  of  our  knowledge  it  is  impossible  sharply  to  differ- 
entiate them  or  satisfactorily  to  classify  them. 

Etiology. — The  disorder  is  most  common  in  the  second  and  third 
decades  of  life,  although  it  occurs  at  all  ages,  and  it  affects  males  rather 
than  females.  The  cause  is  not  known.  By  some  it  is  believed  to  be  an 
infection  or  an  intoxication,  but  neither  the  infectious  agent  nor  the  toxin 
has  been  isolated;  blood  cultures  have  usually  been  negative.  Primary 
disturbances  of  the  nervous  system,  of  the  liver,  of  the  blood,  and  of  the 
bloodvessels  have  been  postulated.  Judging  from  the  perhaps  analogous 
action  of  the  hemorrhagin  of  snake  venom,  it  seems  likely  that  the  essence 
of  the  process  consists  in  an  endotheliolysis  of  the  capillaries  provoked 
by  some  unknown  poison;  the  primary  change  may  occur  in  the  blood. 

Pathology. — There  are  no  characteristic  lesions,  aside  from  the  hemor- 
rhages. In  fatal  cases  there  is  high-grade  anemia  of  the  viscera  with  the 
usual  concomitants.  There  may  also  be  petechial  and  larger  hemor- 
rhages into  the  serous  and  mucous  membranes.  The  spleen  may  be 
enlarged,  and  there  may  be  nephritis  (usually  glomerulo-nephritis). 
No  constant  or  characteristic  changes  have  been  found  in  the  bloodves- 
sels.    During  life  the  blood  reveals  the  ordinary  changes  of  secondary 


PURPURA  389 

anemia,  although  in  some  cases  the  erythrocytes  become  reduced  much 
below  2,000,000  (to  about  500,000  in  some  fatal  cases);  the  blood  platelets 
are  usually  remarkably  reduced  (20,000  or  less  instead  of  the  normal 
200,000  to  700,000).  The  coagulation  time  of  the  blood  is  usually  within 
normal  limits,  although  it  may  be  considerably  increased  (delayed);  the 
clot  often  is  less  firm  than  normally. 

Symptoms. — In  the  simplest  form  (so-called  purpura  simplex),  which 
is  most  common  in  adult  life,  the  cutaneous  hemorrhages,  as  a  rule,  are 
the  only  noteworthy  manifestation.  They  are  usually  small  (petechial), 
occur  in  crops,  and  are  most  common  on  the  legs  and  arms.  Occasionally 
there  is  a  little  fever  or  slight  pain  and  tenderness  in  the  joints  and 
muscles.  The  disorder  usually  lasts  from  two  to  six  weeks;  rarely  there 
are  recurring  attacks  that  last  for  a  year  or  more  (chronic  purpura). 

When  the  articular  symptoms  are  obtrusive  the  disease  is  usually 
spoken  of  as  purpura  (or  peliosus)  rheumatica  (or  arthritica),  or  Schon- 
lein's  disease,  but  it  is  in  no  way  related  to  acute  articular  rheumatism. 
In  about  half  of  the  cases  the  onset  of  the  disease  is  attended  with  fever 
(101°  to  102°),  and  there  may  be  prodromal  or  invasion  symptoms  con- 
sisting of  sore  throat  (tonsillitis),  malaise,  anorexia,  nausea,  neuromus- 
cular and  articular  pains  and  tenderness,  etc.  The  purpuric  eruption  is 
like  that  of  simple  purpura,  perhaps  somewhat  aggravated.  It  may  be 
preceded  by  or  associated  with  urticaria  (purpura  urticans),  or  erythema 
nodosum,  or  rarely  vesiculation  (pemphigoid  purpura).  The  articular 
symptoms  consist  of  pain,  tenderness,  and  swelling;  they  are  most  common 
in  the  knees,  ankles,  and  elbows,  but  may  occur  in  other  joints;  they  may 
antedate  or  occur  with  or  subsequent  to  the  purpura;  and  they  usually 
last  a  few  (four  to  seven)  days,  but  may  recur. 

The  curious  association  of  purpura,  urticaria,  erythema,  angioneurotic 
oedema,  and  visceral  lesions  has  been  especially  studied  by  Osier,  who 
states  that  it  occurs  chiefly  in  children,  and  is  characterized  by  relapses 
or  recurrences,  often  extending  over,  several  years;  cutaneous  lesions, 
which  may  be  simple  purpura,  purpura  urticans,  urticaria,  angioneurotic 
oedema,  and  erythema  in  all  its  multiform  varieties;  gastro-intestinal 
crises — pain,  vomiting,  and  diarrhoea;  joint  pains  or  swelling,  often 
trifling;  hemorrhages  from  the  mucous  membranes;  enlargement  of  the 
spleen;  and  nephritis  (40  to  50  per  cent,  of  the  cases),  which  is  the 
most  frequent  cause  of  death  (which  occurs  in  about  7  per  cent,  of  the 
cases).  The  cases  characterized  by  purpura  or  other  skin  lesions,  gastro- 
intestinal crises,  arthritis,  and  often  nephritis,  are  commonly  spoken  of  as 
Henoch's  or  abdominal  purpura. 

In  another  series  of  cases,  to  the  cutaneous  and  arthritic  lesions  hemor- 
rhages from  the  mucous  membranes  are  added  (hemorrhagic  purjKU-a, 
morbus  maculosus,  AYerlhof).  Nasal  and  oral  hermorrhages  are  the 
most  common;  but  there  may  be  bleeding  from  the  lungs,  stomach, 
intestine,  kidney,  genitalia,  or  rarely  into  the  retiujae,  brain,  etc.  Occa- 
sionally cases  have  been  observed  in  which,  for  a  time  at  least,  the  cutane- 
ous manifestations  were  absent,   while  the  other  symptoms  (such  as 


390  THE  HEMORRHAGIC  DISEASES 

visceral  crises,  epistaxis,  etc.)  seemed  to  justify  the  diagnosis  (so-called 
purpura  without  skin  lesions);  in  some  of  these  cases  skin  lesions  have 
subsequently  appeared.  The  disease  may  terminate  favorably  within  two 
weeks  or  thereabouts;  but  death  may  ensue  from  the  direct  loss  of  blood, 
hemorrhage  into  the  brain,  etc.  Occasionally  in  very  severe  cases  death 
occurs  within  twenty-four  or  thirty-six  hours  or  thereabouts  (purpura 
fulminans). 

Diagnosis. — One  should  distinguish  the  symptomatic  from  the  so- 
called  idiopathic  cases.  The  idiopathic  cases  may  be  distinguished  from 
hemophilia  by  the  absence  of  hereditary  factors;  and  from  scurvy  by  a 
knowledge  of  the  previous  history,  the  absence  of  sponginess  of  the  gums 
(bleeding  from  the  gums  is  not  uncommon  in  purpura),  the  absence  of 
the  hemorrhagic,  sclerodermic,  or  muscular  infiltration  of  the  thighs  (so 
characteristic  of  scurvy),  and  the  effect  of  antiscorbutic  treatment. 

Prognosis. — The  outlook  is  good  except  in  the  event  of  severe  onset 
and  rapid  course  (purpura  fulminans),  very  great  loss  of  blood,  hemor- 
rhage into  the  brain,  nephritis,  and  other  serious  complications. 

Treatment. — The  treatment  of  symptomatic  purpura  is  that  of  the 
primary  or  underlying  disease.  In  the  idiopathic  cases  rest  in  bed,  fresh 
air,  good  food,  iron,  bitter  tonics,  strychnine,  etc.,  are  indicated.  Good 
results  sometimes  attend  the  use  of  arsenic  in  gradually  increasing  doses 
to  the  point  of  toleration;  and  of  aromatic  sulphuric  acid  and  turpentine 
(which  seem  to  check  the  bleeding),  and  of  calcium  lactate  (to  increase 
the  coagulability  of  the  blood).  Accessible  bleeding  spots  may  be  treated 
as  recommended  in  hemophilia. 


HEMOPHILIA. 

Hemophilia  is  a  disorder,  commonly  hereditary,  characterized  by  severe 
and  often  uncontrollable  hemorrhage  and  lessened  coagulability  of  the 
blood,  and  often  associated  with  hemarthrosis  and  arthritis. 

Etiology. — Hemophilia  is  "the  most  hereditary  of  hereditary  diseases" 
(Grandidier),  and,  as  in  the  Appleton-Swain  family,  is  known  to  have 
been  transmitted  to  the  seventh  generation  (within  a  period  of  two 
hundred  years).  Males  usually  exhibit  the  disorder — the  proportion  of 
males  to  females  varying  between  13  to  1  (Grandidier,  657  cases)  and 
4  to  1  (Stempel,  209  cases);  but  the  disease  seems  to  be  transmitted 
almost  exclusively  by  the  females.  The  Anglo-German  races  are  most 
frequently  attacked,  but  even  negroes  are  not  exempt.  Hemophilic 
subjects  usually  are  otherwise  healthy;  commonly  they  are  blondes  with 
soft  delicate  skin;  often  they  are  neurotic;  usually  they  are  remarkably 
fecund. 

The  cause  of  the  disease  is  not  known.  There  is  no  good  evidence  that 
consanguinity  is  of  etiological  significance.  Virchow  believed  in  an 
abnormal  tenuity  and  fragility  of  the  vessels,  but  no  noteworthy  or  con- 
stant changes  are  found.    Sahli  suggests  an  hereditary  deficiency  in  the 


HEMOPHILIA  391 

formation  of  thrombokinase  by  the  vessel  wall.    An  infectious  theory  has 
been  advanced,  but  it  is  not  supported  by  any  trustworthy  evidence. 

Pathology. — The  only  constant  finding  in  fatal  cases  is  high-grade 
anemia  and  its  usual  consequences.  In  a  few  cases  the  arteries  have  been 
found  unusually  thin;  in  others  the  endothelium  of  the  arterioles  has 
proliferated;  in  still  others  the  left  ventricle  has  been  hypertrophied — but 
none  of  these  changes  appears  to  possess  any  special  significance. 

Symptoms. — In  about  three-fourths  of  the  cases  the  disorder  becomes 
manifest  in  the  first  two  years  of  life  (rarely  in  the  newly  born);  occa- 
sionally it  is  delayed  until  the  second  or  the  third  decade,  rarely  until 
advanced  life.  The  characteristic  of  the  disease  is  severe,  often  uncon- 
trollable hemorrhages,  occurring  spontaneously  or  induced  by  slight  (or 
pronounced)  trauma.  The  hemorrhages  may  be  superficial — into  or 
from  the  skin  and  the  mucous  membranes ;  interstitial  or  parenchyma- 
tous— into  the  subcutaneous  and  submucous  tissues  and  the  organs  of  the 
body;  or  they  may  occur  into  the  serous  sacs.  The  chief  sources  of  the 
bleeding  are  the  nose  (50  per  cent,  of  the  cases),  the  mouth  and  gums  (12 
per  cent.),  the  stomach,  intestines,  lungs,  kidneys,  skin  (where  in  con- 
trast to  purpura  they  are  rarely  petechial),  etc.;  but  they  may  occur  from 
any  part  of  the  body,  such  as  the  urethra,  vulva,  uterus,  tear  papilla, 
eyelids,  etc.  The  hemorrhage  is  usually  a  capillary-  oozing  only,  but  it 
may  be  also  arterial  or  venous,  especially  in  the  event  of  incised  or 
lacerated  wounds.  The  bleeding  may  last  for  hours  or  days,  and  on 
account  of  the  large  amount  of  blood  lost  may  promptly  lead  to  death; 
rarely  the  bleeding  continues  for  months.  The  retained  hemorrhages 
may  give  rise  to  smaller  or  larger  hematomas.  Minor  operations,  such 
as  circumcision,  the  eruption  or  extraction  of  a  tooth,  vaccination,  etc., 
may  give  rise  to  severe  and  even  fatal  hemorrhage;  the  hemorrhage  of 
menstruation  and  of  parturition  may  be  excessive,  but  is  usually  not 
unless  there  are  other  phenomena  of  the  disease.  Joint  manifestations, 
involving  especially  the  knees  and  elbows,  but  also  other  joints,  are 
exceedingly  common;  according  to  Konig  they  may  be:  (1)  Hemarthrosis 
(pain,  tenderness,  swelling,  perhaps  fluctuation,  and  visible  hemor- 
rhage about  the  joint);  (2)  arthritis,  with  fever,  resembling  tuberculosis; 
and  (3)  a  condition  resembling  arthritis  deformans.  There  may  be 
associated  muscular  pains,  neuralgias,  etc.  In  some  cases  the  tendency 
to  bleeding  seems  to  be  confined  to  some  particular  part  of  the  body 
(local  hemophilia),  such  as  the  kidney  (so-called  renal  hemophilia), 
the  gastro-intestinal  tract,  the  nose,  etc.,  other  parts  of  the  body  appar- 
ently being  (temporarily  or  permanently)  exempt.  Some  of  the  cases 
of  recurring  epistaxis  are  associated  with  curious  multiple  hereditary 
telangiectases  of  the  nose,  lips,  tongues,  cheek,  etc. 

Following  the  bleedings  there  are  the  usual  changes  of  secondary 
anemia.  There  may  be  a  relative  lymphocytosis.  The  coagulability  of 
the  blood  is  usually  lessened;  in  some  cases  it  has  been  found  remark- 
ably lessened  (the  coagulation  time  being  forty-five  to  sixty  minutes  or 
more);  but  recent  studies  by  Sahli  tend  to  show  tliat  the  coagulabiHty 


392  THE  HEMORRHAGIC  DISEASES 

may  be  normal  or  increased  diu"ing  the  period  of  bleeding  and  lessened 
during  the  intervals.  If  the  hemorrhage  does  not  prove  fatal,  recovery 
is  usually  more  rapid  than  after  other  types  of  bleeding. 

Diagnosis. — The  familial  transmission  of  the  disease,  its  common 
development  in  early  life,  its  usual  persistence  throughout  life,  the 
occurrence  and  recurrence  of  bleeding  upon  little  or  no  provocation,  the 
disproportion  of  the  bleeding  to  the  provoking  trauma,  the  virtual  uncon- 
trollability  of  the  bleeding,  and  the  joint  phenomena  are  cjuite  char- 
acteristic, and  serve  to  exclude  the  hemorrhages  of  the  newborn,  pur- 
pura, and  scurvy. 

Prognosis. — ^Any  hemorrhage  may  be,  but  the  first  is  rarely,  fatal.  Many 
if  not  most  subjects  die  within  the  first  year  of  life,  and  more  than  80  per 
cent,  before  reaching  adult  life.  The  outlook  is  worse  in  boys  than  in 
girls. 

Treatment. — With  a  view  to  preventing  the  disease,  the  daughters  of 
hemophiliacs  should  be  advised  not  to  marry — advice  that  is  likely  not  to 
be  heeded.  The  boys  should  avoid  traumas  of  all  sorts;. they  should  be 
rendered  as  robust  as  possible  by  fresh  air,  good  food,  hydrotherapy, 
massage,  tonics,  etc.,  and  operations,  even  minor  ones,  such  as  circum- 
cision, extraction  of  a  tooth,  etc.,  should  be  interdicted,  except  in  the 
event  of  diseases  otherwise  threatening  life. 

When  hemorrhage  has  occurred,  it  may  sometimes  be  controlled  by 
rest  and  compression,  such  as  plugging  the  nares,  or  the  application  of 
compresses  to  other  accessible  regions.  Adrenalin  chloride  (1  to  1000), 
ice,  cocaine  (2  to  4  per  cent.),  calcium  lactate  or  chloride  (2  per  cent.), 
gelatin  (5  per  cent,  eflfectually  sterilized),  gallic  acid,  tannic  acid,  and 
other  so-called  styptics  may  be  applied  locally  (on  the  compress);  but 
usually  they  are  of  little  avail.  Wright  recommends  the  inhalation  of 
carbon  dioxide  and  oxygen  in  epistaxis.  Internally  calcium  lactate  (15  to 
20  grains,  1  to  1.3  gram,  thrice  daily,  or  50  grains,  3.3  gram,  at  once) 
may  be  given.  It  is  wise  to  intermit  its  administration  after  a  few  days, 
since  continuous  use  sometimes  seems  to  lessen,  after  having  first  in- 
creased, the  coagulability  of  the  blood.  The  best  results  appear  to  attend 
the  use  of  normal  blood  serum  (of  the  rabbit,  horse,  or  man)  locally,  sub- 
cutaneously,  and  intravenously.  A  single  injection  subcutaneously  of 
20  to  30  c.c.  has  sufficed  to  arrest  the  bleeding,  but  it  may  be  necessary 
to  repeat  the  injections  daily  or  every  two  or  three  days  until  the  desired 
result  has  been  secured.  In  the  absence  of  other  serum,  the  ordinary  anti- 
diphtheritic  serum  may  be  used.  The  arthritic  lesions  should  be  treated 
by  rest  (immobilization),  and  after  several  days  by  massage.  Much 
swelling  and  pain  may  necessitate  aspiration.  Extreme  loss  of  blood 
demands  measures  appropriate  for  exsanguination  occurring  under  other 
circumstances,  such  as  physiological  saline  solution  intravenously,  adre- 
nalin chloride,  etc.  (see  acute  secondary  anemia). 


LYMPHANGITIS   AND  LYMPHADENITIS  303 

DISEASES  OF  THE  LYMPH   NODES  AND  LYMPH 

VESSELS. 

Pathological  Physiology. — The  lymph  nodes,  as  has  been  mentioned,  are 
concerned  in  hemopoiesis  to  the  extent  of  forming  perhaps  most  of  the 
circulating  lymphocytes  during  health;  to  some  degree  also  they  serve 
to  protect  the  body  against  bacterial  infections;  they  have  slight  phago- 
cytic properties;  and  they  participate  in  the  processes  of  hemolysis. 
The  formation  of  lymphocytes  becomes  extraordinarily  augmented 
in  some  cases  of  leukemia,  in  which  event  the  nodes  exhibit  various 
degrees  of  hyperplasia  and  metaplasia.  The  protection  exerted  against 
bacterial  infection  is  not,  as  a  rule,  highly  effective,  and  may  become 
totally  overcome,  especially  in  severe  pyococcic  infections.  In  other 
cases,  however,  doubtless  in  consequence  of  chemical  activities,  but 
perhaps  also  of  phagocytic  properties,  bacterial  activity  is  restrained,  if 
not  entirely  abolished;  but,  as  is  well  exemplified  in  some  cases  of  tuber- 
culosis, bacteria  may  remain  for  a  long  time  latent  in  lymph  nodes,  and 
under  auspicious  circumstances  become  activated.  The  hemolymph 
nodes,  certain  nodes  especially  numerous  in  the  abdomen  in  front  of  the 
vertebrae,  and  containing,  in  addition  to  the  structures  of  the  ordinary 
lymph  nodes,  sinuses  filled  with  blood  corpuscles,  in  general  subserve 
the  same  functions  and  are  subject  to  the  same  pathological  conditions 
as  the  lymph  nodes.  In  certain  disorders,  such  as  pernicious  anemia  and 
some  toxic  and  infectious  processes,  they  seem  to  be  unduly  concerned  in 
hemolysis  as  well  as  in  processes  of  immunity  (Warthin).  AMiether 
these  glands  participate  also  in  erythrocytogenesis  has  not  yet  been 
determined.  The  lymph  nodes  may  entangle  metastatic  carcinomatous 
cells,  and  enlarging;  mav  be  the  first  noteworthv  evidence  of  internal 
carcinoma. 

LYMPHANGITIS  AND  LYMPHADENITIS. 

Lymphangitis  and  lymphadenitis,  although  they  may  occur  separately, 
are  usually  associated;  the  process  may  be  acute  or  chronic,  and  is 
always  due  to  bacterial  infection.  The  acute  cases  are  usually  due  to 
the  ordinary  pyogenic  cocci— staphylococci,  streptococci,  pneuraococci, 
etc.;  but  acute  lymphadenitis  is  common  also  in  many  of  the  acute 
specific  infectious  diseases,  such  as  diphtheria,  scarlatina,  measles, 
chickenpox,  erysipelas,  plague,  glandular  fever,  typhoid  fever,  gonor- 
rhoea, chancroid,  as  well  as  rickets,  lymphatic  constitution,  etc.;  the 
chronic  cases  are  due  usually  to  tuberculosis  or  syphilis.  The  infection 
in  lymphangitis  is  usually  acquired  by  means  of  a  wound,  but  this  is  not 
always  necessary,  since  infection  seems  sometimes  to  be  acquired  without 
or  with  only  the  slightest  abrasion,  as  at  necropsies,  operations  on  sep- 
ticopyemic patients,  etc.    The  infectious  agent  may  enter  the  lymph  vessel 


394     DISEASES  OF  THE  LYMPH    NODES  AND  LYMPH    VESSELS 

directly  from  the  wound,  or  it  may  invade  the  vessel  wall  from  without. 
In  lymphadenitis  the  infection  may  be  lymphogenous,  in  which  event  it  is 
likely  to  be  localized;  or  it  may  be  hematogenous,  in  which  event  it  is 
likely  to  be  generalized  (as  in  some  of  the  specific  infectious  diseases). 

Pathology. — Acute  lymphangitis  is  commonly  a  part  of  pyococcic 
infection  (septicopyemia)  and  partakes  of  the  nature  of  such  infections. 
It  may  involve  only  circumscribed  areas  (reticular  lymphangitis),  or  the 
lymphatic  trunks  (tubular  lymphangitis).  The  endothelial  cells  lining 
the  lymph  spaces  swell  and  later  desquamate,  and  together  with  leuko- 
cytes, serum,  and  fibrin  obstruct  the  vessel.  This  inflammatory  exudate 
commonly  coagulates  and  the  vessel  becomes  completely  thrombosed 
and  surrounded  by  more  or  less  inflammatory  congestion  and  oedema 
(perilymphangitis);  occasionally  small  foci  of  hemorrhage  supervene. 
Resolution,  suppuration,  or  organization  may  ensue,  depending  upon 
the  virulence  of  the  infecting  agent  and  the  resistance  of  the  individual. 
In  the  event  of  suppuration,  phlegmonous  infiltration  may  follow.  In 
the  event  of  organization,  proliferation  and  thickening  of  the  vessel  wall 
and  complete  obstruction  of  the  lumen  usually  supervene. 

In  most  cases  the  lymph  nodes  participate  in  the  process  and  local  or 
general  lymphadenitis  results.  The  local  process  is  well  seen  in  infections 
of  the  hands  and  arms  (axillary  nodes)  or  of  the  feet  and  legs  (femoral 
nodes);  in  infections  of  the  mouth,  carious  teeth,  facial  erysipelas,  ton- 
sillitis, etc.  (cervical  nodes) ;  in  pneumonia,  bronchitis,  especially  in  chil- 
dren, tuberculosis,  etc.  (bronchial  nodes);  in  appendicitis,  typhoid  fever 
(mesenteric  and  retroperitoneal  nodes);  in  gonorrhoea  and  chancroid 
(inguinal  nodes,  so-called  bubo) ;  etc.  The  general  process  is  common  in 
the  aforementioned  infectious  diseases,  but  occurs  notably  in  glandular 
fever,  tuberculosis,  syphilis,  plague,  etc.  In  the  acute  cases  the  nodes 
become  enlarged,  swollen,  soft,  and  hyperemic;  resolution  may  occur,  or 
liquefaction,  necrosis,  and  suppuration  may  ensue.  Microscopically  there 
is  lymphoid  hyperplasia,  vascular  dilatation,  polynuclear  leukocytic  infil- 
tration, fibrin  formation,  and  swelling  and  desquamation  of  the  endo- 
thelium of  the  sinuses.  Considerable  necroses  may  occur,  as  in  typhoid 
fever;  or  the  process  may  become  hemorrhagic  or  purulent.  In  the 
chronic  cases  there  is  a  low-grade,  chronic,  inflammatory  process,  with 
the  formation  of  cicatricial  connective  tissue,  in  consequence  of  which 
the  nodes  become  firm,  hard,  and  small;  the  capsule  becomes  thickened, 
the  sinuses  more  or  less  obliterated  or  obstructed,  and  the  lymphoid 
tissue  atrophic. 

Symptoms. — Reticular  lymphangitis  manifests  itself  by  circumscribed, 
red,  swollen,  painful,  and  tender  areas,  which  are  commonly  seen  on  the 
arms  or  legs,  and  progress  usually  from  the  periphery  toward  the  centre; 
frequently  there  is  considerable  collateral  oedema.  Tubular  lymph- 
angitis manifests  itself  in  cord-like,  irregular,  reddish  streaks  beneath 
the  skin,  progressing  from  the  periphery  toward  the  regional  glands. 
As  already  stated,  both  varieties  are  commonly  associated,  and  there 
is   usually   concurrent   inflammation   of   the    regional   lymph   nodes — 


LYMPH  ANGIECT  ASIS  395 

which  become  swollen,  painful,  and  tender.  The  general  symptoms  are 
those  of  pyococcic  infection — malaise,  chilliness,  and  fever,  in  degree 
depending  upon  the  severity  of  the  infection.  In  the  event  of  suppura- 
tion, the  common  symptoms  of  septicopyemia  (chills,  fever,  sweats,  and 
leukocytosis)  supervene,  and  if  the  lymph  nodes  are  involved  they  become 
softened  and  fluctuating,  and  may  rupture.  In  the  event  of  chronic 
proliferation  the  lymph  vessels  become  thickened,  cord-like,  and  chronic 
oedema  due  to  obstruction  occurs,  unless  a  collateral  circulation  develops. 
If  a  large  trunk  is  involved  a  considerable  area  of  the  body  may  become 
chronically  cedematous  or  elephantiatic,  or  chyluria  or  lymphorrhagia, 
etc.,  may  ensue. 

Involvement  of  the  deep  intrathoracic  and  intra-abdominal  lymph 
vessels  and  nodes  may  be  difficult  or  impossible  of  diagnosis,  since, 
aside  from  local  pain  and  perhaps  tenderness,  symptoms  may  be  absent 
or  in  abeyance.  The  considerable  enlargement  of  the  bronchial  nodes 
that  sometimes  occurs  in  children  is  suggested  by  dyspnoea,  respiratory 
stridor,  sometimes  dysphagia,  and  the  physical  signs  of  bronchial  stenosis 
(dulness  over  the  vertebrae,  x-ray  examination,  etc.).  Sudden  death 
occasionally  ensues  from  suppuration  and  rupture  into  the  trachea  or  a 
bronchus. 

The  general  lymphadenitis  of  the  acute  specific  infections  is  manifested 
by  swollen,  painful,  and  tender  nodes  occurring  during  the  course  of 
these  infections.  In  the  chronic  cases,  there  may  be  only  enlargement 
of  the  lymph  nodes;  sometimes  they  are  more  or  less  tender,  and  they 
may  become  quite  hard. 

Diagnosis. — In  the  acute  cases  phlebitis  usually  may  be  excluded 
by  the  fact  that  in  lymphangitis  the  redness  is  more  marked  and  more 
superficial  and  follows  the  lymph  vessels  (rather  than  a  vein),  and  the 
deep-seated  cord-like  induration  in  phlebitis  or  a  thrombosed  vein  is 
absent;  in  addition  the  neighboring  lymph  nodes  are  usually  involved.  In 
the  chronic  cases  one  must  differentiate  between  the  divers  sorts  of 
glandular  enlargement  (see  tumors  and  tumor-like  formations).  Some- 
times it  may  be  necessary  to  excise  one  of  the  enlarged  lymph  nodes  in 
order  to  come  to  a  definite  conclusion. 

Prognosis. — The  prognosis  depends  entirely  upon  the  nature  and 
severity  of  the  infection  and  the  resistance  of  the  patient. 

Treatment. — In  the  acute  cases  the  treatment  is  that  of  the  primary 
pyococcic  infection  together  with  rest  to  the  affected  part,  tiie  local 
applications  mentioned  in  connection  with  erysipelas,  etc.  Surgical 
measures  eventually  may  be  necessary. 


LYMPHANGIECTASIS. 

( Elephantiasis.) 

Lymphangiectasis,  dilatation  of  the  lymph  vessels,  may  be  congenital 
or  acquired.     The  congenital  variety  results  from  mechanical  or  inflain- 


396     DISEASES  OF  THE  LYMPH  NODES    AND  LYMPH   VESSELS 

matory  obstruction  of  the  lymph  vessels  occurring  during  intra-uterine 
Hfe;  but  some  cases  developing  in  adult  life  without  an  obvious  cause 
seem  perhaps  referable  to  a  congenital  or  inherited  predisposition.  The 
acquired  variety  may  be:  (1)  Parasitic,  due  to  obstruction  of  the  vessels 
by  Filaria  bancrofti — the  different  forms  of  tropical  and  subtropi- 
cal elephantiasis,  chylous  ascites,  chyluria,  etc.,  the  result  of  obstruc- 
tion of  the  thoracic  duct,  etc.;  and  (2)  non-parasitic,  which  occasion- 
ally results  from  inflammation  and  thrombosis  of  the  lymph  vessels 
(erysipelas,  eczema,  infected  leg  ulcers,  etc.);  or  it  may  be  secondary 
to  cicatricial  occlusion  of  the  vessels,  to  the  pressure  of  tumors,  to  the 
blocking  of  the  lumen  by  tuberculous  or  carcinomatous  material,  to  the 
extirpation  of  lymph  nodes,  etc.  The  condition,  however,  is  rare, 
despite  the  frequent  operation  of  the  causative  factors,  since  such  is  the 
free  communication  between  the  lymphatics  that  a  collateral  circulation 
is  readily  established. 

Symptoms. — ^The  dilated  vessels,  noticeable  only  when  situated  super- 
ficially, that  is,  in  the  skin  (and  due  then  to  obstruction  of  the  deeper 
lymphatics),  appear  as  soft,  transparent  sacs  or  vesicles,  often  arranged 
in  clusters,  and  filled  with  clear  or  milky  lymph.  These,  which  are 
sometimes  spoken  of  as  circumscribed  lymphangiomas,  are  found  most 
commonly  in  regions  rich  in  superficial  lymph  plexuses,  especially  along 
the  inner  aspect  of  the  thigh,  about  the  genitalia,  on  the  anterior  abdom- 
inal wall,  in  the  mesentery  (chyle  or  lymph  cysts),  etc.  Rupture  of  the 
vesicles  is  not  infrequent,  and  sometimes  results  in  the  escape  of  con- 
siderable lymph  (lymphorrhagia,  chylous  ascites,  etc.).  In  some  cases 
the  obstruction  produces  diffuse  or  widespread  dilatation  of  the  lymph 
vessels — usually  of  the  leg  or  the  external  genitalia  (elephantiasis,  lymph 
scrotum,  lymph  vulva),  although  it  may  occur  anywhere.  The  limb 
(or  other  portion  of  the  body)  becomes  greatly  swollen,  hard,  indurated, 
and  non-reducible — a  condition  of  branny  induration,  due  to  hyperplasia 
and  connective-tissue  overgrowth  of  the  lymph  vessels,  skin,  and  sub- 
cutaneous tissues,  and  chronic  oedema  from  obstruction  of  the  lymph 
vessels.  The  limb  may  be  soft  and  doughy  (elephantiasis  mollis),  or 
quite  hard  (elephantiasis  dura);  and  the  overlying  skin  may  be  thin, 
smooth,  and  translucent,  or  quite  thick  and  horny  (pachydermia). 
Ulceration  may  supervene,  and  permit  of  the  escape  of  more  or  less 
lymph — a  turbid,  milky-white  fluid. 

Prognosis. — The  outlook  is  not  especially  hopeful:  the  condition  is 
usually  permanent. 

Treatment. — In  the  circumscribed  form  relief  may  sometimes,  but 
rarely,  be  obtained  by  extirpation  of  the  dilated  vessels;  but  when  the 
condition  is  diffuse,  temporary  relief  only  may  be  afforded  by  massage, 
an  elastic  bandage,  and  elevation  of  the  limb — in  the  hope  that  a  suffi- 
cient collateral  circulation  ultimately  may  be  established. 


TUMORS  AND  TUMOR-LIKE  FORMATIONS  397 


TUMORS  AND  TUMOR-LIKE  FORMATIONS. 

The  lymph  vessels  are  not  infrequently  the  seat  of  tumor  formations, 
of  which,  two  types  may  be  distinguished — lymphangioma  and  endo- 
thelioma (lymphangiosarcoma).  The  lymphangioma,  which  ordinarily 
is  classed  as  a  benign  tumor,  consists  of  multiplied  and  dilated  lymph 
spaces  (telangiectatic  or  cavernous)  lined  with  endothelium  and  con- 
taining lymph.  They  are  most  common  in  the  skin  and  subcutaneous 
tissues,  but  they  occur  also  in  the  internal  organs,  the  mesentery,  etc. 
Common  examples  are  the  small  plexiform  lymphangiomas  of  the  skin, 
macroglossia,  macrocheilia,  and  certain  cystic  tumors  of  the  neck, 
mesentery,  etc.  The  endothelioma  is  a  tumor  developed  from  the 
endothelium  of  lymphatic  spaces,  and  is  found  most  commonly  in  the 
serous  membranes,  the  salivary  glands,  the  skin,  the  ovary,  the  testicle, 
etc.  In  addition,  the  lymph  vessels  serve  as  the  common  source  of  the 
local  and  distant  spread  of  carcinoma,  rarely  also  of  sarcoma. 

The  lymph  nodes  also  are  the  seat  of  a  number  of  tumors  and  tumor- 
like growths,  which  have  been  variously  described  as  lymphoma, 
lymphadenoma,  lymphocytoma,  lymphosarcoma,  malignant  lymphoma, 
leukosarcoma,  lymphomatosis,  adenie,  pseudoleukemia,  Hodgkin's 
disease,  etc.  Not  only  is  there  much  confusion  in  regard  to  the  identity 
of  the  disease  or  diseases  comprised  in  these  terms,  but  also  in  regard  to 
their  relation  or  supposed  relation  to  leukemia,  on  the  one  hand,  and 
to  syphilis  and  tuberculosis  of  the  lymph  nodes,  on  the  other  hand.  In 
the  majority  of  cases,  however,  one  can  separate  with  tolerable  ease  and 
certainty  the  lymphatic  enlargements  due  to  syphilis  or  tuberculosis; 
and  ordinarily  the  enlargements  due  to  leukemia  present  no  diagnostic 
difficulties.  Most  of  the  other  lymphatic  enlargements  seem  to  be  more 
or  less  related  clinically  and  pathologically;  studying  them  generally, 
they  seem  to  exhibit  gradations  and  stages  of  transition.  Thus,  there 
is  undoubtedly  a  leukemic  and  an  aleukemic  lymphoma;  that  is,  a  dis- 
order characterized  by  enlarged  lymph  nodes  with  or  without  the  leukemic 
blood  picture;  the  one  disease  is  leukemia  in  a  true  sense,  the  other  may 
be  spoken  of  as  pseudoleukemia  or  Hodgkin's  disease.  Differentiation 
is  rendered  difficult  by  the  fact  that,  as  pointed  out  by  Reed,  Longcope, 
and  Warthin,  Hodgkin's  disease  seems  to  have  a  characteristic  histo- 
logical picture;  that  the  other  cases,  of  which  the  histological  charac- 
teristic is  hyperplasia  of  lymphoid  tissue,  sometimes  do  and  sometimes 
do  not  exhil)it  the  leukemic  blood  picture,  that  is,  aleukenu"c  lyniphomas 
sometimes  progress  to  true  leukemia  (perhaps  early  and  late  stages  of 
the  one  disease);  and  that  true  leukemia,  during  the  not  unknown  periods 
of  regression  (occurring  spontaneously,  or  induced  by  treatment),  may 
exhibit  the  blood  j)icture  of  aleukemic  ly]n})h()nia  (sometimes,  however, 
the  blood  is  (|ualitatively  if  not  (|uantitatively  leukemic).  Fnrlhennore, 
there  are  transition  stages  between  some  of  these  cases,  especially  the 
aleukemic  lymphomas,  which  sometimes  are  spoken  of  as  iH-iiigii  lyiii])li- 


398     DISEASES  OF  THE  LYMPH    NODES  AND    LYMPH  VESSELS 

omas,  and  so-called  malignant  lymphomas;  that  is,  there  is  no  sharp 
line  of  demarcation  between  the  cases  of  lymphoid  hyperplasia  that  do 
not  and  those  that  do  infiltrate  and  ultimately  penetrate  the  capsules  of 
the  lymph  nodes  and  invade  the  adjacent  tissues.  The  difference  be- 
tween the  benign  and  the  malignant  lymphoma  (lymphosarcoma)  seems 
to  be  one  of  degree  only.  On  the  other  hand,  the  ordinary  varieties 
of  sarcoma  (round-cell,  spindle-cell,  angiosarcoma,  etc.)  may  implicate 
the  lymph  nodes;  they  differ  from  the  lymphomas  (lymphoid  hyperplasias) 
in  that,  as  do  sarcomas  generally,  they  give  rise  to  hematogenous  metas- 
tases, and  that,  as  a  rule,  they  do  not  progressively  involve  adjacent  sets 
of  lymph  nodes  (as  do  the  lymphomas). 

In  the  present  state  of  our  knowledge  we  may  differentiate  the  follow- 
ing varieties  of  chronic  progressive  enlargement  of  the  lymph  nodes: 

(1)  Those  due  to  specific  infections,  such  as  tuberculosis  and  syphilis; 

(2)  those  due  to  leukemia,  of  which  there  may  be  a  preleukemic,  an  aleu- 
kemic, or  a  subleukemic  stage;  (3)  tumor  formations  (lymphomas), 
among  which  one  may  include  lymphosarcoma  (malignant  lymphoma), 
the  ordinary  types  of  sarcoma  (round-cell,  spindle-cell,  angiosarcoma, 
etc.),  as  well  as  secondary  or  metastatic  carcinomatous  growths;  and 
(4)  Hodgkin's  disease.  The  specific  infections  and  leukemia  have 
already  been  discussed;  some  of  the  cases  included  under  (3)  the  lymph- 
omas, may  be  an  early  stage  or  a  forme  frusie  of,  or  progress  to,  leukemia; 
clinically,  it  is  usually  impossible  to  distinguish  between  the  so-called 
lymphomas  and  Hodgkin's  disease,  except  by  microscopic  examination 
of  an  excised  lymph  node. 


HODGKIN'S  DISEASE. 

Hodgkin's  disease  is  a  disorder  of  the  lymph  nodes  characterized 
anatomically  by  a  peculiar,  chronic,  perhaps  inflammatory  process 
leading  to  well-marked  fibrosis,  and  clinically  by  enlargement  of  the 
lymph  nodes,  progressive  anemia,  and  a  fatal  termination. 

Etiology. — Hodgkin's  disease  is  twice  or  thrice  as  common  in  men  as 
in  women,  and  although  it  may  occur  at  any  age,  it  is  especially  common 
in  young  adults  (fifteenth  to  thirty-fifth  year).  The  cause  of  the  disease 
is  not  known.  A  number  of  cases  have  been  attributed  to  tuberculosis, 
but  there  is  no  doubt  that  although  tuberculosis  of  the  lymph  nodes 
may  follow  an  aberrant  clinical  and  pathological  course,  the  great 
majority,  if  not  all  cases,  can  be  readily  distinguished  from  Hodgkin's 
disease. 

Pathology. — The  lesions  consist  of  progressive  enlargement  of  the 
lymph  nodes,  which  usually  involves  first  the  cervical  nodes,  and  then  in 
order  of  frequency  the  axillary,  the  inguinal,  the  thoracic,  and  the 
abdominal  nodes.  In  some  cases  the  disorder  seems  to  begin  in  the 
deeper  nodes,  the  superficial  nodes  being  involved  later;  in  other  cases 
the  enlargement  is  for  a  long  time  circumscribed  to  one  set  of  nodes,  later 


HODGKIN'S  DISEASE  399 

perhaps  but  sometimes  not  becoming  generalized.  The  lymph  nodes 
vary  much  in  size;  they  are  smooth  and  spheroidal  in  shape,  soft,  and 
inelastic  (sometimes  even  fluctuating),  or  firm  and  discrete,  even  the 
largest  masses  in  many  cases  being  made  up  of  discrete  nodules  bound 
together  by  connective  tissue.  Occasionally,  however,  adjacent  nodules 
fuse  through  penetration  of  the  capsules,  and  they  may  become  adherent 
to  the  overlying  subcutaneous  tissues  and  skin.  On  section  the  nodules 
are  pinkish  and  semitranslucent,  or  grayish  or  yellowish,  especially 
if  softening  and  fibrosis  have  occurred.  The  microscopic  appearances, 
which  are  characteristic,  consist  at  first  of  hyperplasia  of  the  lymphoid 
cells,  especially  of  the  germinal  centres,  with  proliferation  of  the  endo- 
thelial and  reticular  cells — a  process  that  much  resembles  chronic  in- 
flammation. The  cellular  proliferation  and  thickening  of  the  reticulum 
soon  obscure  the  normal  structures,  so  that  only  indefinite  remains 
of  the  lymphoid  tissue  can  be  identified.  In  addition  to  lymphocytes, 
polynuclear  leukocytes,  plasma  cells,  and  endothelioid  cells,  eosinophiles 
and  mononuclear  and  multinuclear  giant  cells  are  found  in  consider- 
able numbers,  and  are  considered  quite  characteristic  (Reed,  Longcope, 
Warthin).  l^ltimately  the  fibrosis  becomes  extreme,  so  that  the  nodes 
become  converted  almost  completely  into  fibrous  tissue.  Nodules  of 
similar  formation  are  sometimes  found  in  the  spleen  (which  may  become 
considerably  enlarged),  in  the  liver,  gastro-intestinal  tract,  kidneys,  lungs, 
bronchi,  thymus,  bone  marrow,  serous  surfaces,  skin,  etc. ;  these  are  most 
likely  not  true  metastases,  but  (as  in  leukemia)  hyperplasias  of  previously 
existing  areas  of  lymphoid  tissues. 

Symptoms. — The  first  symptoms,  as  a  rule,  consist  of  painless  enlarge- 
ment of  the  lymph  nodes,  which,  as  a  rule,  begins  in  one  side  of  the 
neck,  although  it  may  begin  elsewhere;  in  most  cases  the  cervical,  axillary, 
inguinal,  thoracic,  and  abdominal  nodes  become  progressively  involved, 
in  some  cases  soon,  in  some  cases  later;  rarely  the  disease  remains  local- 
ized to  the  set  of  nodes  first  involved.  The  local  mass  of  enlarged 
nodes  often  becomes  very  large,  but,  as  a  rule,  the  individual  nodes  can 
be  distinctly  palpated,  although  rarely  they  fuse  and  perhaps  form 
adhesions  with  the  superjacent  subcutaneous  tissues  and  the  skin.  The 
nodes  may  be  soft  (sometimes  fluctuating)  or  firm;  sometimes,  in  ad- 
vanced cases,  quite  hard.  Divers  symptoms  result  from  local  pressure: 
oedema  and  cyanosis  of  the  neck,  face,  arm,  or  leg;  effusions  within  the 
serous  cavities;  dyspnoea,  generalized  cyanosis,  dysphagia,  and  other 
manifestations  of  mediastinal  tumor;  jaundice,  pyloric  obstruction, 
and  other  gastro-intestinal  disturbances;  sciatica  and  other  local  pains, 
etc.  In  some  cases  the  deep  (thoracic  and  abdominal)  nodes  are  first 
involved,  so  that  these  usually  late  symptoms  of  pressure  may  be  the 
earliest  manifestations.  The  spleen  is  commonly  enlarged,  sometimes 
notably  enlarged;  the  liver  also  is  enlarged  in  about  one-half  the  cases. 
The  skin  may  become  pigmented  (independently  of  the  use  of  arsenic); 
pruritus    and    furuncles    are    often    annoying;    lymphomatous    nodules 


400      DISEASES  OF   THE  LYMPH    NODES   AXD    LYMPH   VESSELS 

sometimes  occur  in  the  skin,  and  subcutaneous  hemorrhages  occasion- 
ally have  been  observed. 

In  the  ordinary,  slowly  progressing  cases,  the  general  health,  aside 
from  more  or  less  malaise,  usually  remains  for  a  long  time  unimpaired. 
In  some  cases  there  is  more  or  less  fever:  it  may  be  a  mild  continued 
fever  (as  high  as  100°  or  101°);  or  especially  toward  the  end  it  may  be 
high  (104°  to  105°)  with  daily  remission  of  three  or  four  degrees  and 
accompanied  with  chills  and  sweats;  or  it  may  be  of  the  relapsing  t^-pe 
( Epstein-Pel j — periods  of  fever  of  ten  to  fourteen  days'  duration  alter- 
nating with  periods  of  apyrexia.  Secondary  anemia,  ultimately  of  high 
grade  r2,000,000  erythrocytes  or  less,  30  to  40  per  cent,  of  hemoglobin), 
emaciation,  and  cachexia  gradually  develop — sometimes  soon  and  pro- 
gress rapidly;  or  the  disorder  previously  quiescent  suddenly  becomes  active 
and  soon  leads  to  death.  The  leukocytes  reveal  no  characteristic  changes ; 
occasionally  there  is  a  slight  leukocytosis  (10,000  to  20,000),  but  rarely  any 
relative  lymphocytosis;  occasionally  an  eosinophilia  has  been  observed. 

Diagnosis. — Clinically  the  disease  is  often  not  an  entity  sharply 
distinguishable  from  other  forms  of  glandular  enlargement.  The 
diagnosis  virtually  depends  upon  painless,  discrete,  progressive  enlarge- 
ment of  the  lymph  nodes  unassociated  with  leukemic  changes  in  the 
blood;  but  in  the  differential  diagnosis  one  must  remember  that  leukemia 
may  have  a  preleukemic,  an  aleukemic,  and  a  subleukemic  stage. 
Excision  and  microscopic  examination  of  an  enlarged  gland  may  be  the 
only  way  to  a  correct  diagnosis  in  some  cases.  Some  cases  of  sarcoma 
(round-cell,  spindle-cell,  lymphosarcoma)  of  the  lymph  nodes  often 
resemble  Hodgkin's  disease,  but,  as  a  rule,  in  sarcoma  growth  is  rapid 
and  often  painful,  infiltration  and  penetration  of  the  capsules  of  the  nodes, 
fusion  of  the  nodes,  and  infiltration  of  the  adjacent  tissues  occur  early, 
metastases  are  common,  and  the  primary  as  well  as  secondary  growths 
may  soften,  ulcerate,  and  discharge  externally.  Sarcoma,  however, 
may  be  painless  and  the  enlarged  nodes  of  Hodgkin's  disease  may  not 
remain  discrete,  so  that  a  differential  diagnosis  may  not  be  possible  in 
the  absence  of  a  microscopic  examination  of  an  excised  node.  Tuber- 
culosis of  the  lymph  nodes  rather  than  Hodgkin's  disease  is  suggested 
by  a  tuberculous  focus  elsewhere  in  the  body,  the  tendency  of  the  en- 
larged nodes  to  fuse,  form  adhesions  with  the  skin,  soften,  suppurate, 
and  discharge,  and  a  response  to  the  tuberculin  tests;  but  a  microscopic 
examination  of  a  node  or  bacteriological  examination  of  the  purulent 
discharge  may  be  necessary  to  establish  the  diagnosis.  Syphilis  may 
be  distinguished  by  the  history  and  concomitant  evidences  of  syphilis 
elsewhere  in  the  body.  The  types  of  splenomegaly  formerly  called 
splenic  pseudoleukemia,  von  Jaksch's  disease,  etc.,  and  the  tumor  for- 
mation known  as  multiple  myeloma,  and  formerly  called  medullary 
or  myelogenous  pseudoleukemia,  are  in  no  way  related  to  Hodgkin's 
disease.  Multiple  myeloma  (occurring  especially  in  the  ends  of  the  long 
bones,  the  ribs,  the  vertebrje,  etc.)  is  characterized  by  deep-seated, 
sometimes   pulsatile   (bone)   pains,   bony  enlargements,   perhaps  .spon- 


DISEASES  OF  THE  THORACIC  DUCT  401 

taneous  fractures,  divers  motor  and  sensory  phenomena  due  to  the 
local  growths,  fever,  anemia  without  leukocytosis  (perhaps  occasion- 
ally relative  lymphocytosis),  and  Bence-Jones  albumosuria  (so-called 
myelopathic  albumosuria,  Kahler's  disease). 

Prognosis. — ^The  disease  is  invariably  fatal.  Most  subjects  rarely 
live  more  than  three  years;  very  mild  and  slowly  progressive  cases  may 
continue  six  years  or  more.  Periods  of  quiescence,  with  spontaneous 
regression  of  the  enlarged  lymph  nodes,  apyrexia,  and  improvement  in 
the  general  health  sometimes  occur,  and  may  last  for  months ;  or  the  dis- 
ease for  some  time  mild  and  non-progressive  suddenly  takes  on  malignant 
characteristics  and  speedily  leads  to  death.  Death  may  result  from  pro- 
gressive anemia,  cachexia,  and  asthenia;  or  from  tuberculosis  or  other 
secondary  infection  (sometimes  answerable  for  the  high  fever  toward 
the  end). 

Treatment. — The  nature  of  the  disease  makes  it  especially  refractory 
to  treatment.  The  best  results  (lessening  of  the  progress  of  the  disease) 
have  been  attained  by  the  use  of  arsenic  and  the  a:-rays,  which  should 
be  employed  as  advised  in  leukemia.  Operative  removal  of  all  the 
regional  lymph  nodes  in  the  localized  form  of  the  disease  has  rarely  been 
of  some  temporary  avail,  but,  as  a  rule,  all  nodes  cannot  be  removed, 
and  those  left  soon  take  on  renewed  growth. 


DISEASES  OF  THE  THORACIC  DUCT. 

The  thoracic  duct  is  formed  by  the  confluence  of  the  main  trunk  or 
trunks  of  the  intestinal  lymphatics  and  the  main  lumbar  trunks  which 
have  resulted  from  the  union  of  the  lymphatics  of  the  pelvis,  genitalia, 
abdominal  wall,  and  lower  extremities.  The  point  of  union  is  on  a  level 
with  the  first  or  second  lumbar  vertebra,  and  is  usually  indicated  by  a 
saccular  dilatation — the  receptaculum  chyli.  Thence  the  thoracic  duct 
courses  through  the  posterior  mediastinum,  and,  being  joined  by  the 
main  trunk  of  the  lymphatics  of  the  upper  part  of  the  body  (except  those 
of  the  right  side  of  the  head  and  thorax),  eventually  empties  into  the  left 
subclavian  vein  distal  to  its  union  with  the  internal  jugular.  The  right 
thoracic  (or  lymphatic)  duct  empties  into  the  right  subclavian  (some- 
times internal  jugular)  vein.  Anatomical  anomalies,  however,  are  by  no 
means  rare. 

Pathology. — ^I'he  thoracic  duct  is  subject  to  divers  disorders  of  con- 
sideral)le  interest  in  clinical  medicine:  (1)  It  is  a  common  source  of  the 
rapid  dissemination  of  tubercle  bacilli  throughout  the  body — by  way 
of  the  lymph  and  l:)lood  streams.  The  duct  often  acts  merely  as  a 
passive  carrier  of  bacilli  discharged  by  a  tuberculous  lymph  node  some- 
where within  the  area  of  collection  of  its  tributaries;  sometimes  it  is 
itself  tuberculous.  There  is  considerable  evidence  also  that  it  is  the 
avenue  of  general  distribution  of  pyococci  in  many  cases  of  septico- 
pyemia; and  of  carcinomatosis  developing  primarily  in  the  abdomen 
26 


402  DISEASES  OF  THE  THYMUS  BODY 

or  pelvis.  (2)  It  is  often  the  seat  of  different  disorders,  of  which  the 
ultimate  consequence  is  obstruction.  This  may  arise  from  thrombi, 
parasites  (Filaria  bancrofti),  secondary  tumor  masses,  etc.,  within  the 
duct;  acute  and  chronic  inflammation  or  primary  tumor  formation 
of  the  duct  itself;  compression  of  the  duct  from  without  by  regional 
inflammatory  exudates,  cicatrices,  enlarged  lymph  nodes,  tumors,  aneu- 
rysm, etc.;  or  thrombosis  of  the  subclavian  vein.  The  consecjuences 
vary  with  the  site  and  degree  of  the  obstruction.  If  the  obstruction  is 
incomplete,  an  efficient  collateral  circulation  may  become  established 
and  there  may  be  no  noteworthy  symptoms ;  this  may  ensue  also  when  the 
obstruction  is  low  down.  When  the  obstruction  is  complete  and  high  up, 
the  duct  usually  becomes  dilated;  the  receptaculum  chyli  may  become 
as  large  as  a  walnut  or  a  hen's  egg  (perhaps  apparent  on  palpation  of  the 
abdomen).  Sometimes  the  dilatation  extends  to  the  peritoneal  tributaries 
of  the  duct,  giving  rise  to  lymph  or  chyle  cysts  (so-called  chyle  angiomas, 
which,  however,  often  have  a  local  inflammatory  peritoneal  cause,  or 
resemble  tumor  formations).  In  some  cases  of  extreme  obstruction 
rupture  of  the  duct  ensues. 

Symptoms, — The  symptoms  are  those  of  stasis  of  chyle,  with  the 
eventual  development,  in  consequence  of  transudation  of  the  chyle  or 
rupture  of  the  vessels,  of  chyloperitoneum  (chylous,  milky,  opalescent 
ascites),  and  chylothorax;  perhaps  also  chylopericardium,  chyluria,  and 
chylous  swelling  of  the  abdominal  wall,  external  genitalia,  legs,  etc. 
In  the  event  of  rupture  of  the  duct  rapid  emaciation  usually  ensues. 

Diagnosis. — It  is  sometimes  difficult  to  distinguish  chylous  from  so-called 
chyliform  fluid  which  (in  the  absence  of  obstruction  of  the  lymphatics) 
sometimes  develops  in  the  peritoneum,  pleura,  etc.;  it  is  due  to  fatty 
metamorphosis  of  leukocytes  (pus  cells),  endothelium,  and  tumor  cells, 
and  has  been  found  in  chronic,  especially  tuberculous,  inflammations  of 
the  serous  membranes,  endothelioma,  chronic  heart  disease,  cirrhosis  of 
the  liver,  etc.  The  presence  of  fine  (rather  than  coarse)  fatty  droplets 
and  of  sugar  suggests,  but  is  not  conclusive  evidence  of,  the  chylous  origin 
of  the  fluid ;  in  some  cases  of  chyliform  fluid  the  origin  of  the  fat  is  evident 
in  the  presence  of  fatty  degenerated  cells. 

Prognosis. — The  prognosis  is  bad,  as  a  rule;  but  it  depends  upon  the 
nature  and  completeness  of  the  obstruction.  Occasionally  an  efficient 
collateral  circulation  becomes  established,  or  a  thrombus,  for  instance, 
may  become  softened  and  permit  of  some  circulation  through  the  duct, 
or  the  course  of  the  obstruction  being  removable,  may  be  removed. 

Treatment. — The  treatment,  in  cases  in  which  any  treatment  is  of 
avail,  is  purely  surgical. 

DISEASES  OF  THE  THYMUS  BODY. 

Pathological  Physiology. — The  thymus  body  ordinarily  attains  its 
greatest  development  at  the  end  of  the  second  year  of  life.  Thereafter 
it  gradually  atrophies  until  puberty,  whereupon  the  atrophic  process 


ENLARGEMENT  OF  THE  THYMUS  403 

becomes  more  rapid,  so  that  in  adult  life  the  body  is  represented  by  a 
small  mass  of  fibro-adipose  tissue  containing  Hassell's  corpuscles  (rem- 
nants of  the  original  epithelial  tissue)  and  a  small  amount  of  lymphoid 
tissue.  Anatomically  and  functionally  the  thymus  is  to  be  classified  with 
the  lymphoid  tissues,  especially  since  nothing  is  known  of  the  function 
of  Hassell's  corpuscles,  and  there  is  no  certain  evidence  that  the  thymus 
produces  a  specific  internal  secretion.  There  is  some  evidence,  however, 
that  an  obscure  and  ill-comprehended  relationship  exists  between  the 
thymus  and  organs  that  do  produce  an  internal  secretion,  such  as  the 
thyroid  (in  Graves'  disease),  parathyroids,  pituitary  body  (in  akromegaly), 
the  ovaries,  testicles  (atrophying  as  the  sexual  organs  develop),  etc.; 
and  extracts  of  the  thymus  are  said  to  cause  a  fall  in  blood  pressure  and 
rapid  action  of  the  heart.  Like  adenoid  tissue  generally,  the  thymus  is 
the  seat  of  lymphocyte  formation,  especially  in  early  life  when  they  are 
produced  in  abundance;  furthermore,  upon  slender  basis,  the  thymus  is 
said  to  exert  some  influence  upon  the  growth  of  the  bone  and  the  develop- 
ment of  the  cerebral  functions,  and  to  participate  in  the  processes  of 
immunity.  The  thymus  persists  in  castrated  animals.  Apparently  the 
thymus  is  rarely  the  seat  of  primary  disease,  the  only  known  disorder  of 
clinical  significance  being  enlargement  or  hypertrophy,  in  some  way 
concerned  in  thymic  asthma  and  thymic  death. 

Enlargement  is  sometimes  found  also  in  leukemia,  Hodgkin's  disease, 
rachitis,  Graves'  disease,  Addison's  disease,  akromegaly,  myasthenia 
gravis,  etc.,  as  well  as  in  tumor  formations  (primary,  that  is,  benign  and 
malignant  lymphoma,  and  secondary),  cyst  formations,  etc.  The  thymus 
may  be  affected  secondarily  also  in  a  number  of  disorders,  such  as  acute 
especially  pyococcic  infection  (acute  simple,  or  suppurative  thymitis), 
chronic  infections  (tuberculosis,  syphilis,  etc.).  Rarely,  pathological 
atrophy  has  been  encountered  in  some  cases  of  infantile  marasmus, 
but  it  is  probably  part  of  the  general  process  rather  than  of  etiological 
significance.  Extracts  (fresh  or  dried)  of  the  thymus  have  been  used 
with  varying  success  in  arthritis  deformans,  rickets,  myxoedema.  Graves' 
disease,  Addison's  disease,  etc. 


ENLARGEMENT  OF  THE  THYMUS. 

(Hi/perlrophi/,  Hi/perplada,  Persistence  of  the  Thyvnis;  Status  Lymphaticus; 
Lymphatism:  Thymic  Asthma:  Thymic  Death;  Thymic  Tracheostenosis.) 

Aside  from  the  disorders  already  mentioned  in  which  the  thvmus 
may  be  enlarged,  enlargement  is  found  in  a  series  of  cases  characterized 
by  stridorous  dyspmra,  asthma,  or  sudden  death.  Some  authors  main- 
tain (although  others  deny)  that  the  thymic  enlargement  is  the  cause  of 
the  stridor,  asthma,  and  death  which  it  is  believed  to  provoke  by  pressure 
on  the  trachea  (tracheal  stenosis),  on  the  vagus,  or  other  of  the  medi- 
astinal tissues  or  organs. 

The  oiihirgeinent   is  a   hypeiphisia  of   luikiiown    cause;    il    has   been 


404  DISEASES  OF   THE   THYMUS  BODY 

referred  to  divers  sorts  of  infections,  intoxications,  and  disorders  of  meta- 
bolism. Often  it  is  associated  with  adenoids,  enlarged  tonsils,  enlarged 
lymph  nodes  generally,  enlarged  spleen,  and  reddish  bone  marrow  (status 
lymphaticus) ;  sometimes  also  there  is  hypoplasia  of  the  heart  and 
aorta,  infantilism,  etc.  There  has  been  much  discussion  as  to  whether 
enlargement  of  the  thymus  can  cause  tracheal  stenosis.  Warthin,  who 
has  studied  the  subject  attentively,  maintains  that  it  may;  suggesting  the 
use  of  the  term  "thymic  tracheostenosis,"  he  states  that  "all  the  symp- 
toms and  all  the  operative  and  postmortem  evidence  point  to  a  suffo- 
cation resulting  from  tracheal  stenosis.  Secondary  laryngeal  spasm 
is  the  chief  if  not  the  only  cause  of  the  fatal  termination.  To  these 
may  be  added  other  effects  of  compression  upon  the  heart,  great  vessels, 
vagi,  and  recurrent  nerves.  To  a  reflex  spasm  of  the  glottis  may  be  added 
a  reflex  cardiac  paralysis,  as  the  latter  may  alone  be  the  direct  cause  of 
death  in  those  cases  of  sudden  death  in  which  all  signs  of  tracheal  stenosis 
or  laryngeal  stenosis  are  wanting."  "Status  lymphaticus  may  be  the 
consequence  of  a  number  of  primary  morbid  processes,  such  as  syphilis, 
rachitis,  some  latent  infection,  auto-intoxication,  etc.,  that  are  character- 
ized by  excessive  demands  upon  the  lymphoid  and  myeloid  tissues.  The 
sudden  death  is  dependent  primarily  and  wholly  upon  the  thymic  enlarge- 
ment, and  the  latter  condition  becomes,  therefore,  the  most  important 
feature  clinically."  Other  observers  believe  that  there  is  a  toxic  ele- 
ment in  the  condition. 

Symptoms. — The  symptoms  are  said  by  Warthin  to  consist  of  respira- 
tory disturbances  resulting  from  the  diminution  of  space  in  the  superior 
thoracic  strait.  He  distinguishes  three  classes  of  cases  according  to  their 
severity — thymic  stridor,  thymic  asthma,  and  thymic  death.  The  stridor 
is  usually  congenital  or  develops  soon  after  birth;  it  is  inspiratory  and 
expiratory;  it  may  be  stationary  or  progressive,  or  it  may  manifest 
itself  suddenly  in  its  most  marked  form;  it  may  be  precipitated  by  a  fit 
of  screaming  or  crying,  or  it  may  come  on  during  one  of  the  acute  infec- 
tions. It  varies  much  in  intensity;  it  is  unassociated  with  changes  in  the 
voice,  and  persists  during  sleep,  although  it  lessens  in  severity.  Thy- 
mic asthma  (Kopp's  asthma,  Millar's  asthma)  is  an  exacerbation  of 
stridor  of  asthmatic  character,  or  it  may  develop  in  a  child  showing  no 
previous  sign  of  stridor.  The  first  attack  may  be  fatal,  or  there  may  be 
periodical  recurrences  of  progressive  character;  but  an  attack  may  sub- 
side quickly.  There  is  no  sharp  line  of  demarcation  between  thymic 
asthma  and  thymic  death,  but  the  term  thymic  death  has  come  to  be 
applied  to  those  cases  in  which  death  occurs  suddenly  without  definite 
history  of  previous  respiratory  difficulty.  It  may  be  induced  by  divers 
causes,  such  as  anesthesia,  slight  surgical  operations,  fright,  etc.  The 
general  picture  is  that  of  a  convulsive  attack  of  thymic  asthma  of 
severest  type  ending  in  death  (Warthin). 

Physical  examination  discloses  an  area  of  dulness  at  the  upper  part 
of  and  somewhat  to  both  sides  of  the  sternum,  merging  with  the  upper 
limit  of  the  cardiac  dulness.     Sometimes  there  is  distinct  bulging,  or  a 


DISEASES  OF  THE  SPLEEN  405 

palpable  swelling  in  the  episternal  notch.  A  shadow  may  be  disclosed 
by  the  a:-rays.  Tracheal  or  bronchial  stenosis  may  be  seen  by  the 
bronchoscope  or  after  tracheotomy.  The  child  may  be  rachitic  or 
anemic.     Examination  of  the  blood  may  reveal  a  relative  lymphocytosis. 

Diagnosis. — A  congenital  chronic  stridor  both  inspiratory  and  expira- 
tory, but  most  marked  on  inspiration,  with  a  tendency  to  exacerbations, 
and  the  production  of  dyspnoea  so  marked  as  to  occasion  intubation 
and  tracheotomy,  and  finally  death,  is  usually  due  to  thymic  enlargement 
(Warthin). 

Prognosis. — The  prognosis  is  bad. 

Treatment. — The  underlying  rickets,  anemia,  or  malnutrition,  should 
be  treated,  so  as  to  prevent,  if  possible,  the  onset  of  symptoms  referable 
to  the  enlarged  thymus.  By  avoiding  excitement,  operations,  etc.,  attacks 
may  be  prevented.  During  the  attack  the  child  should  be  kept  hori- 
zontal, at  least  the  head  forward,  cold  applications  should  be  applied 
to  the  chest  or  the  child  should  be  immersed  in  a  full  warm  bath,  and 
supportive  measures  should  be  used.  Intubation  with  a  long  tube 
through  the  mouth,  or  through  a  tracheotomy  wound,  may  be  resorted  to. 
The  x-rays  may  be  of  service,  as  in  leukemic  conditions,  but  until  more 
data  are  accumulated  they  must  be  employed  with  caution.  The  thymus 
has  been  removed  in  several  cases  with  good  results. 


DISEASES  OF  THE  SPLEEN. 

Pathological  Physiology. — The  functions  of  the  spleen  are  ill  under- 
stood. The  organ  seems  to  be  non-essential  to  life,  and  it  apparently 
does  not  produce  an  internal  secretion — whence  it  cannot  be  classed  with 
the  ductless  glands.  In  general  it  may  be  said  functionally  and  ana- 
tomically to  resemble  the  lymph  nodes — which  take  on  a  compensatory 
hyperplasia  after  splenectomy.  During  foetal  life  the  spleen  is  the  seat 
of  erythrocytogenesis,  a  function  to  which  apparently  it  may  revert  in 
the  stress  of  circumstances  in  later  life.  In  diseases  of  the  hemopoietic 
system,  especially  leukemia,  as  already  mentioned,  it  undergoes  consider- 
able hyperplasia  or  metaplasia,  so  that,  especially  in  myelocytic  leukemia, 
it  may  become  converted  into  a  tissue  much  resembling,  almost  identical 
with,  the  bone  marrow.  It  seems  to  be  actively  concerned  in  hemolysis: 
perhaps  during  health  its  action  in  this  regard  is  rather  passive,  the 
organ  acting  merely  as  a  scavenger,  or  as  a  graveyard  for  blood  corpuscles 
incapacitated  or  destroyed  elsewhere  in  the  economy;  in  diseased  condi- 
tions, however,  hemolysis  seems  to  be  active  in  the  spleen,  and,  as  in 
pernicious  anemia,  this  may  be  a  contributory  factor  in  the  fatal  termina- 
tion. The  spleen  also  is  concerned  in  the  processes  of  immunity;  this  is 
obvious  in  the  splenic  phagocytosis,  but  perhaps  the  organ  exerts  also  a 
chemical  non-phagocytic  immunizing  influence. 


406  DISEASES  OF  THE  SPLEEN 


ANOMALIES  OF  FORM  AND  POSITION  OF  THE  SPLEEN. 

In  association  usually  with  other  errors  of  development,  the  spleen 
may  be  absent,  abnormally  small,  abnormally  large,  or  misplaced  in 
the  abdominal  or  thoracic  cavity;  it  is  sometimes  unusually  lobulated; 
and  small  supernumerary  or  accessory  spleens  are  quite  common.  Clini- 
cal interest  attaches  to  the  presence  of  the  spleen  in  the  right  side  in 
transposition  of  the  viscera. 

Movable  spleen  (floating  spleen,  splenoptosis).  Rarely,  and  then  only 
in  the  event  of  considerable  enlargement,  the  spleen  may  be  unduly 
movable  without  evidences  of  displacement  of  the  other  abdominal 
organs;  but  usually  splenoptosis  is  merely  part  of  general  visceroptosis. 


RUPTURE  OF  THE  SPLEEN. 

Rupture  of  the  spleen  may  occur  spontaneously  or  in  consequence  of 
trauma.  Severe  trauma  may  cause  rupture  of  a  previously  normal 
spleen;  but  commonly  rupture  results  from  slight  trauma,  although  it 
may  occur  spontaneously,  in  a  spleen  already  diseased,  such  as  the 
acute  enlargements  of  typhoid,  relapsing,  or  malarial  fever  (especially 
in  the  tropics),  infarct  and  abscess,  etc.  The  trauma  may  consist  of 
coughing,  rough  handling,  as  in  palpation,  puncture  by  an  exploring 
needle,  etc.  The  symptoms  consist  of  local  pain  and  distress,  and 
the  shock  and  other  phenomena  attending  intraperitoneal  hemorrhage. 
The  treatment  is  surgical,  and  should  be  instituted  immediately. 


THROMBOSIS,  EMBOLISM,  AND  ABSCESS  OF  THE  SPLEEN. 

Thrombosis  of  the  splenic  vein  rarely  develops  in  the  course  of  typhoid 
fever  or  local  inflammatory  disorders  (such  as  of  the  pancreas,  etc.) ;  it  may 
result  from  extension  of  a  thrombus  in  the  portal  or  mesenteric  veins,  or 
follow  sclerosis  and  atheroma  of  the  splenic  vein.  The  symptoms  consist 
in  the  main  of  venous  engorgement,  enlargement  and  perhaps  infarction 
of  the  spleen,  recurring  hematemesis,  and  other  manifestations  suggest- 
ing splenic  anemia,  although  it  differs  in  the  more  common,  acute  onset. 
Embolism  develops  usually  in  the  course  of  acute  or  chronic  valvular 
disease  of  the  heart  and  septicopyemic  processes;  it  may  follow  primary 
splenic  arterial  or  venous  thrombosis.  The  ensuing  infarcts  may  be 
simple  (mechanical)  or  septic  (with  ensuing  abscess  formation).  The 
condition  may  be  suspected  when,  in  the  course  of  the  aforementioned 
diseases,  sudden  pain  develops  in  the  region  of  the  spleen,  becomes 
aggravated  upon  motion  and  respiration,  and  is  accompanied  by  tender- 
ness, especially  on  palpation;  and  when  examination  discloses  enlarge- 
ment of  the  spleen  and  perhaps  palpable  frictions  (acute  perisplenitis), 


SPLENOMEGALY:  SPLENIC  ANEMIA  407 

which  may  be  audible  on  auscuUation.  Irregular  chills,  fever,  sweats, 
and  leukocytosis  may  be  due  to  the  primary  infection,  or  to  the  develop- 
ment of  a  splenic  abscess. 


ENLARGEMENT  OF  THE  SPLEEN. 

Acute  enlargement  of  the  spleen  (acute  splenic  tumor)  occurs  in  many 
infections,  notably  typhoid  fever,  malaria,  and  relapsing  fever,  in  which 
it  attains  considerable  diagnostic  significance;  but  it  may  be  present  also 
in  septicopyemia,  pneumonia,  etc.;  in  acute  portal  obstruction,  in 
embolism  and  thrombosis  of  the  splenic  vein,  etc.  In  venous  obstruction 
its  cause  is  obvious;  in  infection  it  is  attributable  to  a  local  congestive  and 
inflammatory  reaction  to  the  presence  of  microorganisms  or  their  toxins 
or  to  toxic  paralysis  of  the  vasomotor  nerves.  Symptoms  may  be  in 
abeyance,  although  local  pain  and  discomfort  may  supervene,  and  on 
examination  the  spleen  may  be  found  enlarged  and  tender. 

Chronic  enlargement  of  the  spleen  (chronic  splenic  tumor)  occurs 
in:  (1)  Passive  congestion  due  to  chronic  heart  disease,  chronic  liver 
disease  (especially  cirrhosis),  pylephlebitis  and  other  obstructive  dis- 
orders of  the  portal  circulation;  (2)  disorders  of  nutrition,  such  as  rick- 
ets, amyloidosis,  certain  obscure  (especially  tropical)  gastro-intestinal 
intoxications,  arthritis  deformans,  etc.;  (3)  infections,  such  as  malaria, 
syphilis,  tuberculosis,  kala-azar,  and  other  ill-understood,  tropical 
disorders;  (4)  diseases  of  the  hemopoietic  system,  such  as  chlorosis, 
pernicious  anemia,  leukemia,  erythema,  Hodgkin's  disease,  etc.;  (5) 
tumors  and  cysts  of  the  spleen;  and  (6)  certain  ill-understood  diseases 
discussed  under  the  heading  splenomegaly  and  splenic  anemia.  The 
enlargement  of  the  spleen  per  se  may  not  cause  any  noteworthy  symp- 
toms, but  local  distress  and  a  sense  of  weight  are  not  uncommon.  The 
enlargement  is  readily  disclosed  by  physical  examination.  An  enlarged 
spleen  should  not  be  mistaken  for  a  displaced,  though  otherwise  normal, 
spleen. 

SPLENOMEGALY;  SPLENIC  ANEMIA. 

In  a  considerable  number  of  more  or  less  ill-understood  disorders 
enlargement  of  the  spleen  constitutes  a  noteworthy  feature.  The  im- 
perfect state  of  our  knowledge  precludes  a  satisfactory  classification, 
but  several  grou])s  of  cases  may  be  distinguished: 

1.  Congenital  or  Familial  Splenomegaly,  with  Acholuric  Jaundice  (Min- 
kowski). This  is  usually  a  familial  disorder,  and  may  occur  in  suc- 
ceeding generations.  The  splenomegaly  is  often  extreme;  there  is 
slight  jaundice,  but  the  stools  are  not  clay-colored,  and  the  urine  does 
not  contain  l)ile  pigments,  although  it  does  contain  urobilin  and  uro- 
bilinogen. The  blood  reveals  the  changes  of  secondary  anemia.  Ne- 
cropsy has  revealed  chronic  hyperplasia  of  the  spleen  without  cirrhosis 


408  DISEASES  OF  THE  SPLEEN 

of  the  liver  or  angiocholitis.  The  cases  must  be  distinguished  from 
those  of  congenital  jaundice  in  which  angiocholitis  or  obliteration  of  the 
biliary  ducts  has  been  found.  The  general  health  often  remains  notably 
unimpaired. 

2.  Congenital  or  Familial  Splenomegaly,  with  Marked  Constitutional 
Disturbances — stunted  growth,  infantilism,  osseous  changes,  clubbed 
fingers,  pigmented  skin,  enlarged  liver,  and  sometimes  jaundice.  The 
cases  have  been  encountered  especially  in  children  and  young  adults. 
Whether  there  is  any  relationship  between  these  cases  and  the  Min- 
kowski type  of  acholuric  splenomegaly  and'  Hanot's  biliary  cirrhosis  of 
the  liver  remains  to  be  determined. 

3.  Primitive  Splenomegaly.  This  comprises  a  series  of  cases  charac- 
terized by  progressive  enlargement  of  the  spleen  occurring  without  known 
cause.  In  some  cases,  for  many  (ten  to  twenty)  years,  the  general  health 
may  be  scarcely,  if  at  all,  impaired,  the  enlargement  of  the  spleen  con- 
stituting the  only  noteworthy  feature  of  the  disease  (simple  splenomegaly). 
The  spleen  may  reach  extraordinary  dimensions,  extending  to  the  right 
beyond  the  median  line,  and  far  into  the  pelvis.  As  a  rule,  however, 
at  the  end  of  three  or  four  years,  more  or  less  anemia  (splenic  anemia) 
supervenes,  perhaps  attended  or  preceded  by  hemorrhages  (usually 
hematemesis,  but  sometimes  enterorrhagia,  hematuria,  epistaxis,  menor- 
rhagia,  purpura,  etc.).  The  erythrocytes,  as  a  rule,  vary  from  3,500,000 
to  4,000,000,  the  color  index  is  low  (0.5  to  0.7),  and  the  leukocytes  are 
diminished.  With  the  progress  of  the  disease  and  sometimes  in  conse- 
quence of  recurring  hemorrhages,  the  anemia  becomes  more  marked, 
and,  reaching  a  high  grade,  may  lead  to  death;  exacerbations,  as  in 
pernicious  anemia,  are  not  uncommon.  In  some  cases  after  the  lapse  of 
years,  signs  of  portal  cirrhosis  of  the  liver  (ascites,  etc.),  associated  usually 
with  slight  jaundice,  develop  (Banti's  disease).  The  conspicuous  lesions 
found  in  these  cases  of  splenic  anemia  consist  of  chronic  connective 
tissue  hyperplasia  of  the  spleen,  leading  gradually  to  atrophy  of .  the 
lymphoid  tissue,  extraordinary  hyperplasia  of  the  endothelial  cells  of 
the  splenic  sinuses,  and  endothelial  proliferation  and  sclerosis  (even 
atheroma)  of  the  splenic  vein;  sometimes  similar  lesions  involve  also 
the  portal  vein,  both  without  and  within  the  liver,  and  lead  to  stenosis 
and  thrombosis  of  the  branches  of  the  splenic  and  the  portal  veins. 
In  some  cases  the  proliferation  of  the  endothelium  of  the  splenic  sinuses 
constitutes  the  conspicuous  feature  of  the  disease,  and  has  been,  though 
incorrectly,  interpreted  by  some  observers  as  related  to,  if  not  identical 
with,  a  tumor  formation  (splenic  anemia  or  primary  splenomegaly  of 
the  Gaucher  type;  primitive  endothelioma  of  the  spleen) ;  identical  changes 
may  be  found  also  in  the  liver,  lymph  nodes,  and  bone  marrow.  The 
nature  of  the  disorder  is  not  known,  although  the  splenomegaly  is 
assumed  to  be  the  primary  process ;  perhaps  it  develops  in  consequence 
of  some  infective  or  toxic  process  resident  in  the  spleen,  or  to  the  influ- 
ence of  which  the  spleen  may  be  unduly  susceptible.  This  toxin  may  pro- 
voke the  endotheUal  and  other  proliferations  and  ultimately  lead  to  the 


SPLENOMEGALY:  SPLENIC  ANEMIA  409 

anemia  and  the  hepatic  cirrhosis.  The  undoubted  influence  of  the  spleen 
is  evident  in  the  prompt  recovery  and  maintenance  of  health  that  often 
succeed  removal  of  the  spleen  before  the  advent  of  unalterable  changes  in 
the  liver. 

4.  Anemia  in  Children.  In  many  of  the  secondary  anemias  of  infants 
and  children,  such  as  those  due  to  rickets,  syphilis,  poor  food,  faulty 
nutrition,  general  bad  hygienic  conditions,  etc.,  as  well  as  the  more 
common  causes  that  provoke  anemia  in  adults,  the  spleen  is  likely  to  be, 
although  it  is  not  always,  enlarged;  the  enlargement  varies  much  in  dif- 
ferent cases.  The  etiological  factor  should  be  sufficiently  obvious; 
the  blood  changes  are  those  of  ordinary  secondary  anemia,  although 
a  slight  leukocytosis  is  not  uncommon;  the  condition  need  not  be  further 
discussed.  There  are,  however,  other  cases  of  anemia  that  develop  in 
children  without  obvious  cause  and  are  associated  with  more  or  less, 
sometimes  considerable,  enlargement  of  the  spleen;  they  are  sometimes 
spoken  of  as  the  splenic  anemias  of  children.  These  cases  are  difficult 
to  classify :  some  observers  believe  that  the  primary  disturbance  is  in  the 
spleen  (the  disease  being,  therefore,  akin  to  the  splenic  anemia  of  adults); 
others  that  the  splenomegaly  is  the  result  of  or  due  to  the  anemia;  others 
that  both  the  anemia  and  the  splenomegaly  are  the  result  of  a  common 
causative  factor  (perhaps  these  are  allied  to  pernicious  anemia  of 
adults) ;  and  others  that  some  at  least  of  the  cases  are  leukemia  or  Hodg- 
kin's  disease  modified  in  its  clinical  and  anatomical  features  by  the 
young,  more  or  less  undifferentiated,  or  unduly  susceptible,  hemopoietic 
tissues  of  infants  and  children.  Several  grades  of  the  disorder  (or  dis- 
orders) may  be  distinguished:  (1)  That  in  which  the  blood  picture 
is  that  common  to  secondary  anemias  (diminished  erythrocytes  with 
low  color  index)  and  a  normal  number  of  leukocytes,  with  perhaps  a 
relative  lymphocytosis;  (2)  that  differing  from  the  first  mentioned 
only  in  the  presence  of  a  moderate  leukocytosis  (up  to  20,000),  with  little 
if  any  disturbance  in  the  percentage  of  the  different  forms  of  leukocytes ; 
and  (3)  that  characterized  by  more  marked  anemia  (3,000,000  or  less 
erythrocytes),  a  variable,  sometimes  low,  sometimes  rather  high,  color 
index,  considerable  leukocytosis  (20,000  to  50,000  or  more),  poikilo- 
cytosis,  anisocytosis,  polychromatophilia,  megalocytes,  megaloblasts, 
and  a  variable  number  of  myelocytes  (20  to  40  per  cent,  or  more),  in- 
cluding so-called  stimulation  forms — the  disorder  formerly  called  anemia 
infantum  pseudoleuksemica  of  von  Jaksch.  These  three  grades  doubtless 
often,  if  not  always,  represent  stages  or  degrees  of  the  one  process,  and 
although  the  causative  factor  cannot  be  determined,  it  is  not  unlikely 
that  some  of  the  cases  are  due  to  the  sometimes  more  obtrusive  causes  of 
ordinary  secondary  anemia.  Recovery  may  ensue,  even  when  the  blood 
contains  a  large  number  of  myelocytes.  The  treatment  is  that  of  chronic 
secondary  anemia. 


410  DISEASES  OF  THE  SPLEEN 


TUMORS  AND  CYSTS  OF  THE  SPLEEN. 

Tumors  of  the  spleen  may  be  benign  (angioma,  fibroma,  lymph- 
adenoma)  or  malignant  (sarcoma,  endothelioma,  carcinoma),  and  pri- 
mary or  secondary.  The  symptoms  consist  of  local  pain  and  tender- 
ness, enlargement  of  the  organ,  which  may  reveal  nodules,  and  the 
anemia,  emaciation,  and  cachexia  common  to  tumors  in  general.  The 
diagnosis  is  rarely  made  before  operation  (for  enlargement),  or  the 
necropsy.  Cysts  of  the  spleen  may  be  simple  (serous,  hemorrhagic, 
lymphatic),  dermoid,  or  parasitic  (echinococcus  usually),  ^^^len  large, 
the  cyst  may  cause  local  distress  and  reveal  itself  as  a  large  perhaps 
fluctuating  mass.     The  diagnosis  rarely  is  more  than  a  hazard. 


SECTION  VI. 
DISEASES  OF  THE  CIRCULATORY  SYSTEM. 


Pathological  Physiology. — Studies  by  Gaskell,  Keith,  Mackenzie, 
Wenckebach,  Hering,  His,  Erlanger,  and  others  have  tended  to  emphasize 
the  importance  of  the  myogenic  as  contrasted  with  the  neurogenic 
theory  of  the  cardiac  action;  and  although  perhaps  the  two  theories 
may  yet  be  found  to  possess  something  of  truth,  the  five  functions  of  the 
heart  muscle  demonstrated  by  Gaskell  and  Engelmann  constitute  the 
basis  of  the  modern  conception  of  cardiac  physiology  and  pathology. 
These  are:  (1)  Stimulus  production,  the  power  of  producing  stimuli  that 
excite  the  heart  to  contraction;  (2)  excitability,  the  power  of  responding 
to  stimuli  to  contraction;  (3)  conductivity,  the  power  of  transmitting  the 
stimulus  from  one  part  of  the  heart  to  another;  (4)  contractility,  the  power 
of  contracting  in  response  to  stimuli;  and  (5)  tonicity,  the  power  of  main- 
taining such  contraction  of  the  heart  muscle  that  the  total  volume  of 
the  heart  and  the  size  of  the  cavities  are  less  than  they  would  be  were 
full  relaxation  of  the  muscle  to  occur  during  diastole. 

The  power  of  stimulus  production  seems  to  be  inherent  in  the  muscle 
cells  of  the  heart.  The  nature  of  the  stimulus  is  not  known,  but  its 
production  is  much  dependent  upon  the  presence  of  ionized  salts  of 
sodium,  potassium,  and  calcium.  The  stimulus  seems  to  be,  as  it  were, 
a  product  secreted  by  the  cells  and  stored  until  sufl&cient  has  been 
produced  to  excite  a  contraction.  The  contraction  of  the  heart  depends 
upon  its  excitability,  which  disappears  immediately  the  heart  has 
contracted;  the  muscle  fil)ers  are  said  to  be  in  the  refractory  stage. 
This  subsides,  that  is,  excitability  returns,  during  diastole,  so  that,  in 
general,  the  longer  the  period  of  rest  the  weaker  the  stimulus  that  may 
excite  contraction.  The  normal  rate  and  rhythm  of  the  heart  are  de- 
pendent upon  the  normal  interaction  of  the  fwo  functions  of  stimulus 
production  and  excitability.  In  disease  tlie  excitability  may  be  increased 
or  diminished.  Normally  the  stimulus  to  contraction  arises  in  the 
remains  of  the  sinus  venosus,  the  sino-auricular  node  (of  Keith  and 
Flack)  at  the  mouth  of  the  superior  vena  cava  (the  most  excital)le 
portion  of  the  remains  of  the  primitive  cardiac  tube),  and  it  is  trans- 
mitted by  the  muscle  fibers  (perhaps  by  the  bundle  of  Thorel)  along 
the  auricle  to  the  auriculoventricular  bundle  of  His,  and  thence  to  the 
ventricles.    The  regular  succession  of  contractions  of  the  sinus,  auricle, 


412  DISEASES  OF  THE  CIRCULATORY  SYSTEM 

and  ventricle  constitutes  the  normal  or  sinus  rhythm  of  the  heart.  In 
disease  remains  of  the  primitive  cardiac  tube  other  than  the  sino-auri- 
cular  node,  becoming  unduly  excitable,  may  inaugurate  contractions 
(extrasystoles)  independently  of  the  sinus  rhythm,  and  the  conductivity, 
especially  of  the  auriculoventricular  bundle,  may  become  depressed 
(heart  block).  The  power  of  contractility,  the  most  obvious  of  the 
heart  actions,  is  peculiar  in  that  each  contraction  is  maximal  and  is 
followed  by  a  long  refractory  period.  The  fact  of  the  contraction  being 
maximal,  that  is,  as  powerful  as  the  heart  is  at  the  time  capable  of, 
renders  the  heart  independent  of  the  strength  of  the  stimulus,  insures  a 
forceful  response  (contraction)  to  a  weak  stimulus,  and  prevents  an 
excessive  response  to  a  strong  stimulus;  the  refractory  period  insures 
a  period  of  rest  and  renders  tetanization  of  the  muscle  impossible.  In 
general  the  strength  of  the  contraction  is  proportional  to  the  duration 
of  the  immediately  preceding  period  of  rest.  The  power  of  contractility 
may  become  much  depressed  in  disease.  Tonicity  is  a  property  possessed 
by  the  cardiac  musculature  in  common  with  muscular  tissue  elsewhere 
in  the  body;  it  keeps  the  volume  of  the  heart  and  the  size  of  the  cavities 
somewhat  less  than  they  would  be  were  full  relaxation  of  the  muscle  to 
occur  during  diastole.  It  is  the  force,  therefore,  that  opposes  dilatation; 
it  varies  much  in  different  individuals  in  health  and  disease;  it  may  be 
increased  by  drugs,  such  as  digitalis;  and  it  may  be  diminished  by  drugs, 
such  as  muscarin,  and  by  the  toxins  of  infectious  diseases.  Depression 
of  tonicity  is  the  obtrusive  manifestation  of  failure  of  the  heart.  The 
coordinated  activity  of  all  the  functions  of  the  heart  is  essential  to  the 
maintenance  of  the  efficiency  of  the  circulation,  and  this  coordinated 
activity  in  turn  depends  upon  a  sufficiency  of  nutriment. 

In  studying  diseases  of  the  heart  and  interpreting  their  manifestations, 
it  is  essential  to  have  in  mind  not  only  the  myocardium  and  its  nervous 
control  exerted  by  way  of  the  pneumogastric  and  the  accelerator  nerves, 
but  also  its  vascular  or  vasomotor  control  exerted  through  the  elasticity 
and  contractility  of  the  bloodvessels.  This  is  of  importance  because 
of  its  bearing  upon  the  blood  pressure,  which  is  the  resultant  of  the 
resistance  in  the  arterioles  (controlled  by  the  vasomotor  nerves),  of 
the  elasticity  of  the  arterial  walls,  of  the  force  of  the  heart  beat,  and  of  the" 
volume  of  blood.  Without  discussing  the  subject  at  length,  it  perhaps 
suffices  to  point  out  that  the  circulation  may  fail  at  the  periphery  as  well 
as  at  the  heart,  and  that  this  is  more  often  the  case  than  is  usually  sup- 
posed— as  in  shock  generally,  in  the  heart  failure  (more  properly  vaso- 
motor failure)  of  many  infectious  processes,  etc.  Furthermore  the 
beginnings  of  serious  cardiovascular  disease  are  often  in  the  periphery; 
here  divers  endogenous  and  exogenous  poisons  exert  their  deleterious 
influence,  and  in  consequence  of  a  direct  irritant  action  on  the  vaso- 
motor nerves,  or  perhaps  on  the  muscular  coat  of  the  vessels,  increase 
the  blood  pressure,  and  inaugurate  the  series  of  changes  discussed 
under  arteriosclerosis.  It  is  essential,  therefore,  to  study  the  arterial, 
the  capillary,  the  venous,  and  the  pulmonary  circulation. 


PATHOLOGICAL  PHYSIOLOGY  413 

In  all  diseases  of  the  heart  the  major  factor  to  be  determined  is  the 
functional  capacity  of  the  heart,  in  comparison  with  which  other  matters 
are  of  minor  significance.  Noteworthy  incapacity  of  the  heart  is  quite 
obvious  in  symptoms  of  unstable  compensation  or  of  impending  or 
actual  decompensation;  of  these,  several,  such  as  cardiac  pain,  palpita- 
tion, irregularities  of  rate  and  rhythm,  etc.,  are  discussed  under  the  general 
heading  of  neuromuscular  disorders.  There  are  several  others,  common 
to  the  different  forms  of  heart  disease,  such  as  dyspnoea,  cyanosis,  and 
oedema,  that  plainly  disclose  the  functional  incapacity,  the  functional 
failure,  of  the  heart. 

Dyspnoea  is  very  common;  it  may  be  the  only  symptom,  but  is 
often  accompanied  by  a  sense  of  precordial  or  substernal  distress  or 
actual  pain,  and  more  or  less  anxiety  and  apprehension;  and  it 
varies  much  in  degree  from  slight  breathlessness  on  exertion  or  excite- 
ment to  orthopnoea  even  when  the  patient  rests  in  bed.  This  dysp- 
noea is  due  directly  to  deficient  oxygenation  of  the  blood — to  an  excess 
of  carbon  dioxide,  which  in  turn  results  from  a  slow  and  feeble  circula- 
tion; the  excess  of  carbon  dioxide  acts  as  an  irritant  to  the  respiratory 
centre  in  the  medulla  and  increases  the  respiratory  rate.  Contributing 
factors  are  often  present,  such  as  chronic  passive  congestion  with  result- 
ant changes  in  the  alveolar  epithelium  and  encroachment  upon  the 
interalveolar  space  in  consequence  of  dilatation  of  the  capillaries,  loss 
of  elasticity  of  the  lungs,  oedema  of  the  lungs,  chronic  bronchitis, 
bronchopneumonia,  etc.  The  dyspnoea  sometimes  comes  on  paroxys- 
mally  in  attacks — so-called  cardiac  asthma.  These  attacks  are  due  to 
temporary  incapacity  of  the  left  ventricle,  which  may  be  provoked  by 
exertion,  excitement,  a  full  meal,  flatulence,  constipation,  etc.,  or  the 
attacks  may  come  on  without  obvious  cause.  They  are  quite  common 
early  in  the  night,  developing  soon  after  the  patient  has  fallen  asleep. 
Sometimes,  especially  in  arteriosclerotic  subjects  (cardiovascular-renal 
disease)  with  involvement  of  the  brain,  the  respirations  are  peculiarly 
periodical,  longer  or  shorter  periods  of  apnoea  alternating  with 
periods  of  breathing,  at  first  slow  and  shallow,  but  gradually  becoming 
deeper  and  more  rapid  until  they  reach  a  maximum,  whereupon 
they  gradually  decrease  and  finally  again  cease  (Cheyne-Stokes  breath- 
ing). 

Cyanosis  attends  dyspnoea  and  is  due  to  like  causes — to  an  excess  of 
carbon  dioxide  in  the  blood.  In  chronic  cases  the  patients  not  infre- 
quently become  more  or  less  accustomed  to  the  cyanosis,  the  organism 
adapts  itself  to  the  changed  conditions,  and  although  the  cyanosis  may  be 
more  or  less  obvious,  there  may  be  little  or  no  subjective  dyspnoea,  and 
the  functions  of  the  body  may  be  fairly  well  performed.  Cyanosis 
occurs  not  only  in  diseases  of  the  heart,  but  also  in  diseases  of  the  lungs 
interfering  with  proper  oxygenation  of  the  blood;  in  erythremia  (poly- 
cythemia with  cyanosis  and  enlarged  spleen);  rarely  in  conditions  (hie 
to  alteration  of  the  blood  pigment  itself:  that  is,  the  conversion  of  the 
hemoglobin    into   metahemoglobin    (chronic   poisoning   by  acetanilide, 


414  DISEASES  OF   THE   CIRCULATORY  SYSTEM 

phenacetin,  sulphonal,  trional,  etc.);  and  in  so-called  enterogenous 
cyanosis  (intestinal  auto-intoxicationj,  due  in  one  series  of  cases  to  con- 
version of  the  hemoglobin  into  methemoglobin,  the  result  of  the  absorp- 
tion of  nitrites  from  the  intestine  in  chronic  diarrhoea,  and  amenable 
to  a  milk  diet,  and  due  in  another  series  of  cases  to  conversion  of  the 
hemoglobin  into  sulph-hemoglobin,  the  result  apparently  of  putre- 
faction of  the  proteins  in  chronic  constipation  (increased  formation 
or  absorption  of  H2S),  and  amenable  to  treatment  directed  toward  the 
constipation. 

The  oedema  of  cardiac  disease  is  largely  the  result  of  slowing  of  the 
circulation  and  consequent  stasis  of  the  blood;  Vjut  changes  in  the 
endothelium  of  the  capillary  blood  vessels  and  lymph  spaces  are  a  con- 
tributing factor.  This  oedema  from  stasis  is  to  h»e  distinguished  from  so- 
called  inflammatory  oedema,  nephritic  oedema,  and  hydremic  oedema. 

In  many  cases  of  readily  recognized  heart  disease,  compensation  has 
not  failed,  nor  is  it  unstable;  but  it  is  nevertheless  desirable  to  ascertain 
the  functional  capacity  of  the  heart.  This  may  be  roughly  determined 
by  noting  the  amount  of  work  or  excercLse  that  provokes  dyspnoea, 
palpitation  of  the  heart,  precordial  distress,  and  increased  frequency 
of  the  heart  beat;  but  this  is  a  rude  test.  Other  more  or  less  accurate 
and  satisfactory  methods  of  determining  the  functional  capacity  of  the 
heart  have  been  suggested.  The  graphic  methods,  especially  emphasized 
by  Mackenzie,  whereby  it  is  possible  to  recognize  disturbances  of  excita- 
bility, conductivity,  contractility,  tonicity,  and  rhythmicity,  are  excellent; 
but  are  not  often  available  in  clinical  work  outside  a  hospital.  Other 
methods  are  based  upon  the  changes  in  blood  pressure  and  pulse  rate 
provoked  by  a  measured  amount  of  work.  A  simple  test  consists  in 
determining  the  difference  between  the  rate  of  the  heart  beat  in  the 
erect  and  in  the  recumbent  posture;  normally  recumbency  produces  a 
lessening  of  the  heart  beats  of  from  six  to  twenty  per  minute;  this  is 
partly  or  completely  lost  in  cardiac  insufficiency.  ^Mendelsohn  has 
suggested  that  the  functional  capacity  of  the  heart  may  be  estimated 
by  ascertaining  the  time  required  for  the  heart  to  regain  its  normal 
rate  after  a  measured  amount  of  work.  Katzenstein  determines  the 
blood  pressure  and  the  pulse  rate  after  digital  compression  of  both 
femoral  arteries.  In  normal  individuals  this  compression  results  in 
an  increase  of  the  systolic  blood  pressure  in  the  brachial  artery  of 
from  5  to  15  mm.  Hg.,  without  noteworthy  changes  in  the  pulse  rate; 
in  cases  of  efficient  h}'pertrophy  the  blood  pressure  may  be  increased 
15  to  40  mm.  Hg. ;  in  cases  of  slight  cardiac  insufficiency,  the  pressure 
may  not  rise  at  all,  while  the  pulse  rate  becomes  accelerated;  and  in 
cases  of  marked  cardiac  insufficiency  the  blood  pressure  may  fall  and  the 
pulse  rate  become  accelerated.  The  pain  and  mental  excitement  induced 
by  the  procedure  seriously  compromise  the  results,  and  a  marked  in- 
crease in  blood  pressure  is  not  entirely  free  from  danger.  Graupner  has 
drawn  attention  to  the  fact  that  after  a  measured  amount  of  work 
the  systolic  blood  pressure  and  the  pulse  rate  thus  increased,  gradually 


NEUROMUSCULAR  DISORDERS  OF   THE  HEART  415 

return  to  the  normal,  and  that  after  the  pulse  rate  has  declined  to  the 
normal  the  systolic  blood  pressure  begins  to  rise,  attains  its  maximum 
several  minutes  later  than  the  pulse  rate,  and  then  falls  to  (or  below) 
the  normal;  this  so-called  normal  recovery  may  be  delayed  and  di- 
minished in  slight  cardiac  inadequacy,  and  it  may  be  entirely  absent  in 
marked  cardiac  insufficiency,  the  blood  pressure  declining  continuously, 
and  only  reaching  the  normal  after  a  longer  or  shorter  period  of  rest. 
Stair  climbing  or  lifting  weights,  may  be  resorted  to  for  the  measured 
amount  of  work. 


NEUROMUSCULAR  DISORDERS  OF  THE  HEART. 

Disturbances  in  the  sensory  or  motor  activities  of  the  heart  often  either 
dominate  the  clinical  picture  or  constitute  the  sole  discoverable  evidence 
of  cardiac  disease.  These  disturbances,  in  consequence,  are  often  spoken 
of  as  neuroses  or  functional  disorders  of  the  heart,  terms  that  have  some 
justification  in  fact,  but  are  often  misnomers,  since  the  disorders  in 
question  often  constitute  mere  symptoms  or  symptom-complexes  and 
have  an  anatomical  basis.  Convenience,  however,  and  the  grouping  of  the 
phenomena  suggest  their  discussion  together  under  the  designation  neuro- 
muscular or  symptomatic  disorders.  These  may  be  divided  into  the 
sensory  and  the  motor.  The  sensory  disorders  are  represented  by  cardiac 
pain  and  distress  and  the  subjective  sensations  associated  with  palpita- 
tion and  with  some  forms  of  irregularity  or  intermission  of  the  heart;' 
the  motor  disorders  include  disturbances  of  rate  (rapid,  infrequent; 
tachycardia,  bradycardia),  of  rhythm  (the  different  types  of  arrhythmia), 
and  of  force  (strong  and  weak). 

Cardiac  Pain. — Cardiac  pain  varies  much  in  character,  intensity, 
and  in  situation.  It  may  be  a  mere  discomfort,  or  an  actual  pain — dull, 
aching,  stabbing,  or  agonizing,  griping,  constricting,  vise-like.  It  may 
be  referred  to  the  apex  of  the  heart,  to  the  entire  precordium,  to  the 
axillae,  and  it  may  radiate  to  the  back,  to  one  or  both  arms,  etc.  The 
agonizing,  constricting,  vise-like  pain  of  angina  pectoris  is,  of  course,  the 
obtrusive  manifestation  of  the  disorder;  but  since  the  disorder  has  an 
anatomical  basis,  it  should  not  be  called  a  neurosis. 

Cardiac  pain  may  be  due  to  organic  or  so-called  functional  disorders 
of  the  heart:  (1)  The  organic  cases  comprise  all  the  diseases  of  the 
myocardium,  endocardium,  and  pericardium,  and  of  the  aorta,  that 
will  be  discussed  under  the  respective  headings.  (2)  Other  cases  are 
due  to  the  toxic  action  of  tobacco,  alcohol,  tea,  coffee,  etc.,  and  may  or 
may  not  be  associated  with  demonstrable  organic  changes;  the  pain  or 
distress  usually  ceases  in  the  course  of  time  upon  discontinuance  of  the 
exciting  factor.  (3)  A  third  group  of  cases  are  the  so-called  nervous 
cases;  cases  induced  by  shock,  emotional  disturbances,  excessive  venery, 
etc.;  or  associated  with  neurasthenia,  hysteria,  disorder  of  the  genitalia 
(male  and  female)  or  of  the  kidneys,  etc.;  or  apparently  due  to  disorder 


416  DISEASES  OF  THE  CIRCULATORY  SYSTEM 

of  the  vasomotor  system  (Nothnagel's  vasomotor  angina).  (4)  Some 
cases  are  due  solely  to  gastro-intestinal  derangements  associated  with 
flatulence;  they  are  readily  cured  by  attention  to  the  exciting  cause. 

Palpitation  of  the  Heart. — In  health  the  activity  of  one's  heart  is 
entirely  unnoticed;  the  subjective  consciousness  of  the  heart's  pulsation, 
so-called  palpitation,  develops  under  a  variety  of  circumstances.  It  is  a 
normal  phenomena  under  the  stress  of  unusual  exertion  or  excitement,  but 
the  sensations  of  throbbing  thus  experienced  are  perfectly  regular,  as  a 
rule,  and  soon  subside  with  the  initiating  cause.  It  develops  upon  slight, 
sometimes  very  slight,  provocation  in  cases  of  unusual  excitability  of  the 
nervous  system,  in  neurasthenia  and  hysteria;  and  in  women  generally 
rather  than  in  men,  especially  at  times  of  nervous  perturbation,  as  at 
puberty,  during  menstruation,  at  the  climacteric,  and  in  conditions  of 
worry,  anxiety,  and  emotional  disturbances.  It  occurs  also  in  con- 
sequence of  the  toxic  influence  of  tobacco,  alcohol,  tea,  coffee,  etc., 
on  the  heart;  in  the  myocardial  degenerations  associated  with  anemic 
conditions  and  the  acute  infections;  in  the  condition  of  irritable  heart, 
due  to  excessive  muscular  strain;  in  organic  (myocardial  and  endocardial) 
diseases  of  the  heart  generally;  and  in  many  disorders  of  the  abdominal 
organs,  notably  flatulent  dyspepsia. 

The  attacks  vary  much  in  severity — from  a  slight  and  transitory  feeling 
of  fluttering  of  the  heart  to  severe  spells  of  very  forcible  throbbing  of  the 
heart,  attended  by  marked  precordial  distress  or  oppression,  that  may 
continue  for  an  hour  or  more.  The  throbbing  not  infrequently  extends 
to  the  arteries  and  may  lead  to  flushing  of  the  skin  and  perhaps  to 
perspiration  and  transient  polyuria.  Usually  the  heart's  action  is  much 
accelerated,  up  to  150  or  more  per  minute,  and  often  irregular;  but 
occasionally  the  rate  and  rhythm  are  quite  normal;  and  on  the  con- 
trary some  attacks  of  very  rapid  heart  action  (delirium  cordis)  may 
be  entirely  unperceived  by  the  patient.  Examination  of  the  heart,  as  a 
rule,  reveals  only  the  evidence  of  the  hyperactivity.  The  sounds  usually 
are  normal  or  perhaps  somewhat  accentuated,  especially  the  pulmonary 
second  sound.  There  may  be  a  slight  systolic  murmur  in  the  pulmonary 
area,  especially  in  the  anemic  and  neurasthenic  cases. 

Arrhythmia. — ^The  following  varieties  of  arrhythmia  may  be  dis- 
tinguished : 

1.  Respiratory  Arrhythmia  (Juvenile  Arrhythmia;  Sinus  Irregularity 
Mackenzie). — Respiratory  arrhythmia  is  an  exaggeration  of  the  normal 
inspiratory  increase  and  expiratory  decrease  in  the  frequency  of  the  cardiac 
action;  it  is  characterized  by  variations  in  the  duration  of  the  cardiac  cycle, 
dependent  almost  if  not  quite  wholly  upon  prolongation  of  the  diastole. 
It  is  not  associated  with  noteworthy  changes  in  the  size  of  the  individual 
pulse  beats,  nor  is  it  a  condition  of  missed  beats  at  the  wrist  due  to  extra- 
systoles.  It  is  not  uncommon  in  youths  approaching  puberty,  but  rarely 
occurs  in  healthy  adults;  it  is  sometimes  observed  during  convalescence 
from  acute  infections  (diphtheria,  scarlet  fever,  typhoid  fever,  pneumonia, 
etc.),  in  anemic  conditions,  in  neurasthenia,  in  cerebral  disorders,  tuber- 


NEUROMUSCULAR  DISORDERS  OF  THE  HEART  417 

culous  meningitis,  etc.  It  is  often  associated  with  slowing  of  the  heart 
action  and  infrequent  respiration,  and  is  attributable  to  irritation  of  the 
vagus  (exaggeration  of  the  normal  respiratory  reflex).  It  is  readily  recog- 
nized: beats  of  equal  strength  varying  continually  in  time  with  the  phases 
of  respiration,  being,  as  a  rule,  most  infrequent  during  expiration. 
Occasionally  in  children  it  may  be  mistaken  for  continuous  irregularity 
(nodal  rhythm),  but  it  may  be  distinguished  by  a  tracing  of  the  jugular 
vein  which  shows  concurrent  involvement  of  the  auricle,  and  by  its 
being  lessened  or  dissipated  by  atropine  (which  does  not  influence  con- 
tinuous irregularity),  and  by  being  increased  by  digitalis  (which  lessens 
continuous  irregularity).  It  should  not  be  confused  with  the  parodoxic 
pulse — inspiratory  diminution  in  the  force  and  volume  of  the  pulse. 
Of  itself  it  is  of  minor  significance  and  good  prognosis,  and  it  calls  for 
no  special  treatment. 

2.  Extrasystoles. — ^The  majority  of  cases  of  arrhythmia  are  due 
to  extrasystoles,  that  is,  to  "premature  contractions  of  the  auricle  or 
the  ventricle  in  response  to  a  stimulus  from  some  abnormal  point  of  the 
heart,  but  in  which  otherwise  the  fundamental  or  sinus  rhythm  of 
the  heart  is  maintained"  (Mackenzie).  Mackenzie  reasons  that,  since  the 
stimulus  for  contraction  arises  normally  in  the  remains  of  the  sinus 
venosus  at  the  mouths  of  the  great  veins  (the  sino-auricular  node), 
other  remains  of  the  primitive  cardiac  tube,  if  rendered  more  excitable, 
might  start  the  contraction  before  the  sinus;  and  since  this  primitive 
cardiac  tube  in  the  heart  is  represented  also  in  the  auricle,  in  the  auriculo- 
ventricular  node,  and  in  the  auriculoventricular  bundle  after  it  leaves 
the  node,  he  (as  well  as  others)  describe  the  following  types  of  extra- 
systoles : 

1.  Ventricular  extrasystoles,  those  in  which  the  origin  of  the 
extrasystole  is  assumed  to  be  in  the  auriculoventricular  bundle  beyond 
the  auriculoventricular  node  (that  is,  in  the  ventricle).  This  stimulates 
the  ventricle  to  contraction  in  advance  of  the  normal  time;  this  contrac- 
tion (extrasystole)  is  followed  by  the  usual  refractory  period  which 
extends  beyond  the  time  that  the  normal  stimulus  from  the  sino-auric- 
ular node  reaches  the  ventricle;  the  ventricle  in  consequence  remains 
inactive,  a  beat  is  missed,  and  a  large  so-called  compensatory  pause 
ensues,  which  is  terminated  by  a  forcible  (maximal)  contraction  of  the 
ventricle  in  response  to  the  next  ensuing  stimulus  from  the  auricle;  this 
occurs  at  the  proper  time  and  in  normal  rhythm.  Characteristic  of  the 
ventricular  extrasystole  is  the  fact  that  the  time  occupied  by  the  normal 
systole,  the  extrasystole,  and  the  compensatory  pause  is  twice  that  of  a 
normal  cardiac  cycle;  the  number  of  heart  beats  per  minute  may  remain 
normal,  a  premature  ventricular  systole  (extra-systole)  being  inter- 
polated between  two  normal  contractions. 

2.  Auricular  extrasystoles,  those  in  which  the  stimulus  is  assumed 
to  arise  in  the  remains  of  the  primitive  cardiac  tube  incorporated  in  the 
auricle  elsewhere  than  at  the  sinus.  As  in  the  ventricular  extrasystoles,  the 
premature  contraction  of  the  auricle  (extrasystole)  is  followed  by  a  con- 

27 


418  DISEASES  OF  THE  CIRCULATORY  SYSTEM 

traction  of  the  ventricle;  but  the  normal  stimulus  from  the  sinus  finds 
the  auricle  refractory  and  contraction  does  not  take  place.  This  form  of 
arrhythmia  resembles  ventricular  extrasystoles,  and  usually  is  distinguish- 
able only  by  tracings  of  the  jugular  pulse  (which  reveal  the  auricular 
extrasystole) .  As  in  ventricular  extrasystoles  the  time  occupied  by  the 
normal  systole,  the  extrasystole,  and  the  long  pause  may  be  twice  that  of 
a  normal  cardiac  cycle;  but  in  most  cases  it  is  less;  that  is,  the  pause 
is  not  compensatory; 

3.  AuRicuLOVENTRicuLAR  EXTRASYSTOLES  (nodal  extrasystolcs),  those 
in  which  the  stimulus  is  supposed  to  arise  in  the  auriculoventricular 
node  of  Tawara,  and  gives  rise  to  premature  and  simultaneous  con- 
tractions of  auricles  and  ventricles.  This  is  assumed  by  some  ob- 
servers to  be  a  so-called  retrograde  extrasystole,  that  is,  a  ventricular 
extrasystole  in  which  the  stimulus  has  travelled  back  along  the  auriculo- 
ventricular bundle  and  prematurely  stimulated  the  auricle,  an  assump- 
tion that  Mackenzie  believes  untenable. 

Extrasystoles  result  from  the  increased  excitability  of  the  remains  of 
the  primitive  cardiac  tube  (Mackenzie);  perhaps  occasionally  from  an 
exaggeration  of  the  normal  automatism  of  the  heart.  Mackenzie  believes 
that  the  compensatory  pause  is  not  due  to  the  ventricle  being  refractory, 
but  to  the  auriculoventricular  bundle  being  refractory  (impaired  conduc- 
tivity), and  not  conveying  the  stimulus  to  the  ventricle,  which,  therefore, 
stands  still  until  the  next  physiological  stimulus  comes  down  from  the 
auricle.  Clinically  this  type  of  arrhythmia  is  characterized  by  the  occur- 
rence of  two  or  more  approximated  pulse  beats  followed  by  an  unusually 
long  pause  (intermission  of  the  pulse).  The  extrasystole  may  occur  only 
at  long,  irregular  intervals,  at  short  irregular  intervals,  or  at  short  regular 
intervals,  as  after  every  second  beat,  every  three  beats,  etc.,  in  which  latter 
event  it  gives  rise  to  the  so-called  bigeminal,  trigeminal,  quadrigeminal, 
quinquegeminal  pulse,  etc.  A  continuous  series  of  extrasystoles  may 
give  rise  to  a  type  of  paroxysmal  tachycardia  (usually,  however,  this  is 
of  the  nodal  rhythm).  In  some  cases  the  extrasystole  is  more  or  less 
ineffectual,  because  it  occurs  early  in  diastole  (in  the  refractory  period, 
when  the  ventricle  is  incapable  of  much  contractile  effort),  the  ventricle 
contains  very  little  blood,  and  the  pressure  in  the  aorta  is  very  high — so 
that  the  aortic  leaflets  are  opened  slightly,  if  at  all.  This  more  or  less 
ineffectual  extrasystole  produces  little  if  any  perceptible  influence  on  the 
pulse  (although  it  may  be  registrable  on  the  sphygmogram  or  cardio- 
gram); the  pulse  then  appears  to  be  definitely  intermittent — a  beat  is 
missed.  If  this  occurs  with  regularity  after  each  normal  systole  of  the 
ventricle,  the  condition  at  first  may  be  mistaken  for  bradycardia,  which, 
however,  can  be  differentiated  by  tracings  of  the  jugular  pulse  or  of  the 
apex  beat,  and  by  auscultation.  There  is  some  doubt  as  to  the  occurrence 
of  hemisystole  (alternate  contraction  of  the  two  ventricles).  Mackenzie 
and  Hering  believe  that  most  reported  cases  are  really  cases  of  extra- 
systole, and  that  hemisystole  occurs  only  in  a  dying  heart;  von  I.eyden, 
Kraus,  and  Nicolai  believe,  however,  that  rarely  the  ventricles  may  act 


NEUROMUSCULAR   DISORDERS  OF   THE  HEART  419 

asynchronously.  On  auscultation  the  extrasystole,  if  it  occurs  early  in 
diastole  and  is  ineffectual  in  opening  the  aortic  valve,  is  revealed  by  a 
single,  usually  a  muffled,  sometimes  a  loud,  sound;  if  it  occurs  later  in 
diastole,  and  does  lead  to  opening  of  the  aortic  valve,  a  second  sound 
may  also  be  produced;  the  two  normal  sounds  are  quickly  followed  by 
two  weaker  sounds  and  an  unusually  long  pause.  Subjects  are  some- 
times conscious  of  the  extrasystole — a  dull  thud  in  the  region  of  the 
precordiimi,  or  a  sensation  of  stoppage  of  the  heart  and  a  palpable 
intermission  of  the  pulse.  Although,  as  a  rule,  readily  recognizable, 
it  is  sometimes  difficult  to  distinguish  extrasystoles ;  the  several  types 
may  occur  in  varying  combinations,  and  they  may  be  associated  with 
other  forms  of  arrhythmia. 

Extrasystoles  occur  in  a  variety  of  conditions:  (1)  In  neurotic  subjects, 
especially  after  exertion  and  excitement,  at  puberty,  and  the  climacteric, 
during  pregnancy,  in  hysteria,  neurasthenia,  etc.,  and  reflexly  in  indi- 
gestion and  divers  gastro-intestinal  disorders;  (2)  in  toxic  conditions 
such  as  those  due  to  tobacco,  tea,  coffee,  alcohol,  etc.;  (3)  in  infections, 
especially  during  convalescence  from  typhoid  fever,  pneumonia,  diph- 
theria, scarlet  fever,  etc.;  and  (4)  in  the  various  sorts  of  acute  and 
chronic  diseases  of  the  heart,  especially  those  associated  with  hyper- 
tension. In  themselves,  extrasystoles  are  of  minor  clinical  significance, 
of  which  fact  the  patient,  if  aware  of  the  irregularity,  should  be  assured; 
the  associated  conditions,  such  as  infections  and  various  sorts  of  heart 
disease,  may  be  of  great  significance,  even  dangerous.  The  treatment 
should  be  directed  to  the  associated  or  underlying  factors. 

3.  Continuous  Irregularity  (Perpetual  Irregularity;  Nodal  Rhythm; 
Rhythm  of  Auricular  Paralysis;  Ventricular  Rhythm;  Absolutely  Irregular 
Heart). — This  is  characterized  by  irregularity  in  the  force,  ecjuality,  and 
sequence  of  the  pulse  beats,  by  the  absence  of  the  fundamental  or  sinus 
rhythm  of  the  heart,  by  the  presence  of  a  ventricular  (or  positive)  venous 
pulse  (tricuspid  insufficiency  or  auricular  paralysis),  by  the  absence  of 
an  auricular  wave  on  the  jugular  tracing,  and  by  the  permanence  of 
the  phenomena.  The  cardiac  action  may  be  extremely  rapid  (delirium 
cordis);  occasionally  it  may  be  very  rapid  temporarily  (paroxysmal 
tachycardia);  rarely  it  may  be  quite  slow,  especially  under  the  influence 
of  digitalis;  except  when  very  rapid,  the  cardiac  action  is  always  irregular 
and  this  may  be  of  minor  or  of  high  grade.  The  auscultatory  phenomena 
are  similarly  irregular:  the  sounds  vary  in  character  and  intensity,  many 
of  the  systoles  are  not  followed  by  second  sounds,  and  they  occasion  no 
palpable  pulse  at  the  wrist. 

The  condition  is  due  to  the  concurrent  contraction  of  the  auricle 
and  the  ventricle  (sometimes  antecedent  contraction  of  the  ventricle),  in 
response  to  stimuli  arising  at  the  auriculoventricular  node  (Mackenzie), 
or  to  a  block  between  the  sinus  and  the  auricle  (depression  of  conduc- 
tivity, Wenckeback,  Erlanger).  It  is  found  in  all  forms  of  severe  heart 
faihn-e  with  dilatation  of  the  auricles,  particularly  those  of  rheumatic 
origin   (mitral  stenosis  especially)   and   the   fibroid   heart.      Mackenzie 


420  DISEASES  OF  THE  CIRCULATORY  SYSTEM 

believes  that  in  a  great  many  cases  the  immediate  breakdown  is  directly 
attributable  to  the  inception  by  the  heart  of  the  abnormal  rhythm. 
The  condition  is  always  of  serious  moment.  When  once  established 
it  usually  continues  until  death,  although  it  may  be  improved  by  appro- 
priate treatment,  especially  the  use  of  digitalis;  that  is,  some  normal 
beats  occur  and  irregular  beats  become  less  apparent;  but  evidence  of 
auricular  contractions  usually  do  not  again  become  evident,  and  slight 
exertion  sets  up  extreme  irregularity  and  rapid  action  of  the  heart. 

4.  Partial  and  Complete  Heart  Block  (Depression  of  Conductivity). — 
In  some  cases,  the  ventricle  fails  to  contract  after  each  auricular 
contraction,  in  consequence  of  failure  of  the  auriculoventricular 
bundle  of  His  to  conduct  the  stimulus  to  the  ventricle;  the  condition, 
therefore,  is  a  manifestation  of  depressed  conductivity,  and  is  spoken 
of  as  partial  or  complete  heart  block.  But  depression  of  conductivity 
may  occur  without  arrhythmia.  Erlanger  has  shown  experimentally 
that  varying  degrees  of  compression  result  first  in  increase  of  the  inter- 
systolic  period  {a-c  interval;  that  is,  the  time  between  the  beginning  of  the 
auricular  and  the  carotid  waves  in  tracings  of  the  jugular  pulse);  then  in 
a  2  to  1,  3  to  1,  or  4  to  1  auriculoventricular  rhythm  (incomplete  heart 
block);  and  finally  in  independent  auricular  and  ventricular  contrac- 
tions (complete  heart  block).  Mackenzie  states  that  the  stimulus  to  the 
ventricle  may  be,  (1)  delayed;  (2)  prevented  from  crossing  the  bundle 
of  His;  or  (3)  completely  blocked  beyond  the  auriculoventricular  node, 
in  which  event  the  ventricle  contracts  in  response  to  a  stimulus  that 
arises  in  the  uninjured  remains  of  the  auriculoventricular  bundle 
(heart  block,  ventricular  rhythm).  Clinically  the  condition  is  mani- 
fested by  a  slow  ventricular  rate  (slow  radial  pulse;  one  type  of  brady- 
cardia), associated  with  more  frequent  pulsations  of  the  veins  of  the 
neck,  owing  to  preservation  of  the  normal  rate  of  auricular  contractions. 
If  the  ventricular  contractions  are  more  than  thirty-six  per  minute, 
they  may  have  a  distinct  relationship  to  the  auricular  waves  in  the 
jugular  pulse,  the  ventricle  responding  to  every  second,  third,  or  fourth 
auricular  contraction;  when  the  ventricular  contractions  are  about 
thirty  or  less,  they  are  probably  independent  of  the  auricle,  and  the  auricle 
and  the  ventricle  beat  at  independent  rates,  in  response  to  independent 
stimuli.  The  condition  may  be  suspected  when  there  is  a  complete  pause 
in  the  radial  pulse  with  absence  of  heart  sounds  (Mackenzie). 

Temporary  and  incomplete  heart  block  occurs  rarely  in  certain  infec- 
tions (or  during  convalescence),  such  as  typhoid  fever,  pneumonia, 
diphtheria,  scarlatina,  rheumatism,  influenza,  etc.;  it  may  occur  in  the 
fibroid  heart;  and  it  may  be  set  up  by  the  prolonged  use  of  digitalis. 

Complete  heart  block  is  typically  represented  in  the  so-called  Adams- 
Stokes  syndrome,  of  which  the  characteristic  features  are:  (1)  Brady- 
cardia, sometimes  permanent,  sometimes  paroxysmal  and  temporary, 
the  radial  pulse  and  the  ventricular  systoles  falling  to  40,  20,  10  or  less, 
a  minute;  (2)  visible  auricular  pulsation  of  the  veins  of  the  neck  due  to 
auricular  contractions,  and  often  revealing  a  2  to  1,  3  to  1,  or  4  to  1 


NEUROMUSCULAR   DISORDERS  OF  THE  HEART  421 

rhythm  as  compared  with  the  ventricuhir  contractions;  and  (3)  cerebral 
(anemic)  disorders — vertigo,  syncope,  pseudo-apoplectiform  attacks, 
sometimes  associated  with  convulsions  (epileptiform)  of  variable  severity 
and  duration.  The  cases  of  heart  block  that  have  been  carefully 
studied  after  death  have  revealed  more  or  less  destructive  lesions,  espe- 
cially gummas,  sclerosis,  atheroma,  anemic  necrosis,  etc.,  of  the  auriculo- 
ventricular  bundle  of  His,  sufficient  partly  or  completely  to  interrupt 
the  conduction  of  impulses.  It  is  surmised  that  the  less  degrees  of  heart 
block  are  due  to  less-marked,  in  some  cases  perhaps  merely  functional 
lesions  of  the  bundle.  The  cases  due  to  digitalis  are  the  result  of  a 
specific  depressive  action  of  the  drug  on  the  function  of  conductivity. 
The  Adams-Stokes  syndrome  is  a  serious  malady,  ultimately  fatal, 
although  it  may  last  for  years.  The  use  of  the  iodides  often  leads  to 
marked  improvement,  especially  in  the  syphilitic  (gummatous)  cases. 
Strychnine  also  has  proved  of  avail. 

5.  Alternating  Pulse  (Depression  of  Contractility). — The  alternating- 
pulse  consists  of  a  regular  succession  of  large  and  small  pulse 
waves,  and  results  from  depression  of  the  function  of  contractility. 
Mackenzie  states  that  "when  contractility  is  depressed,  if  time  be  allowed 
for  a  full  and  strong  contraction,  the  longer  duration  of  contraction 
encroaches  upon  the  period  of  rest,  so  that  by  the  time  the  next  stimulus 
arrives  the  contractility  has  not  sufficiently  recovered,  and  a  smaller  and 
shorter  contraction  results.  As  this  contraction  is  shorter  in  duration, 
the  period  of  rest  is  thereby  lengthened  before  the  next  stimulus  arrives, 
so  that  the  contraction  will  be  stronger  and  longer;  being  longer,  it  will 
again  encroach  upon  the  period  of  rest,  and  so  the  process  of  alternation 
goes  on."  This  alternating  pulse  is  found  in  conditions  of  exhaustion 
of  the  myocardium,  especially  in  advanced  mitral  stenosis,  coronary  scle- 
rosis, general  arteriosclerosis  with  high  blood  pressure,  angina  pectoris, 
fibroid  heart,  etc.     It  is  of  serious  moment. 

Tachycardia. — ^The  term  tachycardia  is  more  or  less  loosely  applied  to 
abnormal  frequency  of  the  heart  action;  by  some  observers  the  term  is 
restricted  to  extraordinary  frequency  (twice  the  normal — 150  or  more); 
and  it  is  not  infrequently  confused  with  the  term  paroxysmal  tachy- 
cardia, which  seems  to  be  a  distinct  clinical  entity.  Abnormal  frequency 
of  the  pulse  may  be  physiological  or  pathological.  The  physiological 
cases  comprise  those  normal  individuals  in  whom  the  pulse  is  persistently 
above  the  average  of  normal  persons — 80  to  100  per  minute.  The 
pathological  cases  comprise  those  due  to:  (1)  Infections,  which  include 
almost  all  the  infectious  diseases,  in  which,  associated  with  fever,  the  pulse 
becomes  accelerated.  In  perhaps  the  majority  of  cases  the  acceleration 
of  the  pulse  is  proportionate  to  the  increment  of  fever;  in  some  cases, 
notably  scarlatina,  the  pulse  is  disproportionately  rapid;  while  in  others 
such  as  typhoid  fever,  certain  forms  of  meningitis,  although  it  may  be 
of  increased  freriuency,  this  is  not  up  to  the  average  of  other  fever  states; 
in  some  of  these  cases  the  pulse  may  even  be  slowed.  (2)  Intoxications, 
such  as  tobacco,  tea,  coffee,  atropine,  strychnine,  alcohol,  etc-.     (3)  x\ll 


422  DISEASES  OF  THE  CIRCULATORY  SYSTEM 

acute  and  chronic  diseases  of  the  heart,  such  as  irritation,  overstrain, 
valvular  diseases  (notably  mitral  stenosis),  myocardial  disease,  peri- 
cardial disease,  etc.,  especially  in  impending  or  actual  decompensation. 
(4)  Neurotic  disturbances,  such  as  emotional  and  other  shocks,  hysteria, 
neurasthenia,  and  some  organic  nervous  diseases.  (5)  Graves'  disease-. 
(6)  Paroxysmal  tachycardia. 

Paroxysmal  tachycardia  is  a  disorder  characterized  by  paroxysms 
of  extraordinary  frequency  of  the  heart  beat  and  the  pulse.  It  occurs 
in  both  sexes,  especially  in  neurotic  individuals,  and  in  subjects  with  pre- 
viously normal  hearts,  as  well  as  in  cardiopaths.  It  commonly  develops 
in  adult  life,  although  it  may  come  on  during  childhood.  It  is  usually 
attributed  to  paralysis  of  the  inhibiting  centre  (vagus),  but  minor  grades 
(a  pulse  rate  of  less  than  120)  are  sometimes  ascribed  to  irritation  of  the 
sympathetic.  Mackenzie  regards  the  condition  as  a  manifestation  of 
extrasystoles  (transient  and  recurrent  nodal  rhythm).  The  attacks 
come  on  suddenly,  usually  without  obvious  cause,  last  several  minutes, 
several  hours,  or  several  days,  and  usually  end  abruptly;  they  may  recur 
at  irregular  intervals,  days,  weeks,  months,  or  years;  or  perhaps  there 
may  be  only  the  one  attack.  The  attack  is  characterized  by  subjective 
sensations  of  oppression,  tightness,  or  fluttering  in  the  region  of  the 
heart,  associated  with  restlessness  and  weakness,  and  often  dyspnoea  on 
exertion.  The  pulse  is  found  to  be  small  and  rapid,  often  200  or  more 
per  minute  (sometimes  so  rapid  that  it  cannot  be  counted) ;  often  there  is 
no  noteworthy  inequality  in  the  force,  rhythm,  or  volume  of  the  beats, 
but  more  or  less  (even  marked)  arrhythmia  may  develop.  Auscultation 
reveals  the  heart  sounds  to  be  short  and  sharp  (embryocardia;  tic-tac), 
and  often  a  systolic  murmur  (mitral  insufficiency).  The  heart  may 
become  markedly  dilated,  even  within  a  short  time  (according  to  Martins, 
the  disorder  is  a  recurring  acute  dilatation  of  the  heart),  and  the  veins  of 
the  neck  and  the  liver  may  become  distended  and  pulsate.  The  prog- 
nosis depends  upon  the  functional  capacity  of  the  heart  under  the 
abnormal  rhythm,  upon  the  general  circulatory  conditions  under  the 
new  circumstances.  Dyspnoea  and  oedema  are  of  bad  prognostic 
significance.  Mackenzie  believes  that  many  cases  of  rapid  and  fatal 
breakdown,  particularly  in  old  people,  are  due  directly  to  the  inception 
by  the  heart  of  this  rhythm.  The  treatment  comprises  bodily  rest  and 
mental  quietude,  under  which  some  attacks  subside  spontaneously.  The 
bromides,  morphine,  valerian,  and  other  sedatives  may  prove  of  service; 
belladonna,  the  iodides,  nitroglycerin,  etc.,  have  been  recommended 
from  time  to  time.  Attacks  sometimes  may  be  stopped  by  the  patient 
taking  a  long  breath  or  a  series  of  long  breaths  and  fixing  the  chest  in 
full  inspiration,  by  the  use  of  ice-cold  douches  to  the  chest,  by  irritation 
of  the  vagus  nerve  in  the  neck  (pinching,  faradization,  etc.). 

Bradycardia. — The  term  bradycardia  is  more  or  less  loosely  applied 
to  abnormal  infrequency  of  the  pulse;  supposedly  the  cardiac  action  is 
at  the  same  time  infrequent,  but  in  reality  this  is  not  always  so.  Follow- 
ing Mackenzie,  the  cases  of  diminished  frequency  of  the  pulse  may  be 


DISEASES  OF  THE  MYOCARDIUM  423 

divided  into  four  classes:  (1)  Those  in  which  all  die  chambers  of  die 
heart  participate  in  the  slow  action  (true  bradycardia);  (2)  those  in 
which  the  slow  pulse  rate  is  due  to  a  missed  beat,  the  ventricle  having 
contracted  but  the  resulting  pulse-wave  being  too  feeble  to  reach  the 
wrist  (extrasystolic  form  of  arrhythmia);  (3)  certain  cases  of  nodal 
rhythm  in  which  the  auricle  has  ceased  to  beat,  or  beats  synchronously 
with  the  ventricle  (mild  heart  block);  and  (4)  cases  in  which  the  stimulus 
is  blocked  between  the  auricle  and  the  ventricle  so  that  the  auricle  beats 
at  its  normal  rhythm  and  the  ventricle  does  not  respond  to  the  auricular 
systole,  but  pursues  an  independent  and  slow  rhythm  (complete  heart 
block).  The  cases  are  due  then  to  stimulation  of  the  vagus  (inhibition), 
or  to  depressed  conductivity  and  contractility  of  the  myocardium. 

True  bradycardia  may  be  physiological  or  pathological.  The  physio- 
logical cases  comprise  certain  normal  individuals  in  whom  the  pulse  is 
always  abnormally  slow — 60  or  less;  the  pulse  may  become  slowed  also 
during  pregnancy,  less  than  60,  even  50,  40,  or  less,  and  in  starvation 
(but  this  perhaps  verges  on  the  pathological).  The  pathological  cases 
comprise  those  due  to:  (1)  Infections,  such  as  typhoid  fever,  pneumonia, 
diphtheria,  influenza,  rheumatism,  etc.,  in  convalescence  from  which 
it  is  rather  common;  (2)  intoxications,  such  as  alcohol,  coffee,  tea,  lead, 
tobacco,  uremia,  digitalis  poisoning,  etc.;  (3)  disease  of  the  heart, 
especially  the  fatty  heart,  chronic  myocarditis,  aortic  stenosis,  etc. ;  (4)  dis- 
orders of  the  lung,  especially  emphysema;  (5)  divers  disorders  of  the 
gastro-intestinal  tract,  such  as  gastric  carcinoma,  jaundice,  cholelithiasis 
(especially  during  colic),  etc.;  (6)  nervous  disorders,  such  as  apoplexy, 
meningitis,  brain  tumor,  injury  of  the  medulla,  vagus  stimulation  by 
tumors,  coma,  epilepsy,  etc.;  and  (7)  anemic,  cachetic,  and  exhausting 
disorders  of  wide  diversity.  In  true  bradycardia  the  pulse  rate  is  rarely 
less  than  40.  The  condition  is  not  serious;  it  may  last  for  many  years. 
The  use  of  atropine,  since  it  accelerates  the  cardiac  activity  in  the  vagus 
cases,  may  help  to  distinguish  these  from  the  myocardial  cases. 


DISEASES  OF  THE  MYOCARDIUM. 

In  the  introductory  remarks  on  the  pathological  physiology  of  the 
cardiovascular  system  the  prime  importance  of  the  myocardium  has  been 
emphasized,  and  later  certain  disorders  to  which  the  myocardium  is 
subject  under  divers  circumstances  have  been  grouped  together  under 
the  designation  neuromuscular  disorders.  An  attempt  to  separate 
diseases  of  the  myocardium  and  to  discuss  them  apart  from  other  diseases 
of  the  heart,  however,  is  a  matter  of  extreme  difficulty,  if  not  impossibility. 
The  relationships  that  the  myocardium,  in  health  and  in  disease,  bear 
to  the  normal  and  the  perverted  activity  of  the  heart  are  so  intimate 
that  one  can  scarcely  be  thought  of  independently  of  the  other.  What- 
ever the  disorder  of  the  heart  under  consideration,  the  major  diagnostic, 
prognostic,  and  therapeutic  considerations   must   be   based  upon   the 


424  DISEASES  OF  THE  MYOCARDIUM 

condition  of  the  myocardium.  In  chronic  valvular  disease,  for  Instance, 
although  the  condition  of  the  valves  or  orifices  is  of  significance,  the 
efficiency  of  the  circulation,  the  comfort  of  the  patient,  and  the  dura- 
tion of  life  depend  upon  the  functional  capacity  of  the  myocardium  under 
the  new  or  changed  conditions;  this  is  true  also  in  diseases  of  the  peri- 
cardium, notably  in  chronic  adhesive  pericarditis,  and  likewise  one  may 
also  say  in  the  advanced  anemic  and  cachetic  stages  of  general  disorders 
in  which  degenerative  changes  in  the  myocardium  are  prone  to  develop. 
The  classification  of  diseases  of  the  myocardium,  therefore,  is  exceed- 
ingly intricate;  no  classification  is  entirely  satisfactory.  It  is  even 
difficult  to  draw  a  line  between  the  primary  and  the  secondary  diseases 
of  the  myocardium.  Hypertrophy  and  dilatation,  for  instance,  are  due 
to  many  factors,  each  more  or  less  separate  and  distinct  in  itself  and 
productive  of  varying  grades  of  mischief;  bacterial  toxins,  chemical 
poisons  of  widely  diverse  nature,  and  anemic  conditions  may  engender 
degenerative  changes  in  the  myocardium  that  may  be  expressed  in 
myocardial  weakness  or  dilatation,  the  phenomena  of  which  may  domi- 
nate the  clinical  picture;  the  fibroid  heart  may  be  viewed  as  a  disease  of 
the  myocardium  or  of  the  coronary  arteries,  to  which  in  the  great  majority 
of  cases  it  is  directly  due;  and,  finally,  the  nutrition  of  the  heart  under 
all  conditions,  its  functional  capacity,  its  ability  to  hypertrophy  under  the 
stress  of  unusual  demands,  its  failure  to  adapt  itself  to  new  or  changed 
conditions,  etc.,  are  due  wholly  to  the  condition  of  the  coronary  circula- 
tion— generally  as  well  as  locally.  In  the  absence  of  a  satisfactory 
classification,  the  subjoined  arrangement  of  diseases  of  the  myocardium, 
may  be  adopted  tentatively;  it  comprises  more  or  less  well-defined 
clinical  entities  with  associated  pathological  changes,  which,  however, 
gradually  merge  into  other  conditions. 


THE   WEAK  OR  INSUFFICIENT  HEART. 

(Myocardial  Weakness  or  In-sufficiency ;   Congenital  Weakness  of  the  Myocardium; 
Acquired  Weakness  of  the  Myocardium;  Cardiac  Asthenia.) 

Etiology. — There  is  a  more  or  less  diversified  group  of  disorders  of 
the  heart,  of  which  the  pathological  lesions  are  inconspicuous,  and  of 
which  the  noteworthy  clinical  manifestation  is  myocardial  w^eakness; 
the  other  clinical  manifestations  and  the  etiological  factors  may  be 
quite  dissimilar.  These  disorders,  therefore,  not  only  differ  more  or 
less  among  themselves,  but  they  cannot  be  sharply  separated  from  other 
disorders  of  the  myocardium.  Unquestionably  some  of  these  cases  are 
congenital:  the  subject  is  born  with  a  "weak  heart;"  other  cases  are 
acquired.  In  the  congenital  cases  the  weakness  occasionally  is  more 
or  less  obviously  represented  in  smallness  in  the  size  of  the  heart  or  in 
thinness  of  its  walls;  often  the  structure  is  apparently  normal,  but  the 
organ  is  physiologically  inadequate;  in  either  event  the  heart  is  unable 
to  meet  the  requirements  of  ordinary  life.     The  acquired  cases  result 


THE   WEAK  07?  INSUFFICIENT  HEART  425 

from  damage  to  a  heart  originally  norm'al.  The  important  etiological 
factors  are:  (1)  The  infectious  diseases.  In  these  disorder  of  the  heart 
may  develop  as  described  under  the  infectious  febrile  heart;  usually 
the  heart  returns  to  its  previously  normal  condition,  but  it  may  remain 
for  some  time  or  permanently  weak  or  insufficient.  (2)  Intoxicants — 
such  as  alcohol,  tobacco,  coffee,  tea,  etc.,  especially  when  taken  in 
excess.  (3)  Anemic  and  cachectic  states.  (4)  Neurotic  disturbances, 
exemplified  in  undue  reaction  to  emotional  and  extraneous  influences, 
or  in  general  nervous  incapacity  with  special  involvement  of  the  heart. 
In  some  cases  the  damage  is  doubtless  not  confined  to  the  myocardium, 
but  involves  also  the  nervous  mechanism;  but  the  discoverable  changes 
are  inconspicuous. 

Symptoms.  —  Many  persons,  subjects  of  congenitally  weak  hearts, 
conscious  perhaps  of  other  cardiac  deficiency,  or  readily  made  aware 
thereof  upon  slight  exertion,  lead  a  quiet  and  retired  life — well  within 
the  functional  capacity  of  their  hearts — and  suffer  no  noteworthy  ill 
consequences.  Others,  however,  endeavoring  to  attain  the  average  of 
human  activities,  suffer  upon  slight  or  moderate  exertion,  with  precordial 
distress  or  oppression,  palpitation  of  the  heart,  rapid  heart  action  (120 
or  more  per  minute),  with  an  unstable  or  irritable  pulse,  dyspnoea,  general 
muscular  weakness,  etc.  These  symptoms  may  become  of  high  grade 
and  associated  with  more  serious  evidences  of  cardiac  inadequacy 
should  the  patient  lead  an  altogether  ill-advised  life,  engage  in  athletic 
exercises,  attempt  feats  of  mountain  climbing,  etc.  (consult  the  over- 
strained heart);  or  they  may  develop  precipitously  after  some  sudden 
severe  exertion  (consult  acute  dilatation  of  the  heart). 

In  the  acquired  cases  the  symptoms,  as  a  rule,  are  analogous.  In 
the  postinfectious  cases  the  patient  during  quietude  does  not  suffer, 
but  more  or  less  distress,  palpitation,  and  dyspnoea  ensue  upon  activity, 
and  the  patient  is  generally  weak.  In  the  alcoholic  and  tobacco  cases 
the  patient  may  be  conscious  of  palpitation,  fluttering,  or  irregularity 
of  the  heart  even  when  quiet,  and  dyspnoea  develops  upon  exertion. 
These  symptoms  are  often  assopiated  with  other  evidences  of  intoxica- 
tion, such  as  so-called  indigestion,  general  nervousness,  headache,  and 
other  mental  symptoms.  The  disorder  of  the  heart,  of  course,  gradually 
passes  over  into  well-recognized  anatomical  lesions  (degenerative,  chronic, 
fibrotic,  etc.). 

In  the  anemic  and  cachectic  cases,  in  addition  to  the  general  manifes- 
tations of  anemia,  there  is  more  or  less  precordial  distress,  cardiac  pal- 
pitation, rapid  heart  action,  weak  apex  beat,  feeble  pulse,  dyspnea, 
syncopal  attacks,  etc.;  these  are  referable  in  part  to  the  anemia  as  such, 
but  they  are  due  also  in  part  to  the  weakened  and  usually  dilated  myo- 
cardium the  result  of  insufficient  nourishment.  The  condition  gradually 
merges  into  parenchymatous  and  fatty  degeneration  and  chronic;  dilata- 
tion of  the  heart. 

The  neurotic  cases  are  well  exemplified  in  tlie  more  or  less  fleeting 
attacks  that  occur  usually  in  neurotic  women  under  most  diverse  circum- 


426  DISEASES  OF  THE  MYOCARDIUM 

stances,  and  are  manifested  by  sensations  of  stoppage  of  the  heart  or  pre- 
ordial  fluttering,  pallor  of  the  lips  and  face,  and  a  general  feeling  of  appre- 
hension, "sinking,"  impending  syncope,  or  paresthetic  phenomena;  the 
pulse  is  usually  weak  and  somewhat  accelerated  (not  the  pulse  of  syncope 
— ^which  does  not  occur).  The  attack  lasts  a  variable  time,  and  may  be 
followed  by  considerable  exhaustion.  In  other  cases,  especially  following 
a  long  period  of  mental  overwork,  worry,  etc.,  the  heart,  sometimes 
quite  suddenly,  becomes  weak  and  may  necessitate  the  patient's  taking 
to  bed;  in  aggravated  cases  any  position  other  than  the  prone  leads  to 
syncope,  weak  heart  action,  and  feeble  pulse.  The  apex  beat  is  weak, 
the  first  sound  is  short  and  valvular,  the  second  sound  is  rarely  accen- 
tuated; the  action  of  the  heart  is  often  irregular  and  readily  disturbed  in 
rate  and  rhythm  by  various  influences.  There  are  no  hysterical  symp- 
toms.   Recovery  may  not  ensue  for  several  or  many  months. 

Diagnosis. — The  diagnosis  of  the  acquired  cases  is  not  difficult  as 
a  rule.  The  congenital  cases  often  pass  unnoticed,  until  at  least  more  or 
less  dilatation  has  ensued,  whereupon  the  condition  is  scarcely  to  be 
distinguished  from  dilatation  arising  from  other  causes.  In  the  early 
stages  the  history  of  the  patient,  the  absence  of  etiological  factors,  the 
development  of  symptoms  upon  the  slightest  exertion  and  their  aggra- 
vation upon  exertion  well  borne  by  the  average  individual,  and  the 
absence  of  noteworthy  physical  signs,  aside  from  the  rapidity  and  overac- 
tion  of  the  heart  and  smallness  and  frequency  of  the  pulse,  should  serve 
for  the  recognition  of  the  disorder. 

Prognosis. — In  the  congenital  cases  the  outlook  depends  upon  the 
mode  of  life  of  the  patient,  upon  his  living  within  the  capabilities  of 
his  heart.  The  postinfectious  cases  usually  eventuate  in  recovery,  but 
this  may  be  long  delayed.  The  cases  due  to  alcohol,  tobacco,  tea, 
coffee,  etc.,  are  likely  to  improve  in  the  course  of  time,  if  the  causative 
poison  is  discontinued  and  irreparable  damage  has  not  been  done. 

Treatment. — ^The  treatment  is  largely  hygienic.  In  the  congenital 
cases  the  patient  should  be  well  nourished  and  should  be  given  tonics 
to  improve  the  general  blood  condition  and  nutrition,  and  he  should 
indulge  in  carefully  regulated  exercise  under  competent  supervision 
with  a  view  to  strengthening  his  myocardium;  considerable  improvement 
often  follows.  The  treatment  of  the  postinfectious  cases  is  similar; 
iron  is  often  a  very  useful  remedy,  but  rest  to  the  disabled  he^vt  may 
be  required  for  a  long  time.  Digitalis,  strychnine,  and  similar  drugs 
often  do  harm;  they  may  be  required,  in  the  event  of  failing  cardiac 
compensation,  but  rapid  or  unstable  action  of  the  heart  of  itself  is  not 
an  indication  for  their  use.  The  cases  due  to  alcohol,  tobacco,  and 
the  like  usually  improve  with  discontinuance  of  the  causative  factor, 
but  the  bromides,  valerian,  and  aconite  often  render  material  service 
in  quieting  the  overactive  heart.  The  transient  disorders  that  occur 
in  neurotic  women  demand  little  else  than  stimulation  and  other  meas- 
ures useful  in  syncope;  speaking  generally,  there  is  no  danger  in  the 
attacks  except  that  which  lies  in  the  habit  of  taking  drams  to  cure  or 


THE  OVERSTRAINED  OR  IRRITABLE  HEART  427 

})reveiit  them  (Allhutt).  Tlie  more  severe  and  prolonged  neurotic  cases 
are  best  treated  by  rest  in  bed,  massage,  hydrotherapy,  nutritions  food, 
strychnine,  alcohol,  iron,  and  arsenic.  Later,  benefit  accrues  from 
carefullv  regulated  exercises. 


THE  OVERSTRAINED  OR  IRRITABLE  HEART. 

{Cardiac  Strain;  Muscular  Strain  of  the  Heart;  The  Soldier's  Heart; 
The  A'thlete's  Heart.) 

Etiology. — The  term  overstrained  heart  is  used  as  a  convenient 
designation  of  the  condition  that  results  from  excessive  muscular  effort. 
Probably,  however,  the  term  might  be  employed  to  comprise  in  addition 
all  the  conditions  of  the  heart  in  which  the  myocardium,  relatively  or 
absolutely,  is  at  a  disadvantage  (functionally  insufficient)  in  relation 
to  the  intracardiac  and  arterial  pressure,  and  in  which  in  consequence 
overstrain  ensues;  these  comprise  cases  of  chronic  valvular  disease, 
the  fibroid  heart,  diseases  of  the  coronary  arteries,  arteriosclerosis,  etc., 
all  of  which  are  discussed  under  appropriate  headings.  Although  it  may 
be  difficult  to  estimate  the  importance  of  strain  in  an  individual  case, 
inasmuch  as  it  is  often  bound  up  with  other  etiological  factors  of  cardio- 
vascular disease,  such  as  syphilis,  alcoholism,  gout,  plumbism,  renal 
disease,  etc.,  its  prime  importance  is  manifest  when  we  compare  the 
heart  disorders  of  men  with  those  of  women  of  the  same  station  in  life; 
and  when  we  compare  the  heart  disorders  of  men  engaged  in  laborious 
occupations,  such  as  draymen,  ironworkers,  blacksmiths,  etc.,  with 
those  of  men  not  engaged  in  laborious  occupations,  but  equally  but  not 
more  given  to  the  vices  of  intemperance  and  sexual  immorality,  such  as 
clerks,  business  and  professional  men.  In  estimating  the  etiological 
significance  of  strain,  one  must  take  into  consideration  all  of  the  factors 
in  the  individual  case;  and  one  may  no  more  cursorily  and  without 
investigation  attribute  to  strain  certain  manifest  diseased  conditions 
in  a  patient  than  he  may  elect  to  overlook  the  possible  etiological  impor- 
tance of  a  sudden  and  severe  strain  to  which  the  patient  himself  may 
attribute  the  onset  of  his  ailment.  It  is  quite  conceivable,  indeed,  it  is 
quite  true,  that  the  healthy  individual — the  individual  with  his  muscles, 
heart,  bloodvessels,  and  lungs  developed  proportionately  to  the  demands 
that  he  makes  upon  them — may  endure  a  considerable  amount  of  pro- 
longed or  sudden  strain  without  obvious  ill  consequences.  This  we 
observe  almost  every  day  in  athletes  and  like  persons.  But  we  also 
observe  very  frequently  the  disastrous  results  to  the  heart  and  the 
general  economy  of  sudden  severe  strain  and  of  prolonged  strain  ill- 
advisedly  persisted  in,  not  only  in  a  certain  proportion  of  those  engaged 
in  athletic  contests,  but  also  in  those  whose  occupation  necessitates 
considerable  strain,  in  those  poorly  endowed  by  nature,  who  soon  use 
u])  their  reserve  strength,  and  in  those  with  hearts  weakened  by  typhoid 
fever,  influenza,  and  other  infections,  anemic  states,  etc. 


428  DISEASES  OF   THE  MYOCARDIUM 

Cardiac  overstrain,  in  the  restricted  sense  in  which  it  is  here  employed, 
results:  (1)  From  sudden  violent  muscular  effort,  such  as  may  occur 
in  lifting  unusually  heavyweights,  in  rowing  races  and  similar  contests, 
etc.;  and  (2)  from  repeated,  long-continued,  and  ill-directed  muscular 
exertion,  such  as  may  occur  in  college  and  other  athletes,  in  all  persons 
who  engage  unduly  and  inadvisedly  in  exercise,  in  soldiers  subjected  to 
forced  and  prolonged  marches,  etc.  This  overstrain  of  the  heart,  in 
view  of  the  etiological  factors,  is  largely  a  disorder  of  early  adult  life 
and  of  the  male  sex,  but  it  is  sometimes  encountered  in  young  women 
overzealous  in  the  pursuit  of  athletics.  It  may  develop  in  a  heart  pre- 
viously normal,  as  well  as  in  a  heart  damaged  by  myocardial  or  valvular 
disease  or  weakened  by  general  causes,  such  as  fever  states,  anemia,  etc. 

Pathology. — In  sudden  death  from  acute  heart  strain,  all  the  chambers 
of  the  heart  are  dilated  and  filled  with  blood,  and  the  lungs  and  the 
venous  system  are  markedly  engorged.  In  the  chronic  cases  the  heart 
shows  more  or  less  hypertrophy  and  dilatation,  myocardial  degeneration, 
perhaps  mitral  endocarditis,  coronary  arteriosclerosis,  etc.;  in  a  word, 
the  more  common  concomitants  of  general  and  coronary  arteriosclerosis. 

The  chief  causative  factors  of  cardiac  overstrain  are  increased  arterial 
pressure  and  increased  and  accelerated  flow  of  venous  blood  to  the  heart, 
both  of  which  are  provoked  by  muscular  exertion.  The  increased  arterial 
pressure  occasions  an  insufficient  and  incomplete  emptying  of  the 
left  ventricle,  which  in  turn  leads  to  a  gradually  increasing  residuum 
of  blood  within,  and  dilatation  of,  the  ventricle;  at  the  same  time  the 
increased  and  accelerated  flow  of  venous  blood  leads  to  a  similar  condition 
of  the  right  ventricle.  Dilatation  of  the  right  ventricle  is  the  more  com- 
mon in  the  ordinary  athletic  contests,  and  can  commonly  be  demonstrated 
by  increased  cardiac  dulness  to  the  right  and  a  systolic  murmur  in  the 
tricuspid  region  (tricuspid  insufficiency;  safety-valve  action  of  the 
tricuspid  valve).  With  cessation  of  the  causative  factor  the  heart, 
if  previously  healthy,  reverts  to  its  normal  condition  and  no  ill  conse- 
quences ensue.  Permanent  damage,  however,  may  follow  the  too 
frequent  repetition  of  athletic  contests  or  other  muscular  exertion, 
ill-directed  athletic  training,  the  non-adaptation  of  exercise  to  the  indi- 
vidual— which  is  the  essential  etiological  factor;  this  permanent  damage 
occurs  especially  in  young  S^dults  of  poor  physique,  such  as  many  college 
students,  soldiers,  etc.  In  the  case  of  soldiers,  to  the  other  etiological 
factors  one  may  add  the  weight  of  accoutrements,  which  embarrass 
respiration,  the  fatigue  of  prolonged  marches,  the  abuse  of  tobacco 
and  alcohol,  venery,  etc.,  all  of  which  may  gradually  lead  to  what 
Da  Costa  so  aptly  described  as  the  soldier's  "irritable"  heart. 

Symptoms. — A  person  subjected  to  severe  muscular  exertion  in  excess 
of  the  capabilities  of  his  heart,  complains  of  a  sense  of  fulness,  or  dis- 
tress beneath  the  sternum  and  in  the  region  of  the  heart,  perhaps  of 
actual  pain  that  may  radiate  throughout  the  chest  and  into  the  arms; 
there  is  also  palpitation  of  the  heart,  dyspnoea,  general  muscular  weak- 
ness, vertigo,  and  sometimes  even  syncope.     Observation  discloses  a 


THE  OVERSTRAINED   OR  IRRITABLE  HEART  429 

livid  and  anxious  expression,  with  prominent  eyes  and  dilated  pupils, 
and  excessive  perspiration;  fulness  and  pulsation  of  the  veins  of  the  neck; 
marked  and  widespread  precordial  pulsation;  increased  area  of  cardiac 
dulness  especially  to  the  right,  with  loud,  clear,  valvular  heart  sounds, 
a  systolic  murmur  in  the  tricuspid  area  (relative  tricuspid  insufficiency; 
safety-valve  action  of  the  tricuspid  valve),  perhaps  a  systolic  murmur 
elsewhere,  and  a  weak  pulse.  These  phenomena  are  to  be  interpreted 
as  the  manifestations  of  an  acutely  embarrassed  heart.  As  a  rule,  espe- 
cially in  previously  healthy  subjects,  they  subside  and  leave  no  ill  con- 
sequences; in  rare  instances,  especially  in  those  the  subjects  of  previous 
heart  disease,  they  may  lead  to  an  immediately  fatal  issue;  in  other  cases, 
the  acute  phenomena  subside,  but  the  patient  finds  himself  in  the 
future  more  or  less  incapacitated.  The  original  distressing  symptoms 
and  embarrassed  cardiac  action  are  again  provoked  in  the  athlete  by 
contests,  such  as  football,  basket  ball,  running,  rowing,  bicycling,  etc.; 
in  some  cases  even  moderate  exercise  serves  to  bring  on  the  symptoms; 
whereas,  especially  in  older  subjects  with  perhaps  some  myocardial  de- 
generation, even  the  slightest  exertion  (climbing  stairs  or  a  hill),  perhaps 
even  a  full  meal,  or  too  much  tobacco  or  alcohol,  or  constipation  with 
intestinal  distention,  leads  to  more  or  less  distress  (precordial  distress, 
dyspnoea,  palpitation  of  the  heart,  irregular  or  quickened  heart  action, 
etc.);  that  is,  the  heart  is  unusually  sensitive  to  extraneous  influences 
well  borne  by  a  normal  heart:  it  is  said  to  be  irritable.  Comparative 
comfort  or  freedom  from  distress  may  be  secured  by  the  patient's  leading 
a  quiet  life  and  avoiding  all  muscular  strain.  The  physical  signs  may  be 
entirely  normal,  or  there  may  be  signs  of  hypertrophy  with  some  dilata- 
tion of  the  heart. 

The  more  chronic  cases,  such  as  result  from  long  continued  excessive 
muscular  exertion,  present  the  common  evidences  of  increased  arterial 
pressure  and  hypertrophy  of  the  heart,  together  with  a  marked  tendency 
to  the  occurrence,  upon  exertion,  of  the  aforementioned  signs  of  cardiac 
embarrassment.  The  physical  signs  are  those  of  hypertrophy  and  dilata- 
tion of  the  heart,  of  which  the  one  or  the  other  may  predominate  in  the 
individual  case. 

Diagnosis. — In  the  acute  cases  the  history  and  the  mode  of  life  of  the 
individual  are  of  great  importance  in  determining  the  cause  of  the 
symptoms,  especially  in  cases  in  which  the  physical  signs  are  equivocal. 
The  effect  of  exertion  purposely  undertaken  under  the  observation  of 
the  physician  may  be  of  service  in  establishing  a  diagnosis.  In  the 
chronic  cases  the  diagnosis  depends  upon  a  history  of  long  continued 
overexertion  and  the  physical  signs  of  heightened  blood  pressure  and 
dilated  hypertrophy  of  the  heart. 

Prognosis. — In  the  acute  cases  the  outlook  depends  entirely  upon  the 
future  life  of  the  individual,  upon  his  avoiding  the  causes  known  to  pro- 
voke cardiac  distress.  The  prognosis  in  tlie  chronic  cases  is  that  of 
hypertrophy  and  dilatation  of  the  heart. 


430  DISEASES  OF   THE  MYOCARDIUM 

Treatment. — Overstrain  of  the  heart  should  be  prevented — by  thorough 
physical  examination  of  the  heart  of  ail  intending  athletes,  soldiers,  etc., 
by  the  avoiding  of  muscular  exertion  obviously  too  severe  for  the  sub- 
ject, and  by  proper  training  under  supervision.  By  graduated  exercises 
a  weak  but  otherwise  normal  heart  may  be  made  stronger,  and  capable 
of  sustaining  greater  efforts.  Sudden  severe  overstraining  of  the  heart 
often  leads  to  more  or  less  irreparable  damage  to  the  heart.  The  acute 
symptoms  are  best  met  by  rest  in  the  recumbent  posture  and  diffusible 
stimulants,  such  as  whiskey,  brandy,  aromatic  spirit  of  ammonia, 
compound  spirit  of  ether,  etc.;  in  rare  cases  bleeding  may  be  required. 
After  recovery  from  these  acute  symptoms,  rest  for  a  long  time  is  impera- 
tive. The  patient  must  avoid  all  factors  that  in  the  least  tend  to  irritate 
or  accelerate  the  heart:  not  only  exercise,  but  also  alcohol,  tobacco, 
tea,  coffee,  etc.  After  the  lapse  of  several  months  graduated  exercise, 
most  carefully  supervised,  is  often  of  service.  The  overacting,  irritable 
heart  may  often  be  quieted  by  the  use  of  the  bromides,  valerian,  aconite, 
etc.  Cardiac  tonics,  such  as  digitalis,  strychnine,  etc.,  are  of  little  service, 
except  in  the  more  chronic  cases  with  dilatation,  the  treatment  of  which 
is  that  of  failing  cardiac  compensation  in  general. 


THE  FATTY  HEART. 

Etiology. — The  term  fatty  heart  is  applied  to  two  conditions,  fatty 
degeneration  and  fatty  infiltration.  Although  they  may  occur  together, 
in  well-marked  cases,  they  represent  two  quite  distinct  diseases.  Fatty 
degeneration  usually  follows  and  is  associated  with  parenchymatous 
degeneration,  and  is  due,  therefore,  to  like  causes;  but  it  occurs  also  in 
many  forms  of  hypertrophy,  in  old  age,  etc.  Fatty  infiltration  or  over- 
growth is  an  excess  of  the  normal  subpericardial  fat,  and  is  a  part  of 
general  obesity. 

•Pathology. — Usually  the  fatty  deposit  is  most  marked  along  the 
course  of  the  larger  coronary  vessels  and  in  the  auriculoventricular 
furrows;  but  it  may  entirely  envelop  the  heart  in  a  thick  casing  and  may 
infiltrate  between  the  muscular  fibers  even  to  the  endocardium.  In  some 
regions  the  muscular  fibers  may  be  entirely  replaced  by  the  fatty  tissue. 
Aside  from  the  fatty  deposit,  the  heart  may  be  quite  normal,  but  it  is 
usually  somewhat  enlarged,  hypertrophied  in  consequence  of  excessive 
food  and  drink,  and  dilated  in  consequence  of  muscular  weakness. 
In  addition  to  the  fatty  deposit  there  is  usually  some  fatty  degeneration 
and  simple  and  brown  atrophy  of  the  muscular  fibers;  the  coronary 
arteries  often  reveal  some  sclerosis,  and  there  are  consecutive  areas  of 
fibrosis  of  the  myocardium. 

It  is  difficult  in  many  cases  to  determine  to  what  degree  the  symptoms 
are  due  to  the  fatty  deposit.  It  is  not  improbable  that  a  large  encasement 
of  fat  more  or  less  seriously  compromises  the  functional  activity  of  the 
heart,  but  there  are  many  cases  of  well-marked  fatty  infiltration  of  the 


THE  INFECTIOUS  FEBRILE   HEART  431 

heart  that  present  no  symptoms  until  the  advent  of  dilatation,  and  many 
fatty  hearts  with  symptoms  reveal  in  addition  coronary  sclerosis  and 
fibroid  myocardium — which  may  well  be  answerable  for  the  symptoms. 
Perhaps  in  many  cases  the  fatty  deposit  is  secondary  to  primary  atrophy 
of  the  muscular  fibers. 

Symptoms. — The  majority  of  obese  subjects  sooner  or  later  complain 
of  dyspnoea,  slight  cyanosis,  and  palpitation  of  the  heart  on  exertion 
(these  are  often  due,  in  part  at  least,  to  the  obesity  itself  and  interference 
with  the  action  of  the  muscles  of  respiration);  others  have  periodical 
attacks  of  so-called  asthma  (perhaps  induced  by  overeating  or  over- 
drinking), or  of  bronchitis;  still  others  complain  of  vertigo,  pseudo- 
apoplectic  attacks,  with  Cheyne-Stokes  breathing,  anginoid  pains,  or 
angina  pectoris.  Examination  of  the  heart  (rendered  difficult  by  the 
excessive  panniculus  adiposus)  reveals  increase  in  the  area  of  cardiac 
dulness  and  weak  or  muffled  cardiac  sounds;  and  the  pulse  is  small  and 
weak.  In  the  course  of  time,  unless  properly  and  efficiently  treated, 
the  symptoms  of  failing  compensation  (dyspnoea,  passive  congestion  of 
the  viscera,  and  oedema),  with  a  murmur  of  relative  mitral,  and  perhaps 
tricuspid,  insufficiency,  may  develop;  or  the  patient  may  die  suddenly 
in  an  anginoid  attack. 

Diagnosis. — The  diagnosis,  which  rests  upon  cardiac  enfeeblement 
in  an  obese  subject,  is  always  precarious;  the  symptoms  doubtless 
are  often  due  less  to  the  fat  about  the  heart  than  to  associated  lesions. 

Prognosis. — The  prognosis  virtually  is  that  of  obesity  plus  the  asso- 
ciated cardiac  conditions. 

Treatment. — ^^Fhe  treatment  is  that  of  obesity,  associated  with  appro- 
priate measures  to  invigorate  the  action  of  the  heart.  The  so-called 
Oertel  treatment  (regulated  diet,  largely  protein,  limitation  of  the  fluid 
intake,  and  graduated  exercises  up  hill)  here  finds  an  especial  field  of 
utility. 

THE  INFECTIOUS  FEBRILE  HEART. 

{Myocardial  Degeneration;  Parenchimatous  ami  Fatty  Degeneration  of  flie  Heart; 

Acute  Myocarditis.) 

The  infectious  febrile  heart  is  a  somewhat  inapt  and  perhaps  ill-chosen 
term  designed  to  describe  the  condition  of  the  heart  in  the  acute  infec- 
tious processes;  the  lesions  are  chiefly  degenerative,  but  to  these  in  some 
cases  inflammatory  changes  are  added. 

Etiology. — The  etiological  factors  are  the  toxins  of  the  acute  infections 
generally,  but  notably,  acute  rheumatic  fever,  typhoid  fever,  pneumo- 
coccic  and  other  pyococcic  infections  (septicopyemias),  influenza, 
diphtheria,  etc.  These  toxins  perhaps  act  upon  the  nervous  mechanism, 
stimulating  the  accelerator  nerves,  since  fever  of  itself  is  accompanied 
by  an  accelerated  heart-rate.  The  chief  influence  of  the  toxins,  however, 
is  exerted  on  the  mvocardium  and  the  vasomotor  svstem. 


432  DISEASES  OF   THE  MYOCARDIUM 

Pathology. — The  changes  vary  considerably  in  different  cases.  In  some 
they  are  shght  and  apparently  inconsequential,  transitory  in  nature, 
and  leave  no  permanent  ill  consequences.  In  others  there  is  a  varying 
reaction  of  the  myocardium  to  the  toxin;  whereas  in  still  others  there 
may  be  also  endocarditis  or  pericarditis,  or  what  may  be  properly  spoken 
of  as  carditis  or  pancarditis.  Endocarditis  and  pericarditis  are  described 
elsewhere,  but  it  is  perhaps  wise  to  point  out  here  that  most  of  the 
symptoms  and  signs  of  these  disorders,  such  as  precordial  distress, 
dyspnoea,  cardiac  and  pulse  irregularities,  changes  in  the  size  of  the 
cardiac  dulness,  as  well  as  some  murmurs,  etc.,  are  of  myocardial  origin. 

At  the  necropsy,  after  a  fatality  in  one  of  the  aforementioned  acute 
infections,  the  myocardium,  to  the  unaided  eye,  is  usually  pale  and  opaque, 
and  flabby  or  friable;  occasionally  it  is  streaked  with  yellowish  lines, 
especially  that  of  the  left  ventricle  and  the  papillary  muscles.  The  heart 
may  be  more  or  less  dilated;  the  cavities  may  be  filled  with  laminated 
and  anemic  clots;  but  sometimes  in  sudden  death  they  are  quite  empty 
(vasomotor  collapse).  Microscopically  the  muscle  fibers  are  swollen 
and  opaque,  the  seat  of  more  or  less  advanced  albuminous,  granular, 
or  parenchymatous  degeneration  (cloudy  swelling).  The  lesions,  if 
unchecked,  proceed  to  fatty  degeneration  (the  yellowish  streaks  in  the 
muscle  of  the  ventricles  or  the  papillary  muscles) ;  or  there  may  be  asso- 
ciated hyaline  or  amyloid  degeneration.  The  nerves  may  reveal  degenera- 
tive changes.  The  interstitial  tissue  often  reveals  little  if  any  change. 
In  some  cases,  especially  of  severe  infections,  or  associated  with  endo- 
carditis or  pericarditis,  there  is,  in  addition  to  the  myocardial  degen- 
eration, more  or  less  vascular  dilatation  and  cellular  exudation  and 
proliferation  (acute  interstitial  myocarditis).  The  lesions  may  subside 
or  give  rise  to  a  form  of  chronic  myocarditis.  In  septicopyemia  there 
may  be  embolism  of  the  small  coronary  vessels,  with  scattered  foci  of 
suppuration  containing  the  causative  microorganisms  (suppurative 
myocarditis).  In  favorable  cases  the  small  abscesses  become  inspissated 
and  a  cicatrix  ultimately  forms,  leading  to  a  form  of  chronic  localized 
myocarditis,  with  perhaps  the  later  development  of  an  aneurysm  of  the 
heart;  in  other  cases  the  abscess  may  increase  in  size  and  ultimately 
rupture  into  the  pericardium  or  a  cavity  of  the  heart. 

Symptoms. — From  the  nature  of  the  etiological  factors  cardiac  symp- 
toms are  often  in  abeyance,  being  masked  by  those  of  the  primary 
disorder.  In  many  of  the  infections  there  may  be  no  complaint  whatever 
while  the  patient  is  at  rest  in  bed;  dyspnoea  and  palpitation  of  the  heart, 
however,  not  infrequently  follow  even  slight  exertions,  and  excitability  of 
the  heart  is  shown  in  attacks  of  rapid,  irregular,  and  intermittent  action 
upon  slight  "starts,"  emotional  and  other  disturbances,  etc.  (toxic  depres- 
sion of  conductivity  and  the  dropping  out  of  ventricular  systoles).  In 
other  cases  the  pulse  is  persistently  rapid.  In  the  majority  of  infectious 
or  toxic  cases  the  symptoms  develop  as  the  patient,  convalescing,  begins 
to  substitute  the  activity  of  returning  health  for  the  prone  and  quiet 
posture  of  disease.      The  first  symptom  may  be  a  sudden  and  fatal 


THE  INFECTIOUS  FEBRILE   HEART  433 

attack  of  heart  or  vasomotor  failure,  such  as  not  infrequently  occurs 
during  convalescence  from  diphtheria.  In  other  cases  less  severe 
attacks  of  heart  fkilure  occur;  syncope  attends  the  upright  posture 
or  the  getting  out  of  bed;  in  other  cases  the  heart  becomes  rapid,  and  is 
subject  to  periods  of  irregularity  and  intermittency  on  exertion  or 
excitement.  But  in  a  notable  series  of  cases  the  patient  presents  general 
evidence  of  cardiac  inadequacy  (depression  of  tonicity) ;  he  complains  of 
muscular  lassitude  and  of  cold  hands  and  feet  and  nose;  while  generally 
pallid,  his  toes  and  finger  tips  and  nose  and  ears  may  be  bluish  (capillary 
stasis);  he  is  mentally  torpid  and  does  not  respond  to  mental  or  other 
stimuli ;  the  urine  is  of  low  specific  gravity,  reduced  in  amount,  and  may 
contain  a  slight  trace  of  albumin;  and  there  may  be  vomiting.  In  many 
of  these  cases,  to  the  cardiac  inadequacy  vasomotor  failure  is  added; 
this  may  readily  be  determined  by  a  rapid  pulse  and  low  blood  pressure. 
Systolic  pressures  of  100  mm.  Hg.  are  not  uncommon;  less  than  80  mm. 
may  be  found  in  severe  infections,  and  is  of  serious  moment.  In  unusual 
cases,  instead  of  rapidity  there  may  be  unusual  slowness  of  the  heart 
action,  proceeding  even  to  heart  block.  Influenza  sometimes  attacks 
the  heart  with  special  severity.  During  the  attack  there  may  be  marked 
prostration,  with  dyspnoea,  cardiac  palpitation,  syncope,  and  very 
feeble  heart  sounds;  after  the  attack  has  subsided  dyspnoea  and  tachy- 
cardia often  persist,  and  may  be  associated  with  precordial  pain  and 
distress  or  anginoid  pains  on  exertion. 

Examination  reveals  the  heart  action  rapid,  irregular,  or  intermittent; 
usually  but  not  always  there  is  some  dilatation;  the  apex  beat  is  weak 
and  diffuse;  the  first  sound  at  the  apex  is  muffled  and  prolonged,  or  weak, 
short,  and  valvular;  or  it  may  be  replaced  by  a  variable  blowing  systolic 
murmur  (relative  mitral  insufficiency  from  stretching  of  the  mitral  ring, 
or  from  irregular  or  incoordinated  action  of  the  papillary  muscles) ;  the 
pulmonary  second  sound  is  usually  accentuated;  and  the  blood  pressure, 
as  a  rule,  is  low  (often  less  than  100  mm.  Hg.),  but  fluctuates  much  from 
time  to  time  and  is  unusually  responsive  to  divers  sorts  of  extraneous  influ- 
ences. Added  sounds  (extrasystoles)  may  be  audible.  The  heart  may 
also  be  observed  to  dilate  under  exertion  or  excitement. 

Diagnosis. — The  diagnosis  should  be  apparent  from  the  etiological 
factors  and  the  obvious  evidences  of  weak,  irritable,  or  unstable  cardiac 
action,  especially  a  rapid,  irregular,  and  feeble,  or  a  very  feeble,  slow 
pulse,  capillary  stasis,  weak  apex  beat,  weak  and  valvular  first  sound 
of  the  heart,  evidences  of  dilatation,  variable  apex  murmur,  and  low 
blood  pressure. 

Prognosis. — As  a  rule,  most  cases  eventuate  in  recovery  with  the  cure 
of  the  initiating  disorder;  but,  as  in  the  influenzal  and  other  cases,  this 
may  be  longer  delayed.  Occasionally  the  heart  remains  for  a  long  time 
or  permanently  susceptible,  and  dyspnoea  and  palpitation  develop  on 
slight  provocation. 

Treatment.  Attempts  should  be  made  to  minimize  the  damage  to  the 
heart  by  the  use  of  antitoxin  in  diphtheria;  by  hydrotherapeutic  measures 
28 


434  DISEASES   OF   THE  MYOCARDIUM 

to  reduce  the  fever,  especially  in  cases  of  long  continued  or  high  fever; 
and  by  free  elimination  in  all  toxic  conditions.  Absolute  rest  in  bed  is 
the  most  important  element  of  the  treatment;  it  should  be  prolonged 
especially  in  diphtheria,  scarlatina,  severe  pneumonia,  influenza,  etc., 
and  the  getting  up  and  about  should  be  gradual  and  controlled  by  the 
effect  on  the  heart  and  the  pulse.  Especial  attention  should  be  paid  to  the 
diet,  which  should  be  wholesome,  highly  nutritious,  and  readily  digestible. 
Iron,  quinine,  the  bitter  tonics,  and  alcohol  are  the  most  suitable  remedies; 
these  may  be  augmented  by  cold  affusions  and  other  simple  hydrothera- 
peutic  measures,  which  are  of  the  utmost  value  in  restoring  tone  to  the 
cardiac  muscle  and  the  vasomotor  system.  Cardiac  tonics,  such  as  digi- 
talis, strophanthus,  strychnine  (except  in  very  small  doses),  are  contra- 
indicated,  in  the  early  stages  at  least.  In  protracted,  slowly  progressing 
cases,  small  doses  of  digitalis  often  prove  serviceable.  In  these  cases 
also  massage  and  graduated  exercises  are  of  value. 

Attacks  of  acute  failure  of  the  heart  are  to  be  met  with  diffusible 
stimulants,  such  as  aromatic  spirit  of  ammonia,  compound  spirit  of 
ether,  brandy,  whiskey,  hot  coffee,  etc.,  by  the  mouth;  or  whiskey, 
caffeine,  camphor  in  oil,  strophantin,  adrenalin  chloride,  etc.,  hypo- 
dermicly,  with  adrenalin  chloride  and  physiological  saline  solution 
by  the  bowel,  hypodermically,  or  intravenously.  The  acute  failure 
with  marked  dilatation  of  the  heart  is  sometimes  promptly  relieved  by 
venesection,  ( 

THE  FIBROID  HEART. 

(Chronic  Interstitial  Myocarditis;  Fibroid  Degeneration  of  the  Myocardium; 
Sclerosis  of  the  Coronary  Arteries.) 

Etiology. — In  the  great  majority  of  cases  the  fibroid  heart  is  a  result 
of  sclerosis  of  the  coronary  arteries,  which  in  turn  may  be  a  more  or  less 
independent  disorder,  but  usually  is  merely  part  of  general  arteriosclerosis ; 
the  causes  of  the  one,  therefore,  are  the  causes  of  the  other,  notably 
alcoholism,  syphilis,  habitual  and  excessive  muscular  work;  but,  as  in 
arteriosclerosis  generally,  excessive  eating,  gout,  prolonged  and  exces- 
sive mental  efforts,  lead  poisoning,  etc.,  also  are  of  significance.  The 
disorder,  therefore,  is  more  common  in  the  male  sex  and  after  the 
fortieth  year;  and  in  some  cases  it  seems  to  be  predisposed  to  by  heredi- 
tary influences.  Occasionally  chronic  myocarditis  results  from  or  is  a 
sequel  of  acute  myocarditis,  representing  the  healing  and  cicatrization 
of  the  acute  lesions;  or  it  is  associated  with  endocarditis  and  pericarditis, 
representing  an  extension  into  the  myocardium  of  the  lesions  of  either 
of  these  two  disorders;  or  it  is  intimately  bound  up  with  the  conditions 
of  hypertrophy  and  dilatation,  and  of  the  so-called  fatty  heart.  Finally, 
the  disorder  may  be  merely  an  expression  of  advancing  age. 

Pathology. — The  lesions  may  be  diffused  or  circumscribed.  The 
circumscribed  lesions  implicate  especially  the  left  ventricle,  more  par- 
ticularly the  apex,  and  less  frequently  the  septum,  the  right  ventricle, 


THE  FIBROID  HEART  435 

the  papillary  muscles,  and  the  auricles.  They  consist  of  firm,  whitish 
streaks  or  patches,  of  variable  size,  interspersed  between  the  muscular 
fibers.  Usually  these  areas  can  be  demonstrated  to  be  directly  related 
to  sclerotic  changes  in  the  finer  branches  of  the  coronary  arteries.  In 
consequence  of  lessening  of  the  lumen  of  these  small  vessels  (obliterating 
endarteritis)  the  portion  of  myocardium  thereby  supplied  with  blood 
becomes  imperfectly  nourished,  gradually  undergoes  degenerative  and 
atrophic  changes,  and  is  ultimately  replaced  by  connective  tissue. 
Occasionally  the  interruption  in  the  arterial  supply  is  sudden  (thrombosis 
or  embolism),  and  if  the  patient  does  not  die  immediately,  an  area  of 
anemic  or  hemorrhagic  infarction  ensues  and  is  usually  replaced  by  a 
scar.  Associated  with  the  fibrosis  there  is  more  or  less  hypertrophy  and 
dilatation,  varying  in  grade  in  different  parts  of  the  heart.  Since  a  heart 
ill  supplied  with  blood  cannot  hypertrophy,  the  hypertrophy  must  be 
due  to  extracardiac  factors,  notably  an  antecedent  valvular  disease, 
general  arteriosclerosis,  chronic  nephritis,  idiopathic  hypertrophy,  or 
localized  hypertrophy  of  the  non-involved  portion  of  the  myocardium, 
etc.;  the  dilatation  is  the  result  of  the  gradual  yielding  of  a  weakened 
myocardium  to  the  intracardiac  pressure.  Sometimes  the  yielding 
is  limited  to,  or  marked  at,  a  small  area  (scar  of  a  healed  infarct),  and  a 
so-called  cardiac  aneurysm  results;  exceptionally  this  or  the  initial  area 
of  infarction  may  rupture  and  give  rise  to  sudden  death.  In  those  cases 
in  which  there  is  extensive  fatty  change,  the  sclerosis  has  usually  involved 
the  larger  branches  of  the  coronary  arteries  rather  than  the  smaller 
twigs,  and  leads  to  a  general  interference  with  the  nutrition  of  the 
myocardium. 

Symptoms, — ^The  symptoms  are  extremely  variable.  In  some  cases 
there  are  no  noteworthy  symptoms  whatever,  more  or  less  extensive 
myocardial  fibrosis  being  found  after  death  from  other  causes.  In  these 
cases,  of  course,  the  demands  made  upon  the  myocardium  were  still 
within  the  limit  of  its  capabilities.  Symptoms  when  they  develop  are 
those  of  embarrassed  or  insufficient  heart  action,  developing,  as  a  rule, 
gradually  in  a  man  past  middle  life.  Sometimes  the  symptoms  are 
precipitated  by  an  intercurrent  disorder,  such  as  pneumonia  or  other 
infection,  or  by  some  intoxication,  such  as  an  alcoholic  debauch  or  an 
attack  of  acute  gout,  or  by  some  unusual  exertion  or  excitement  precipi- 
tating dilatation  of  the  heart.  In  the  cases  beginning  thus,  more  or 
less  suddenly,  the  symptoms  are  those  of  more  or  less  well-marked 
cardiac  decompensation.  In  the  cases  of  more  gradual  development 
the  patient  begins  to  notice  general  sallowness  of  the  integument,  weak- 
ness, and  languor;  he  is  readily  tired,  and  less  capable  than  formerly 
of  mental  or  physical  exertion:  the  first  induces  fatigue  and  mental 
depression,  and  the  second  dyspnoea,  palpitation  of  the  heart,  precordial 
distress,  and  perhaps  syncopal  attacks  (cerebral  anemia).  With  increas- 
ing dilatation  of  the  heart,  the  phenomena  of  failing  compensation 
(cyanosis,  oedema,  passive  congestion  of  the  viscera,  etc.)  develop. 
Another  series  of  cases  is  characterized  by  anginoid  pains  or  attacks 


436  DISEASES  OF  THE  MYOCARDIUM 

of  true  angina  pectoris.  In  another  series  of  cases  the  phenomena  of  the 
Stokes-Adams  syndrome  develop;  or  a  person  apparently  in  good  health 
dies  suddenly  (coronary  thrombosis  and  anemic  infarcts,  fatty  degenera- 
tion of  the  heart,  or  extensive  fibrosis);  or  the  symptoms  may  be  merely 
those  of  advancing  age. 

Examination  of  the  heart  reveals  variations  in  accordance  with  asso- 
ciated conditions,  arteriosclerosis,  chronic  nephritis,  valvular  disease, 
chronic  pericarditis,  emphysema,  etc.  Usually  there  is  more  or  less 
hypertrophy  with  dilatation.  The  apex  beat  is  displaced  downward 
and  outward  in  accordance  with  the  predominating  hypertrophy  and 
dilatation,  and  it  is  feeble;  often,  indeed,  it  is  entirely  absent.  The 
first  sound  of  the  heart  varies:  it  may  be  feeble  or  muffled,  suggesting 
irregularity  of  the  muscular  contractions ;  or  it  may  be  loud  and  valvular 
(disproportionately  loud  as  compared  with  the  feeble  apex  beat)  suggesting 
more  or  less  complete  loss  of  the  muscular  element ;  or,  and  this  is  quite 
significant,  there  may  be  a  distinct  gallop  rhythm.  This  may  be  of  the  pre- 
systolic type,  in  which  the  new  thirdsound  immediately  precedes  the  normal 
first  sound  of  the  heart,  and  is  due  to  a  strongly  acting  hypertrophied 
auricle,  or,  if  heard  in  weak  and  rapidly  acting  hearts,  is  due  to  a  delay 
in  conductivity  and  sufficient  separation  in  time  of  the  auricular  and 
the  ventricular  contractions  to  enable  one  to  differentiate  the  separate 
sounds  produced  by  both;  or  the  gallop  rhythm  may  be  of  the  proto- 
diastolic type,  in  which  the  new  third  sound  occurs  in  the  early  part 
of  diastole  immediately  following  the  normal  second  sound,  or  it  may 
be  mesodiastolic,  in  which  the  new  sound  occurs  in  the  middle  of  diastole; 
in  both  of  these  the  new  sound  is  ventricular  in  origin  and  is  perhaps 
due  to  loss  of  tonicity  of  the  ventricular  muscle  and  its  sudden  dis- 
tention by  an  ample  and  rapid  volume  of  blood.  The  second  sound 
may  be  reduplicated,  but  this  is  less  frequent  than  in  valvular  disease. 
There  are  commonly  no  murmurs  until  the  disease  is  fairly  well  ad- 
vanced, when  a  systolic  murmur  of  relative  mitral  insufficiency  and  per- 
haps also  of  tricuspid  insufficiency,  may  ensue,  the  consequence  of  inco- 
ordination of  the  papillary  muscle  or  dilatation  of  the  arterioventricular 
rings.  The  cardiac  action  and  the  pulse  are  often  irregular  in  rhythm 
and  force;  the  pulse  is  usually  small  and  feeble;  it  may  be  rapid,  but 
it  is  often  characteristically  slow,  60,  50,  or  less  to  the  minute,  and  not 
uncommonly  exhibits  extrasystoles  (pulsus  bigeminus). 

Diagnosis. — The  diagnosis  is  often  difficult  and  sometimes  impossible, 
but  special  significance  attaches  to  the  manifestation  of  a  failing  or 
embarrassed  heart  in  a  middle-aged  person  without  the  etiological 
factors  and  concomitant  signs  o^  valvular  disease;  and  especially  to  a 
slow,  irregular  pulse,  attacks  of  anginoid  pains  or  syncope,  and  evidences 
of  sclerosis  of  the  palpable  arteries. 

Prognosis. — The  prognosis  is  always  grave,  since  restitution  to  the 
normal  is  impossible ;  but  with  care  and  the  adoption  of  a  suitable  mode 
of  life  the  patient  may  live  many  years. 


HYPERTROPHY   AND  DILATATION  OF   THE   HEART        437 

Treatment. — In  the  cases  of  gradual  onset  and  slow  prog-ress,  as  well 
as  in  the  heart  of  fatty  overgrowth,  much  can  often  be  done  to  arrest 
the  progress  of  the  disorder  by  regulation  of  the  mode  of  life,  especially 
as  regards  eating  and  drinking,  and  Vjy  properly  regulated  rest  and 
exercise.  The  so-called  Oertel  cure  (regulated  diet,  largely  protein, 
limitation  of  the  fluid  intake,  and  graduated  exercises  up  hill)  and  the 
Schott  or  Nauheim  treatment  (effervescing  baths  and  resisted  exercises) 
are  often  very  advantageous.  Cases  developed  upon  a  syphilitic  basis 
may  perhaps  be  benefited  by  the  use  of  the  iodides,  which  also  may  be 
given  in  any  case  of  arteriosclerosis;  benefit  sometimes  attends  its 
prolonged  use.  Cases  of  obvious  cardiac  insufficiency,  manifested  by 
dyspnoea,  cyanosis,  oedema,  and  rapid  and  irregular  pulse,  etc.,  are  to 
be  treated  as  is  the  decompensation  of  valvular  disease.  The  cases  with 
slow  pulse  and  no  signs  of  dilatation  are  to  be  treated  with  diffusible 
and  other  stimulants,  and  with  morphine  (in  the  event  of  restlessness, 
nervousness,  anxiety,  etc.),  and  nitroglycerin  (in  the  event  of  high  blood 
pressure);  digitalis  is  contra-indicated. 


HYPERTROPHY  AND  DILATATION  OF  THE  HEART. 

{Enlnrgement  of  the  Heart.) 

Enlargement  of  the  heart  may  be  due  to  hypertrophy,  to  dilatation, 
or  to  both.  By  simple  hypertrophy  is  meant  a  simple  increase  in  the 
thickness  of  the  muscular  walls  without  increase  in  the  size  (or  capacity) 
of  the  heart  cavities;  by  eccentric  hypertrophy  is  meant  increase  in  the 
thickness  of  the  muscular  walls  with  increase  in  the  capacity  of  the 
cavities.  Increase  in  the  thickness  of  the  walls  with  diminution  in  the 
size  of  the  cavities  probably  never  occurs  (formerly  so-called  eccentric 
hypertrophy). 

Etiology. — Hypertrophy  and  dilatation,  although  often  the  obtrusive 
evidence  of  disorder  of  the  heart,  are,  in  the  great  majority  of  cases,  the 
expression  of  the  activity  of  more  or  less  remote  causative  factors.  In 
most  cases  the  hypertrophy  and  dilatation,  which  are  usually  combined, 
are  readily  referred  to  a  manifest  valvular  defect;  but  occurring  inde- 
pendently of  valvular  disease,  the  hypertrophy  or  dilatation  is  frequently 
overlooked,  or,  being  detected,  is  set  down  as  a  primary  disorder,  when 
in  reality  it  is  a  result  or  part  and  parcel  of  other  diseased  conditions. 

In  general,  hypertrophy  or  dilatation  is  an  expression  of  the  functional 
capacity  of,  and  of  the  demands  made  upon,  the  heart;  it  represents  the 
relationship  between  the  power  possessed  by  the  heart  and  the  work  that 
it  is  called  upon  to  perform.  In  health  there  is  a  balance  between 
these,  and,  to  the  astonishment  of  all  who  think  of  it,  the  heart  that 
never  ceases  its  activity  remains  normal.  When,  upon  occasion,  the  heart 
is  called  upon  temporarily  to  perform  some  unusual  work,  its  reserve 
force  is  such  that  it  is  usually  enabled  to  do  it  without  damage  to  itself. 
Such,  however,  mav  be  the  inherent  weakness  of  the  heart,  or  the  dis- 


438  DISEASES  OF  THE  MYOCARDIUM 

proportionately  great  amount  of  work  that  it  is  called  upon  to  perform, 
that  it  succumbs  (cardiac  overstrain),  and  acute  dilatation  results. 
On  the  other  hand,  the  increased  amount  of  work  may  be  moderate 
in  amount  but  frequently  repeated,  in  which  circumstance  the  heart 
fortifies  itself  by  hypertrophy — in  many  respects  a  conservative  process. 
In  this  manner  the  heart  is  enabled  to  perform  the  increased  amount  of 
work  for  some  time — until  its  nutrition  suffers  or  the  work  becomes 
too  great,  whereupon  dilatation  and  the  usual  evidences  of  embarrassed 
circulation,  of  failing  cardiac  compensation,  result.  Thus,  dilatation, 
both  acute  and  chronic,  not  infrequently  occurs  without  associated 
hypertrophy;  but  wdiether  hypertrophy  ever  occurs  independently  of 
dilatation  may  well  be  doubted — most  if  not  all  cases  of  so-called  con- 
centric hypertrophy  reported  being  examples  of  postmortem  contrac- 
tion of  the  heart. 

Hypertrophy  and  dilatation  may  affect  the  heart  as  a  whole,  or  may  be 
confined  to  one  side  or  to  one  of  the  four  great  divisions  of  the  organ. 
Usually  there  is  associated  disease  of  both  sides,  and  not  uncommonly 
of  all  four  divisions.  The  hypertrophy  and  dilatation  of  valvular  disease 
is  discussed  under  the  appropriate  headings;  occurring  independently 
of  valvular  disease,  there  are  the  following  clinical  varieties:  (1)  Acute 
dilatation;  (2)  chronic  dilatation;  and  (3)  hypertrophy,  or,  as  it  is 
sometimes  called,  dilated  hypertrophy. 

Acute  Dilatation. — ^Acute  dilatation  is  a  common  event  in  the  course 
of  many  of  the  acute  infective  diseases,  and  not  infrequently  leads  to 
death  (see  the  infectious  febrile  heart).  Acute  dilatation  may  be 
observed  also  in  certain  chronic  diseased  states,  such  as  are  attended  by 
grave  secondary  anemia  and  degenerative  alterations  of  the  myocardium. 
In  some  of  these  cases  the  heart,  gradually  failing,  may  suddenly  dilate, 
although  chronic  dilatation  is  the  more  common  event.  Acute  dilatation 
results  also  from  sudden  violent  exertions — from  the  attempting  of  work 
altogether  disproportionate  to  the  natural  and  reserve  force  of  the  heart. 
Thus,  we  find  it  in  draymen  and  ironworkers  who  suddenly  exert  all  their 
muscular  power  in  the  effort  to  lift  heavy  weights;  in  athletes,  oarsmen, 
runners,  football  players,  etc.,  after  participation  in  some  unduly  stren- 
uous contest;  in  mountain  climbers,  especially  in  those  who  attempt 
difficult  ascents  to  which  they  are  unaccustomed,  etc.  It  is  a  feature  also 
of  what  is  known  as  angiospastic  dilatation  of  the  heart. 

Chronic  Dilatation. — Chronic  dilatation,  occurring  independently 
of  valvular  disease,  is  common  in  states  of  general  malnutrition  attended 
by  grave  secondary  anemia.  It  attends  fatty  degeneration  of  the  heart 
muscle,  myocarditis,  fibroid  heart,  and  pericardial  adhesions.  It  is  a 
terminal  event  in  hypertrophy  from  whatever  cause  arisen,  unless  the 
subject  dies  of  an  intercurrent  affection.  It  results  from  gradual  weak- 
ness (loss  of  tonicity)  of  the  heart  muscle,  which  becomes  less  and  less 
able  to  perform  its  allotted  work. 

Hypertrophy. — Hypertrophy  of  the  heart,  occurring  independently 
of  valvular  disease,  may  be  due  to  a  variety  of  causes.     The  hypertrophy 


HYPERTROPHY  AND  DILATATION  OF  THE  HEART        439 

that  efi'ects  especially  the  right  ventricle  is  due  to  increased  pressure  in 
the  pulmonary  circulation,  and  is  found  most  commonly  associated 
with  emphysema,  fibroid  lung,  chronic  bronchitis,  chronic  pleural 
adhesions  with  contraction,  etc.  It  is  really  a  part  of  these  diseases — a 
conservative  process  on  the  part  of  the  heart,  a  condition  that  arises 
in  response  to  increased  demands  upon  the  heart.  It  may  persist  for 
years,  enabling  the  heart  to  do  the  increased  work  well,  and  the  patient 
may  die  of  an  entirely  independent  affection.  In  many  cases,  however, 
dilatation  and  its  attendant  phenomena  ultimately  result. 

Hypertrophy  of  the  left  ventricle,  occurring  independently  of  valvular 
disease,  results  from  increased  pressure  in  the  systemic  circulation,  and 
from  increased  activity  of  the  heart.  Among  the  rarer  causes  are  con- 
genital hypoplasia  of  the  aorta,  such  as  is  sometimes  observed  in  chlorosis 
and  other  conditions;  narrowing  of  the  aorta,  usually  congenital  and 
occurring  in  the  neighborhood  of  the  ductus  Botalli;  aneurysm  of  the  aorta, 
usually,  however,  associated  with  general  arteriosclerosis  or  aortic  valve 
disease;  pressure  on  and  obstruction  of  the  aorta,  such  as  may  be  ob- 
served in  intrathoracic  tumor  and  indurative  mediastino-pericarditis,  etc. 
Practically,  however,  in  the  majority  of  cases,  hypertrophy  of  the  left 
ventricle  partakes  of  one  of  three  varieties:  (1)  That  due  to  arterio- 
sclerosis; (2)  that  due  to  renal  disease;  and  (3)  that,  for  want  of  a  better 
name,  known  as  idiopathic  hypertrophy  of  the  heart.  In  some  cases  it 
is  difficult  to  refer  the  hypertrophy  to  one  or  the  other  of  these  classes, 
inasmuch  as  two  or  three  may  be  concerned  in  the  causation  of  the 
hypertrophy  in  the  individual  case.  Thus,  arteriosclerosis  and  renal 
disease  are  frequently  associated,  and  the  subject  of  one  or  both  of  these 
is  frequently  exposed  to  the  causative  factors  of  the  so-called  idiopathic 
hypertrophy. 

The  hypertrophy  of  arteriosclerosis  is  common  in  advanced  life — when 
to  a  considerable  extent  it  is  a  conservative  process.  But  it  occurs  fre- 
quently enough  in  relatively  early  life,  when  it  is  bound  up  etiologically 
with  syphilis,  alcoholism,  plumbism,  rheumatism,  gout,  etc.  In  the  early 
stages  the  hypertrophied  and  contracted  arterioles  oppose  a  barrier  to 
the  onward  movement  of  the  blood,  and  high  tension  results.  To  over- 
come these,  the  heart,  reacting  to  the  stimulus  of  increased  work,  hyper- 
trophies. Later  the  arteries  become  rigid  and  more  or  less  incapable  of 
contracting.  Thus,  an  important  adjunct  to  the  onward  movement  of 
the  blood — the  activity  of  the  arteries  themselves — is  lost,  and  the  heart 
must  compensate  by  hypertrophy.  Ultimately  the  entire  arterial  svstem 
may  become  extremely  rigid  and  permanently  distended,  whereupon  the 
heart  must  furnish  almost  if  not  quite  all  the  power  for  the  movement 
of  the  blood,  and  this  is  possible  only  through  marked  hypertrophy. 
At  the  same  time,  the  coronary  arteries  participate  in  the  process,  the 
nutrition  of  the  heart  does  not  keep  pace  with  its  increase  in  size,  and 
chronic  dilatation  ensues. 

The  hypertrophy  of  the  heart  of  rejial  disease  occiu's  in  all  types  but 
not  in  all  cases  of  nephritis;  it  is  most  common  and  most  marked  in 


440  DISEASES  OF   THE  MYOCARDIUM 

chronic  diffuse  indurative  (or  interstitial)  nephritis,  in  which  it  is 
properly  looked  upon  as  part  and  parcel  of  widespread  disease  of  the 
cardiovascular  and  renal  systems.  In  the  majority  of  cases  the  disorder 
doubtless  commences  in  the  kidneys,  but  it  speedily  implicates  the  heart 
and  the  blood  vessels ;  in  some  cases  the  lesions  begin  simultaneously  in 
the  kidneys  and  in  the  cardiovascular  apparatus.  The  primary  factor 
is  always  increased  blood  pressure,  which  is  discussed  in  detail  under 
nephritis 

Idiopathic  Hypertrophy  of  the  Heart. — In  a  certain  proportion  of 
cases  of  cardiac  hypertrophy  (usually  associated  with  some  dilatation) 
none  of  the  ordinary  causes  can  be  determined  upon.  There  is  neither 
valvular  disease  nor  disease  of  the  coronary  or  systemic  arteries;  no 
disorder  of  the  myocardium  as  such,  no  pulmonary  emphysema  or  other 
disease  of  the  lung,  no  chronic  nephritis,  no  arteriosclerosis,  and  yet  there 
is  cardiac  hypertrophy.  Eliminating  the  other  and  rarer  causative 
factors  previously  mentioned,  these  cases — for  want  of  a  better  term — 
are  known  as  cases  of  idiopathic  hypertrophy  of  the  heart. 

Some  at  least  of  these  cases  are  due  to  nervous  causes,  to  persistent 
overactivity  of  the  heart  induced  by  undue  irritability  or  overstimulation 
of  the  nervous  mechanism.  This  is  sometimes  seen  in  nervous  persons, 
in  those  susceptible  and  unduly  exposed  to  psychic  disturbances;  it  is 
found  also  in  some  cases  of  exophthalmic  goitre;  and  .is  sometimes 
due  to  the  misuse  of  tea,  coffee,  tobacco,  etc. 

Another  class  of  cases  is  undoubtedly  due  to  excessive  eating  and 
drinking.  There  can  be  little  doubt  that  excessive  eating  temporarily 
increases  the  specific  gravity  of  the  blood,  and  excessive  drinking  the 
total  volume  of  the  blood;  these,  together  with  the  stimulating  effect  of 
certain  metabolic  products,  result  in  increasing  temporarily  the  blood 
pressure  and  the  frequency  and  quickness  of  the  heart's  action.  The 
frequent  repetition  of  this  calls  for  more  work  on  the  part  of  the  heart, 
and  when  its  reserve  force  has  been  exhausted  hypertrophy  ensues. 
This  is  seen  well  exemplified  in  the  great  hypertrophy  of  the  heart  in 
beer  drinkers  (the  Munich  beer-heart),  and  in  the  obesity  of  indulgence, 
especially  in  men  over  forty  years  of  age.  Alcohol  in  these  cases  is 
probably  a  contributing  factor,  but  it  is  probably  less  answerable  for 
the  hypertrophy  (which,  as  already  mentioned,  is  to  a  certain  extent  a 
conservative  process)  than  it  is  for  arterial  alterations  and  subsequent 
degenerative  changes  in  the  heart. 

Finally,  one  of  the  most  interesting  causes  of  cardiac  hypertrophy 
is  excessive  muscular  strain  (which  has  been  discussed  under  the  over- 
strained heart). 

Pathology. — The  conspicuous  alterations  are  increase  in  the  size  of 
the  heart,  increase  in  the  thickness  of  the  walls,  and  change  in  the  shape. 
The  normal  heart  weighs  from  250  grams  (woman)  to  300  grams  (man); 
in  hypertrophy  with  dilatation  the  weight  is  often  twice  or  thrice  this, 
sometimes  more.  In  health  the  left  ventricle  measures  8  to  14  mm. 
in  thickness,  the  right  4  to  7  mm.,  the  left  auricle  2  to  3  mm.,  and  the 


HYPERTROPHY   AND  DILATATION  OF  THE  HEART       441 

right  auricle  1  to  2  mm.  When  fhseased,  tlie  left  ventricle  may  measure 
20  to  25  mm.,  the  right  ventricle  8  to  15  mm.,  the  left  auricle  3  to  4  mm., 
the  right  auricle  2  to  3  mm.  The  papillary  muscles  share  in  the  hyper- 
trophy. W^ien  there  is  marked  dilatation,  thinning  of  the  walls  is  often 
more  apparent  than  real,  being  relative  only.  The  cavities  of  the  heart 
are  greatly  increased  in  capacity,  being  doubled,  or  even  tripled;  such 
may  be  the  distention  that  relative  insufficiency  of  otherwise  normal 
valves  ensues.  The  heart  is  variously  altered  in  shape,  depending  upon 
the  portion  of  the  heart  especially  affected.  In  general,  the  apex  becomes 
broader  and  blunter;  this  is  especially  the  case  in  hypertrophy  of  the  right 
ventricle,  in  which  the  heart  as  a  whole  becomes  globular,  and  the  entire 
apex  may  be  made  up  of  the  thickened  right  ventricle;  in  hypertrophy 
of  the  left  ventricle,  although  the  apex  is  broader  than  normally,  the  heart 
still  preserves  its  conical  shape.  When  dilatation  supervenes  the  heart 
becomes  generally  rounded.  In  the  early  stages  of  hypertrophy  the 
heart  muscle  is  firm  to  the  touch,  and  dark  red  brown  in  color;  in  increas- 
ing dilatation,  however,  it  loses  its  firmness,  and  becomes  flaccid,  and  in 
high  degrees  of  dilatation  it  is  commonly  a  misshapen,  toneless  mass 
of  tissue  at  the  necropsy.  Microscopically  there  is  an  increase  in  the 
number  and  size  of  the  muscular  fibers ;  in  late  stages  fatty  degeneration 
of  the  myocordium  and  fibroid  alterations  ensue. 

Symptoms. — Hypertrophy  of  the  heart,  since  it  is  a  conservative 
process  on  the  part  of  nature,  frequently  exists  for  a  considerable  time 
without  occasioning  symptoms;  indeed,  by  its  presence  it  obviates 
certain  symptoms  that  otherwise  would  develop  on  account  of  the 
diseased  condition  which  it  endeavors  to  correct.  Sometimes,  however, 
there  are  unpleasant  sensations  in  the  region  of  the  heart,  evidences 
of  overactivity  of  the  heart,  precordial  distress,  rarely  amounting  to 
pain,  subjective  appreciation  of  the  heart's  action,  etc.  These  are 
especially  noticeable  after  exertion  or  excitement,  when  they  may  be 
accompanied  by  slight  dyspnoea,  vertigo,  etc.  Sooner  or  later,  however, 
there  are  symptoms.  These,  in  large  part,  are  not  to  be  distinguished 
from  those  of  failing  cardiac  compensation  occurring  in  the  course  of 
myocarditis  or  chronic  endocarditis.  The  early  symptoms  in  such  cases, 
however,  differ.  Thus,  in  athletes  and  others  whose  hypertrophy  is  due 
to  excessive  muscular  exercise,  and  who  rather  suddenly  cease  this 
muscular  activity,  there  may  be  the  subjective  manifestations  of  over- 
activity of  the  heart,  precordial  distress,  dyspnoea,  cough,  hemoptysis, 
tinnitus  aurium,  vertigo,  flushings,  disturbed  vision,  etc.  (consult 
the  overstrained  heart).  In  other  cases  more  or  less  constant  and 
persistent  dyspnoea  precedes  the  final  breakdown. 

The  symptoms  of  acute  dilatation  are  those  already  mentioned  un(ler 
acute  cardiac  overstrain  and  under  the  infectious  febrile  heart.  The 
symptoms  of  chronic  dilatation  are  those  of  decompensation,  described 
under  chronic  valvular  disease  of  the  heart — precordial  distress  and 
pain,  cough,  dyspncx'a,  cyanosis,  crdema,  congestion  of  the  viscera,  etc. 


442  DISEASES  OF  THE  MYOCARDIUM 

Physical  Signs. — The  physical  signs  vary  somewhat,  depending  upon 
the  portion  of  the  heart  affected. 

Left  Ventricle. — Inspection  and  palpitation  reveal  bulging  of  the 
precordium,  which  in  young  subjects  may  cause  marked  asymmetry 
of  the  chest,  widening  of  the  intercostal  spaces,  increase  in  the  force 
of  the  apex  beat,  and  a  widely  diffused  heart  beat.  The  apex  beat 
may  be  as  low  as  the  sixth,  seventh,  or  eighth  intercostal  space,  and 
2  to  5  cm.  outside  the  mid-clavicular  nipple  line  (13  to  18  cm.  from  the 
median  line).  The  apex  beat  is  peculiarly  deliberate  and  heaving  in 
character,  increased  in  strength,  and  about  2  fingers'  breadths  in  width. 
In  some  cases  of  well-marked  hypertrophy  a  double  apex  beat  may  be 
felt,  the  second  being  attributed  to  a  rebound  of  the  heart  transmitted 
from  the  aortic  valve.  Percussion  reveals  an  increase  in  the  area  of 
dulness,  which  is  more  ovoid  than  in  health,  the  long  axis  of  the  ovoid 
being  directed  in  the  long  axis  of  the  heart.  The  dull  area  (deep  or 
relative  dulness)  may  extend  upward  to  the  third  rib,  rarely  to  the  second 
interspace,  to  the  left  2  to  5  cm.  beyond  the  mid-clavicular  line,  while 
to  the  right,  in  uncomplicated  hypertrophy  of  the  left  ventricle,  the 
increase  of  dulness  is  relatively  slight — not  more  than  2  cm.  (|  inch)  beyond 
the  right  edge  of  the  sternum.  On  auscultation,  if  the  valves  are  still 
competent,  the  heart  sounds  are  normal,  or  the  first  sound  is  dull,  some- 
what louder,  and  more  prolonged  than  normally  (due  to  increase  of 
the  muscular  element).  The  aortic  second  sound  is  usually  accentuated, 
sometimes  reduplicated  or  split.  The  pulse  is  regular,  of  good  volume, 
increased  in  strength  and  in  tension. 

Right  Ventricle. — Inspection  and  palpation  reveal  bulging  of  the 
precordium,  especially  at  the  xyphoid  cartilage  and  adjacent  right 
cartilages,  with  some  widening  of  the  intercostal  spaces.  The  heart-beat 
is  diffuse — the  strongest  beat  not  infrequently  being  at  the  low^er  part 
of  the  sternum.  The  apex  beat  also  is  diffuse,  wider  than  normally — 
2  to  3  fingers'  breadths  in  width — and  extends  to  the  left  bevond  the 
mid-clavicular  line;  it  is  rarely  dislocated  downward,  and  when  so,  not 
below  the  sixth  intercostal  space.  Percussion  reveals  great  increase  in 
the  deep  cardiac  dulness  transversely,  to  the  left  slightly,  and  to  the 
right  considerably  — 2  to  5  cm.  (|  to  2  inches)  beyond  the  right  border  of 
the  sternum.  The  area  is  irregularly  ovoid — transversely  ovoid.  On 
auscultation  the  heart  sounds  may  be  normal;  the  first  sound  usually  is 
slightly  dull  and  prolonged,  and  the  second  sound  is  accentuated  or 
reduplicated  in  the  pulmonary  area.  The  pulse  is  usually  regular,  and 
increased  in  volume  and  tension. 

Hypertrophy  of  the  auricles  does  not  occur  in  the  absence  of  asso- 
ciated disease  of  the  ventricles  or  of  valvular  disease,  and  is  scarcely 
to  be  diagnosticated  in  the  absence  of  such  associated  disease.  Hyper- 
trophy of  the  left  auricle  commonly  causes  enlargement  anteropos- 
teriorly,  since  that  the  chamber  of  the  heart,  as  a  rule,  does  not  come 
in  contact  with  the  chest  wall;  upon  occasion,  however,  there  may  be 
some  increased  dulness  in  the  third  or  the  second  left  intercostal  space, 


ANEURYSM  OF  THE  HEART  443 

together  with  a  visible  and  palpable  presystolic  (auricular  systolic)  pulsa- 
tion. Hypertrophy  of  the  right  auricle  gives  rise  to  dulness  to  the  right 
of  the  sternum  and  a  visible  and  palpable  presystolic  (auricular  systolic) 
pulsation  in  the  third  and  fourth  right  intercostal  spaces,  occasionally  also 
in  the  third  left  intercostal  space. 

With  the  onset  of  dilatation  the  apex  beat  grows  weaker,  more  diffuse, 
and  irregular;  often,  although  a  diffuse  wave  may  be  seen,  none  can  be 
felt  (or  scarcely  felt);  the  dulness  is  increased,  especially  to  the  right, 
the  heart  sounds  lose  their  muscular  element  and  become  sharp,  higher- 
pitched,  valvular,  and  later  quite  feeble  and  indistinct.  Murmurs 
of  relative  mitral  and  tricuspid  insufficiency  frequently  develop;  gallop 
rhythm  may  supervene;  autochthonous  pulsations  appear  in  the  jugular 
veins  and  the  liver;  the  pulse  becomes  small,  quick,  and  irregular;  and 
other  evidences  of  failing  cardiac  compensation  develop.  At  times  death 
occurs  suddenly,  and  without  premonition. 

Prognosis. — ^The  prognosis  depends  upon  the  etiological  factors  and 
the  associated  conditions.  Hypertrophy  itself  is  a  conservative  process; 
so  long  as  it  remains  efficient  the  outlook  is  good.  From  the  nature  of  the 
process,  however,  the  final  prognosis  is  bad,  since  ultimately  the  nutrition 
does  not  keep  pace  with  the  enlargement  of  the  heart,  and  degenerative 
processes  and  finally  dilatation  ensue.  The  prognosis  in  dilatation 
depends  upon  its  cause  and  degree. 

Treatment. — The  treatment  of  hypertrophy  and  dilatation  is  so 
intimately  bound  up  with  the  causal  factors  that  it  can  scarcely  be  dis- 
cussed apart  from  them.  In  general,  an  overactive  hypertrophied 
heart  is  much  benefited  by  rest,  the  avoidance  of  tobacco,  coffee,  tea, 
alcohol,  etc.,  and  the  use  of  sedatives,  such  as  the  bromides,  valerian, 
aconite,  etc.  The  treatment  of  dilatation  is  that  of  decompensation 
in  valvular  disease. 


ANEURYSM  OF  THE  HEART. 

Aneurysm  may  involve  the  myocardium  or  the  valves.  Valvular 
aneurysm  may  result  from  acute  valvular  endocarditis,  which  leads  to 
softening  and  weakness  of  a  leaflet,  and  permits  of  its  distention  in  re- 
sponse to  the  influence  of  the  blood  pressure.  This  is  most  common  at 
the  aortic  orifice,  where  the  aneurysm  usually  forms  an  ovoid  or  spheroid 
projection  into  the  left  ventricle;  rarely  a  similar  condition  occurs  at  the 
mitral  valve.  Rupture  may  occur  and  give  rise  to  valvular  insufficiency. 
Otherwise  the  condition  cannot  be  recognized  during  life. 

Myocardial  aneurysm  may  follow  an  area  of  localized  weakening; 
this  is  usually  due  to  fibroid  myocarditis,  a  scar  of  a  healed  infarct, 
a  gumma,  mural  endocarditis,  etc.  The  common  seat  is  the  left  ventricle 
near  the  apex.  The  aneurysm  is  usually  saccular,  rarely  a  rather  diffuse 
dilatation.  There  are  no  characteristic  symptoms.  Occasionally 
there  may  be  a  localized  pulsating  prominence  near  the  region  of  the 


444  DISEASES  OF  THE  MYOCARDIUM 

apex  beat,  and  an  irregular  area  of  dulness.  The  condition  may  be 
revealed  by  a  Rontgen-ray  examination.  The  prognosis  is  bad,  ru})ture 
ensuing  eventually.    Treatment  is  unavailing. 


RUPTURE  OF  THE  HEART. 

Rupture  of  the  heart  is  a  rare  event  that  may  occur  in  cases  of  degene- 
rated or  softened  myocardium.  This  occurs  especially  in  aneurysm  of  the 
heart,  in  the  fibroid  heart,  in  the  fatty  heart,  in  softening  (myomalacia 
cordis)  due  to  obstruction  (embolism  or  thrombosis)  of  the  coronary 
artery,  in  suppurative  myocarditis,  gummas,  ulceration  endocarditis,  etc. 
It  occurs  most  commonly  in  men  over  sixty  years  of  age,  and  is  usually 
due  to  some  exertion.  The  rupture  may  occur  anywhere,  but  is  most 
common  in  the  wall  of  the  left  ventricle  near  the  septum.  Occasionally, 
also  a  valve  leaflet  may  be  ruptured  and  lead  to  valvular  insufficiency; 
usually  it  results  from  severe  exertion  or  traumatism  to  the  chest,  or  from 
ulcerative  endocarditis.  The  symptoms  of  rupture  of  the  heart  are  rarely 
unequivocal.  Usually  there  is  sudden  death  without  premonitory  symp- 
toms. Occasionally  there  is  sudden,  perhaps  agonizing,  pain  in  the  pre- 
cordium,  a  sensation  as  of  something  giving  way  in  the  chest,  dyspnoea, 
anxiety,  collapse,  and  death  from  the  pressure  of  the  ensuing  hemoperi- 
cardium  upon  the  heart;  death  may  be  delayed  for  twelve  hours  or 
more,  rarely,  even  for  days.  The  diagnosis  is  rarely  made;  it  is  sug- 
gested by  the  aforementioned  symptoms  and  the  physical  signs  of  fluid 
in  the  pericardium.     The  prognosis  is  hopeless  and  treatment  ineffectual. 


TUMORS  AND  PARASITES  OF  THE  HEART. 

Tumors  of  the  heart  are  rare;  but  lipoma,  fibroma,  myoma,  sarcoma, 
and  carcinoma  have  been  observed.  Sarcoma  and  carcinoma  are 
usually  secondary,  and  may  be  single  or  multiple.  There  are  no  sig- 
nificant symptoms;  decompensation  may  ensue  ultimately. 

Parasites  of  the  heart  also  are  rare.  The  most  common  is  Echino- 
coccus  granulosa.  Cysticercus  cellulosae,  Trichinella  spiralis,  Strepto- 
thrix  actinomyces,  etc.,  have  also  been  observed. 


DISEASE  OF  THE  CORONARY  ARTERIES. 

Disease  of  the  coronary  arteries  can  scarcely  be  separated  from 
disorders  to  which  it  gives  rise  or  with  which  it  is  associated.  The  integ- 
rity of  the  myocardium,  of  course,  depends  upon  an  efficient  coronary 
circulation — which  may  become  disordered  in  toto  or  locally,  slowly 
or  suddenly.  The  chief  consequences  are:  (1)  Infarction  and  softening. 
This  is  due  to  occlusion  of  a  larger  or  smaller  twig  (end  artery),  and  is 


ACUTE  ENDOCARDITIS  445 

most  common  in  the  area  of  distribution  of  the  anterior  coronary  artery. 
The  absence  of  such  infarction  in  some  cases  of  arterial  occlusion  is 
attributable  to  abnormal  anastomoses  or  to  an  efficient  circulation 
through  the  vessels  of  Thebesius.  The  softened  infarcted  area  is  gradu- 
ally replaced  by  scar  tissue,  which  later  may  be  the  seat  of  an  aneurysm 
or  of  rupture  of  the  heart.  (2)  The  fibroid  heart  (which  see).  (3)  An- 
gina pectoris  (which  see).  (4)  Sudden  death.  A  not  uncommon  cause 
of  sudden  death  is  occlusion  of  one  coronary  artery  or  of  one  of  its  main 
branches.  The  occlusion  is  usually  due  to  thrombosis  of  a  vessel 
somewhat  sclerosed  and  more  or  less  narrowed;  the  circulation  has 
been  perhaps  for  some  time  precarious,  but,  the  final  interruption  of  the 
circulation  being  rather  sudden,  death  may  ensue  immediately. 


DISEASES   OF   THE   ENDOCARDIUM. 


ACUTE  ENDOCARDITIS. 

Etiology. — Acute  endocarditis  is  rarely  a  primary  disorder;  usually  it 
is  secondary  to  infectious  processes  elsewhere  in  the  body.  It  occurs 
most  frequently  in  association  with  rheumatic  fever,  the  likelihood  of 
its  development  increasing  with  recurrence  of  attacks  of  rheumatism; 
75  per  cent,  or  more  of  endocarditic  subjects  are  or  have  been  rheumatic, 
and  others  give  a  history  of  such  related  disorders  as  tonsillitis  (the  portal 
of  entry  of  the  infectious  agent),  chorea,  neuromuscular  (growing) 
pains  (especially  significant  in  children),  erythema  nodosum,  etc. 
Acute  endocarditis  occurs  also  in  association  with  scarlatina,  pneumonia, 
pyococcic,  gonococcic,  and  typhoid  infections,  dysentery,  influenza, 
and  occasionally  also  with  diphtheria,  tuberculosis,  measles,  etc.  The 
local  lesions  in  the  heart  may  be  provoked  by  the  primary  infective  agent, 
but  frequently  they  are  set  up  by  secondary  pyococcic  invaders.  The 
disorder  is  most  common  in  adolescents  and  young  adults,  corresponding 
with  the  period  of  greatest  prevalence  of  the  aforementioned  infections. 
It  is  predisposed  to  by  diabetes,  chronic  nephritis,  gout,  syphilis,  carci- 
noma, and  chronic  anemic  and  debilitating  disorders  in  general,  and  in 
consequence  it  is  not  uncommonly  a  terminal  event  in  older  subjects. 
It  is  often  engrafted  on  an  old  or  chronic  endocarditis. 

Pathology. — Different  types  or  forms  of  the  disease  may  be  distin- 
guished— rheumatic,  staphylococcic,  streptococcic,  pneumococcic,  gono- 
coccic, typhoid,  influenzal,  etc.;  simple  (or  benign)  and  ulcerative  (or 
malignant);  verrucose  and  ulcerative;  and  valvular  and  mural.  Except 
etiologically,  no  sharp  line  of  demarcation  can  be  drawn  between  these 
types. 

The  lesions  are  most  common  in  the  left  side  of  the  heart,  the  relative 
frequency  being  as  follows:    The  mitral  valve  in  50  per  cent,  or  more  of 


446  DISEASES  OF  THE  ENDOCARDIUM 

the  cases  when  affected  alone,  in  80  per  cent,  when  associated  with  lesions 
elsewhere;  the  aortic  valve  in  15  per  cent,  when  affected  alone,  in  40  per 
cent,  when  associated  with  lesions  elsewhere;  the  tricuspid  valve;  the 
pulmonary  valve;  the  wall  of  the  left  auricle  and  ventricle;  and  the  wall 
of  the  right  auricle  and  ventricle.  Endocarditis  developing  during 
intra-uterine  life  is  more  common  in  the  right  side  of  the  heart,  which 
fact  is  attributed  to  the  greater  strain  and  stress  to  which  the  right  and 
the  left  side  of  the  heart  respectively  is  subjected  in  intra-uterine  and 
extra-uterine  life;  there  are,  however,  other  more  or  less  ill-understood 
factors,  such  as  anomalies  of  development,  etc. 

In  the  simplest  form,  the  lesions  consist  of  small,  grayish,  translucent 
vegetations  or  excrescences  attached  to  the  line  of  closure  of  the  valves, 
that  is,  to  the  surface  opposed  to  the  blood  current,  the  auricular  surface 
of  the  mitral  valve,  and  the  ventricular  surface  of  the  aortic  valve.  Often 
the  vegetations  are  extremely  small,  1  to  2  mm.  in  diameter,  bead-like; 
they  may  be  larger,  and  have  a  fissured  or  wart-like  surface;  sometimes 
they  are  attached  by  a  pedicle,  that  is,  polypoid.  They  are  most  commonly 
situated  along  the  line  of  closure  of  the  valves,  which  appears  to  be  re- 
lated to  the  fact  that  the  regions  most  exposed  to  strain  and  traumatism 
are  most  likely  to  be  less  resistant,  and  that  the  infection  is  probably 
effected  through  the  medium  of  the  blood  circulating  through  the 
cavities  of  the  heart,  rather  than  that  circulating  in  the  coronary  vessels, 
although  this  is  still  a  debated  point.  The  vegetations  developing  on  the 
valves  may  spread  to  the  chordae  tendinese,  the  wall  of  the  cavities,  etc. 
They  consist  for  the  most  part,  of  fibrin,  leukocytes,  and  blood  platelets 
(coagulable  elements  of  the  blood),  superimposed  upon  an  area  of 
desquamating  and  proliferating  endothelial  cells.  Occasionally  there 
is  a  surrounding  area  of  reactive  congestion,  but  often  this  is  entirely 
absent.  The  causative  microorganisms  may  be  found  in  the  vegetations, 
but  they  are  not  infrequently  absent  when  sought — which  suggests  that, 
having  initiated  the  lesions,  the  microorganisms  may  die  out,  or,  as  is 
likely,  that  toxins  suffice  to  set  up  the  lesions.  Insufficiency  of  the  valve 
is  a  common  concomitant,  being  the  result  of  malposition  of  the  leaflets 
dependent  upon  the  vegetations  or  upon  a  consecutive  deformity  of  the 
leaflets;  but  when  the  vegetations  are  small  the  insufficiency  is  often  due 
less  to  the  vegetations  per  se  than  to  myocardial  disorder  and  inter- 
ference with  the  normal  action  of  the  valve  leaflets  and  papillary  muscles. 

The  subsequent  course  of  events  varies:  (1)  In  the  course  of  time 
the  proliferating  endothelial  cells  and  fibroblasts  may  invade  the  vegeta- 
tion, and  by  a  process  akin  to  organization  gradually  lead  to  its  replace- 
ment, so  that  ultimately  the  lesion  is  represented  by  a  scar.  In  rare  cases, 
in  which  the  lesions  have  been  minor  in  grade,  restitution  to  the  normal 
may  perhaps  ensue;  but  this  is  doubtful,  and  very  unlikely  in  a  given  case. 
The  scar  usually  contracts  and  leads  to  thickening,  induration,  and 
distortion  of  the  valve  leaflets — chronic  valvular  disease.  (2)  The  lesions 
may  progress  to  what  is  often  spoken  of  as  ulcerative  or  malignant 
endocarditis.     This,  merely  an  aggravation  of  the  more  benign  lesion, 


ACUTE  ENDOCARDITIS  447 

usually  begins  on  the  valves,  but  it  is  likely  to  spread  to  the  chordae  ten- 
dineae  and  the  mural  endocardium,  and  while  it  is  most  frequent  in  the 
left  side  of  the  heart,  it  is  not  uncommon  also  in  the  right  side.  It  is  char- 
acterized not  only  by  the  most  exuberant  vegetations,  but  also  by  more 
or  less  extensive  necrosis  and  ulceration  of  the  underlying  tissues;  so 
that  to  the  previously  existing  valvular  insufficiency,  stenosis  of  the  orifice 
(from  blockage  by  vegetations)  is  not  infrequently  added.  The  ulcera- 
tion may  be  superficial,  involving  perhaps  only  the  endocardium;  but 
usually  it  is  more  extensive,  and  not  uncommonly  leads  to  aneurysmal 
dilatation  and  perforation  of  a  valve  leaflet,  destruction  of  the  chordae 
tendinese  or  papillary  muscles,  perhaps  considerable  necrosis,  suppura- 
tion, even  perforation  of  the  cardiac  septa  or  walls.  The  lesions  may 
also  spread  to  the  aorta  and  the  pulmonary  vessels.  The  vegetations  are 
likely  to  become  disintegrated,  and  being  detached  in  part  or  in  whole 
and  swept  into  the  circulation,  cause  embolism  and  infarction  in  differ- 
ent organs,  especially  the  spleen,  kidneys,  brain,  intestine,  etc.  (or  in 
the  lung  in  involvement  of  the  right  side  of  the  heart).  Multiple  abscesses 
(so-called  arterial  pyemia)  ensue,  if  the  emboli  are  infected.  The 
lesions  in  the  heart  thus  are  often  relatively  insignificant,  being  over- 
shadowed by  those  of  the  primary  disorder  and  the  metastatic  phe- 
nomena. Often  the  cardiac  lesions  are  widespread,  involving  the 
endocardium,  the  myocardium,  and  the  pericardium,  so  that  the  term 
pancarditis  is  most  appropriate. 

Symptoms. — The  milder  grades  of  acute  endocarditis  frequently  run 
their  course  entirely  unsuspected;  of  themselves  they  occasion  no  note- 
worthy or  unequivocal  symptoms,  and  frequently  are  disclosed  only  by 
the  necropsy.  Since  the  disease  is  especially  common  in  rheumatic 
fever,  the  likelihood  of  its  occurrence  should  be  borne  in  mind;  its 
development  should  be  suspected  in  the  event  of  precordial  distress  or 
oppression,  palpitation,  dyspnoea  on  slight  exertion,  rapid  and  irregular 
cardiac  action,  and  persistence  or  sudden  increase  of  fever  without 
adequate  articular  or  other  signs  to  explain  it.  The  more  marked 
grades  of  the  disorder  exhibit  gradual  progression  in  symptomatology 
to  that  of  frank  septicopyemia — irregular  chills,  fever  (remittent  or  high 
and  continuous),  sweats  (often  profuse),  rapid  loss  of  flesh  and  strength, 
progressive  anemia,  polynuclear  leukocytosis,  enlargement  of  the  spleen, 
diarrhoea,  pyococcic  or  other  bacteremia,  etc.  These  phenomena  are 
not  essentially  different,  whether  they  occur  in  septicopyemia  attended 
or  unattended  with  endocarditis;  but  they  are  especially  significant  if 
there  be  no  adequate  cause  to  explain  them,  or  if  they  occur  in  a  subject 
of  old  valvular  disease. 

In  most  cases  the  diagnosis  depends  upon  the  occurrence  of  embolic 
phenomena  and  the  results  of  a  physical  examination  of  the  heart.  Of 
embolic  phenomena  the  most  important  and  suggestive  occur  in  the 
skin — petechiifi;  in  the  kidneys — renal  pain,  albumin,  blood,  and  tube 
casts  in  the  urine;  in  the  spleen — splenic  pain,  palpable  and  audible 
frictions;   in    the   lungs — pain,   hemoptysis,   perhaps   localized   dulness, 


448  DISEASES  OF  THE  ENDOCARDIUM 

bronchial  breathing,  and  fine  rales;  in  the  cerebrum — hemiplegia, 
monoplegia,  aphasia,  blindness,  convulsions;  in  the  eye — retinal  hemor- 
rhages and  optic  neuritis,  as  well  as  petechial  hemorrhages  in  the  palpe- 
bral conjunctiva;  in  the  long  bones — local  pain  and  tenderness;  in 
the  joints — local  pain,  swelling  and  tenderness;  painful  ephemeral 
erythematous  nodules  in  the  fingers,  toes,  hands,  and  feet;  and  in  the 
extremities — gangrene  from  vascular  obstruction.  The  joint  symptoms 
are  often  fugitive  and  much  resemble  the  articular  manifestations  of 
rheumatism;  they  are  doubtless  toxic  in  nature,  as  are  also  some  of 
the  skin  manifestations,  such  as  certain  roseolas,  erythemas,  urticarias, 
etc. 

The  extreme  variability  in  the  symptomatology  has  led  to  a  classificar 
tion  of  the  disorder  into  several  types:  (1)  The  cardiac  type,  in  which 
cardiac  distress  and  obvious  valvular  lesion  with  attendant  failure  of 
cardiac  compensation  constitute  the  noteworthy  features;  (2)  the  septic, 
or  pyemic  type,  which  cannot  be  distinguished  from  septicopyemia,  of 
which  in  reality  it  is  a  manifestation;  (3)  the  typhoid  type,  resembling 
typhoid  fever  in  the  toxemia,  asthenia,  and  prostration ;  and  (4)  the  cere- 
bral type,  resembling  meningitis.  These  terms,  however,  are  largely 
misnomers,  since  the  disease  necessarily  is  always  cardiac  and  toxemic 
or  septicopyemic,  and  the  irregularity  and  multiplicity  of  the  lesions  and 
symptoms  do  not  really  permit  of  such  classification. 

The  physical  signs  are  extremely  uncertain.  In  some  cases  there  may 
be  no  discernible  deviation  from  the  normal,  especially  in  some  of  the 
streptococcic,  gonococcic,  and  pneumococcic  forms.  The  cardiac  action 
is  often  persistently  excited  (without  obvious  adequate  cause),  and 
sometimes  peculiarly  unstable,  attacks  of  tachycardia  (120  to  150  heart 
beats  per  minute)  often  developing  suddenly  and  ceasing  quite  as  sud- 
denly (without  apparent  cause);  this  is  of  some  diagnostic  importance. 
In  some  cases  the  first  sound  at  the  apex  becomes  impure  or  muffled,  and 
finally  replaced  by  a  murmur,  and  other  signs  of  mitral  insufficiency 
develop;  in  other  rarer  cases  the  signs  of  aortic  insufficiency  or  other 
valvular  defect  ensue.  Extreme  variability  in  the  character  of  the 
murmur  from  day  to  day  (perhaps  related  to  changes  in  the  vegeta- 
tions, or  due  to  incoordinated  action  of  the  papillary  muscles)  is  quite 
significant,  but  is  not  always  present. 

The  clinical  course  of  the  disease  is  quite  variable,  but  permits  of 
o'rouping  of  the  cases :  (1)  Mild  cases,  which  are  common  in  rheumatic 
fever,  and  occur  also  in  typhoid  fever  and  other  infections  and  in  de- 
bilitated conditions,  perhaps  as  a  terminal  infection.  The  clinical  phe- 
nomena are  slight  or  altogether  absent,  but  if  the  patient  survives,  the 
lesions  usually  lead  to  chronic  valvular  disease.  (2)  Severe  cases,  which 
are  especially  common  in  pyococcic  infections  (puerperal  infection,  wound 
infection,  pneumonia,  gonorrhoea,  scarlatina,  etc.),  although  they  may 
occur  also  in  milder  infections,  rheumatic  fever,  etc.  The  clinical  phe- 
nomena may  be  more  or  less  obtrusive,  and  the  lesions  may  subside  leav- 
ing a  \alve  or  valves  more  or  less  damaged;  or  a  fatal  result  may  ensue 


ACUTE  ENDOCARDITIS  449 

within  several  weeks;  or  a  chronic  septic  process  may  be  set  up  and 
continue  for  months.  (3)  Recurring  or  relapsing  cases,  which  may  be 
interpreted  aS  relighting  of  an  obsolete  infection  or  reinfection  of  a 
damaged  valve — a  form  of  chronic  endocarditis. 

Diagnosis. — ^The  diagnosis  of  the  simple  or  mild  cases  is  difficult,  and 
is  often  a  matter  merely  of  conjecture.  Increase  of  the  cardiac  dulness, 
an  apical  systolic  murmur,  and  an  accentuated  pulmonic  second  sound 
are  not  uncommonly  due  to  toxic  degeneration  of  the  myocardium 
provoked  by  divers  infections  (rheumatic  fever,  etc.).  The  gradual 
development  of  the  murmur  is  suggestive  of  endocarditis;  but  since  anemia 
and  degeneration  of  the  myocardium  usually  supervene  at  about  the 
time  endocarditis  may  develop,  the  diagnosis  cannot  always  be  made, 
and  often  must  await  the  passage  of  time;  persistence  of  the  physical 
signs  after  convalescence  from  the  infection,  of  course,  is  conclusive 
evidence  of  a  valvular  defect.  The  development  of  a  diastolic  murmur 
during  the  infection  is  of  itself  almost  conclusive  of  aortic  endocarditis. 
The  diagnosis  of  the  more  severe  cases  may  be  based  upon  the  symptoms 
of  septicopyemia,  embolic  phenomena,  and  the  physical  signs  referable 
to  the  heart  already  mentioned.  In  obscure  cases  blood  cultures  may 
afford  material  diagnostic  assistance. 

Typhoid  fever  may  be  excluded  by  the  absence  of  the  prodromes, 
especially  the  persistent  headache  and  nose-bleed,  roseola,  tympanites, 
delirium,  dry  tongue,  Gruber-Widal  reaction,  and  typhoid  bacilli  from 
the  feces,  urine,  roseola,  and  blood,  and  by  the  presence  of  a  source  of 
infection,  irregular  and  repeated  rigors,  intermittent  fever,  profuse  perspi- 
ration, rapid  and  unstable  pulse,  undue  dyspnoea,  the  early  occurrence 
of  marked  prostration,  the  rapid  development  of  anemia,  leukocytosis, 
embolism,  and  the  detecting  of  the  infecting  microorganism  in  the  blood. 
The  spleen  is  said  to  become  less  enlarged,  although  more  tender,  in 
endocarditis  (and  sepsis)  than  in  typhoid  fever.  It  is  well  also  to  bear 
in  mind  that  the  typhoid  bacillus  may  set  up  the  endocarditis,  either 
primarily  or  by  infecting  an  old  lesion.  In  acute  tuberculosis,  as  con- 
trasted with  acute  endocarditis,  variations  in  the  temperature  and  pulse 
rate,  and  excessive  perspirations  occur  with  more  regularity,  wasting 
is  more  rapid,  a  local  focus  of  tuberculous  disease  may  be  detected  in 
some  part  of  the  body — in  the  lungs  (tubercle  bacilli  in  the  expectora- 
tion), in  the  pleura,  in  the  abdomen,  in  the  brain  (tubercle  bacilli  in  the 
cerebrospinal  fluid  obtained  by  lumbar  puncture),  etc. ;  physical  examina- 
tion of  the  heart  reveals  no  signs  of  valvular  disease  (except  in  the  rare 
cases  in  which  there  is  an  associated  valvular  lesion);  and  embolism 
does  not  occur.  The  detecting  of  choroidal  tubercles  in  the  one  case, 
and  of  retinal  hemorrhages  in  the  other,  is  of  the  greatest  diagnostic 
value.  Malaria  may  l)e  excluded  l)y  the  irregularity  of  the  attacks 
of  chills,  fever,  and  sweats,  polynuclear  leukocytosis,  absence  of  malarial 
Plasmodia  from  the  blood,  and  the  administration  of  quinine. 

Prognosis. — The  prognosis  varies  with  the  severity  of  the  lesions — 
which  has  already  been  referred  to.     The  seriousness  of  the  lesions, 
29 


450  DISEASES  OF   THE   ENDOCARDIUM 

however,  sometimes  cannot  be  judged  from  the  cHnical  manifestations, 
so  that  for  a  time  at  least  the  prognosis  as  regards  Kfe  may  be  doubtful; 
that  as  regards  the  heart  is  always  bad,  since  chronic  valvular  disease 
almost  certainly  results.  Rarely  even  severe  so-called  malignant  endo- 
carditis may  eventuate  in  recovery,  with  more  or  less  permanent  damage 
to  the  heart.  Usually,  however,  it  ends  in  death,  or  the  acute  symptoms, 
fever,  etc.,  subside  within  two  or  three  months. 

Treatment. — The  treatment  resolves  itself  largely  into  that  of  the 
primary  infection — whether  rheumatic  or  non-rheumatic.  It  is  perhaps 
possible  in  some  cases  of  rheumatism,  to  prevent  the  development  of 
endocarditis — by  prompt  and  efficient  treatment  of  the  rheumatism. 
The  patient  should  be  absolutely  at  rest  in  bed,  and  should  be  brought 
promptly  under  the  influence  of  the  salicyl  preparations — ^large  doses 
to  the  point  of  mild  intoxication.  This  not  only  relieves  the  rheumatic 
manifestations,  but,  counteracting  the  poison  it  should  tend  to  prevent 
the  occurrence  of  endocarditis;  there  is  some  evidence  that  it  does. 
Some  observers  believe  that  the  addition  of  the  alkalies  (in  twice  the  dose 
of  the  salicyl  preparation)  is  of  much  value.  Caton  insists  on  the 
importance  also  of  small  repeated  blisters  to  the  precordium,  and  he  as 
well  as  others  extol  the  advantage  of  prolonged  rest  in  bed — six  weeks 
to  three  months. 

The  treatment  of  developed  endocarditis  also  is  largely  that  of  the 
primary  disorder — in  rheumatic  cases  that  just  mentioned;  in  other 
cases,  that  of  the  initiating  pyococic,  gonococcic,  pneumococcic  infection, 
etc.  Should  it  be  possible  to  cultivate  the  provoking  microorganism 
from  the  blood,  a  vaccine  may  be  prepared  and  used  with  hope  of  good 
result.  The  serums  used  heretofore  have  not  been  especially  successful. 
Colloidal  silver  also  is  scarcely  to  be  recommended.  Indeed,  in  severe 
cases,  it  is  doubtful  if  any  measures,  aside  from  general  supportive, 
can  achieve  much  good.  In  the  event  of  palpitation  or  cardiac  distress 
an  ice-bag  should  be  applied  to  the  precordium,  or  aconite  may  be  used 
in  small  doses. 

CHRONIC  ENDOCARDITIS. 

Etiology. — ^Acute  endocarditis,  if  it  does  not  lead  to  death,  usually 
subsides  within  two  or  three  months,  and  leaves  the  cardiac  valves  per- 
manently damaged  (chronic  valvular  disease),  although  rarely  the 
lesions  may  be  limited  to  the  mural  endocardium.  In  a  few  cases,  how- 
ever, the  endocarditic  phenomena  are  protracted — for  many  months; 
and  in  many  cases,  having  become  more  or  less  quiescent,  they 
are  relighted  (recurring  or  relapsing  endocarditis).  The  etiological 
factors  in  these  chronic  cases  are  the  bacterial  agents  that  set  up  acute 
endocarditis;  but  the  later  attacks  in  the  recurring  cases  are  not  always 
provoked  by  the  bacterial  cause  of  the  primary  attack;  the  damaged 
valves  are  especially  vulnerable  to  the  attack  of  any  pathogenic  bacterium. 


CHRONIC  ENDOCARDITIS  451 

Pathology. — The  lesions  vary  much  in  different  cases.  In  most  cases 
(relapsing  form)  they  consist  of  the  various  lesions  more  particularly 
described  under  valvular  disease,  to  which  the  lesions  characteristic 
of  acute  endocarditis  are  added;  in  some  cases  to  the  deformity  of  the 
valve,  more  or  less  exuberant,  sometimes  rather  firm,  vegetations  are 
added ;  in  other  cases  there  are  more  or  less  superficial  or  deep  ulcerations. 

Symptoms. — The  symptoms  in  general  are  like  those  of  acute  endo- 
carditis, but  protracted  or  recurrent.  In  one  series  of  cases  (chronic 
recurrent  or  relapsing  endocarditis),  aside  from  the  symptoms  due  to  the 
associated  valvular  disease,  there  are  recurring  attacks  of  chills,  fever, 
and  sweats,  and  leukocytosis  (mild  septicopyemia),  with  intervening 
periods  of  good  health.  During  the  attack  the  cardiac  symptoms  may 
be  in  abeyance,  ot  those  previously  present  may  become  aggravated, 
and  the  embolic  phenomena  of  acute  endocarditis  may  supervene.  In 
another  series  of  cases  the  symptoms  are  continuous  from  the  beginning; 
they  do  not  differ  essentially  from  those  of  acute  endocarditis,  although 
perhaps  they  are  less  severe;  but  rarely  chills,  fever,  sweats,  and  leuko- 
cytosis may  last  for  months.  In  certain  rare  and  protracted  cases  per- 
sistent fever  (100°  to  102°)  is  the  characteristic  and  dominant  mani- 
festation; chills  and  sweats  are  much  less  common  than  in  the  acuter 
cases,  but  they  may  occur  from  time  to  time,  and  are  then  usually 
associated  with  an  added  increment  of  fever.  Occasionally,  after  the 
lapse  of  months,  the  lesions  may  subside  and  the  patient  become  apy- 
retic,  but  recurrence  of  the  symptoms  is  likely.  Rarely  there  is  a  slight 
cough  and  the  patient  may  emaciate  (suggesting  tuberculosis).  There 
are  usually  the  physical  signs  of  mitral  or  aortic  valve  disease,  although 
occasionally  for  long  periods  or  throughout  the  disease  there  may  be 
no  murmur  whatever.  Embolic  phenomena  occur,  but  they  are  less 
common  than  in  the  acuter  forms  of  the  disease. 

Diagnosis. — The  basis  of  a  diagnosis  is  the  same  as  that  of  acute 
endocarditis;  but  special  importance  attaches  to  the  knowledge  of  an 
old  valvular  disorder,  increase  in  the  size  of  the  heart,  changes  in  the 
character  of  the  cardiac  murmurs,  the  development  of  new  murmurs, 
embolic  phenomena,  recurring  attacks  of  fever,  etc.  In  cases  that 
present  little  else  than  persistent  fever  it  may  be  quite  impossible  for 
some  time  to  eliminate  typhoid  fever  or  tuberculosis.  A  blood  culture 
may  reveal  the  nature  of  the  infection.  Malaria  should  be  readily  ex- 
cluded. 

Prognosis. — The  prognosis  is  bad.  Rarely  cases  in  which  the  symp- 
toms continue  unabated  from  the  beginning  may  last  a  year  or  more. 
The  relapsing  cases  may  continue  for  several  years,  the  duration  being 
determined  by  the  periods  of  apyrexia,  the  permanent  damage  done 
to  the  cardiac  valves,  and  the  ensuing  changes  in  the  myocardium. 

Treatment. — The  treatment  is  that  of  acute  endocarditis  plus  that  of 
the  associated  valvular  disorder. 


452  DISEASES  OF  THE  ENDOCARDIUM 


CHRONIC  VALVULAR  DISEASE  OF  THE  HEART. 

Etiology. — Two  types  of  chronic  valvular  disease  of  the  heart  may  be 
distinguished:  (1)  The  chronic  inflammatory,  and  (2)  the  arterio- 
sclerotic or  atheromatous;  but  a  sharp  line  of  distinction  cannot  always 
be  drawn  between  them,  and  the  final  lesions  in  both  are  much  alike.  The 
first  or  chronic  inflammatory  type  most  frequently  involves  the  mitral 
valve,  is  most  common  in  young  subjects  and  in  women,  and  usually 
results  from  acute  endocarditis;  the  causes  of  the  one,  therefore,  are  the 
causes  of  the  other,  the  chronic  lesions  representing  the  results  of  healing 
of  the  acute  process.  In  a  minority  of  the  cases,  the  lesions  may  be 
chronic  from  the  beginning,  initiated  perhaps  by  the  toxins  of  attenuated 
microorganisms  or  by  certain  ill-understood  autotoxins.  The  second, 
arteriosclerotic  or  atheromatous  type,  most  frequently  involves  the 
aortic  valve,  is  most  common  in  male  adults,  and  occurs  with  increasing 
frequency  in  both  sexes  as  the  subjects  advance  in  years.  The  especially 
important  etiological  factors  are  alcoholism,  syphilis,  and  excessive  and 
long-continued  muscular  strain,  but  it  is  due  also  to  gout,  plumbism, 
chronic  nephritis,  diabetes,  and  the  divers  other  factors  related  causally 
to  arteriosclerosis  and  high  arterial  tension.  In  some  cases,  especially 
of  mitral  valve  disease,  no  etiological  factor  can  be  determined  with 
certainty.  A  few  cases,  especially  of  aortic  valve  disease,  are  apparently 
traumatic  in  origin,  developing  in  consequence  of  sudden  undue  muscular 
strain,  severe  contusions  or  compression  of  the  chest,  etc.,  which  lead 
directly  to  rupture  of  a  valvular  leaflet.  Heredity  seems  to  play  a  role 
in  some  cases.  Lesions  of  the  right  heart  are  usually  congenital.  Acute 
lesions  are  not  infrequently  superadded  to  the  chronic:  this  may  be  a 
frank  acute,  more  or  less  severe  (or  malignant)  endocarditis,  due  usually 
to  the  pyococci ;  or  it  may  be  the  relighting  of  a  more  or  less  quiescent  or 
obsolete  infection  (recurring  or  relapsing  endocarditis). 

Pathology .^ — ^Among  1058  cases  collected  by  Parrot,  the  mitral  valve 
was  involved  in  621  (58.7  per  cent.),  the  aortic  in  380  (36  per  cent.), 
the  tricuspid  in  46  (4.3  per  cent.),  and  the  pulmonary  in  11  (1  per  cent.); 
the  left  side  of  the  heart  in  1001  (94.7  per  cent.),  the  right  side  of  the 
heart  in  57  (5.3  per  cent.).  In  minor  or  slight  cases  the  lesions  consist 
of  opacity,  or  of  slight,  perhaps  nodular,  thickening  and  induration  near 
the  free  margin  of  the  valve  leaflets,  just  within  the  margin  in  mitral 
and  tricuspid  disease,  and  about  the  corpora  aurantii  in  aortic  disease; 
these  may  be  interpreted  as  the  results  of  so-called  organization  of  the 
acute  vegetations,  or  as  the  analogue  of  the  early  changes  of  arteriosclero- 
sis (which  may  be  associated).  The  body  of  the  valve  leaflets  may  reveal 
grayish-white  opacities  or  yellowish  areas  of  fatty  degeneration.  The 
newly  formed  fibrous  tissue,  of  which  the  opacities  and  thickenings  are 
made  up,  gradually  undergoes  contraction  and  leads  to  varying  degrees 
of  curling  or  puckering  of  the  edge  of  the  leaflets,  or  of  stiffness,  indura- 
tion, shortening,  and  deformity  of  the  leaflets  as  a  whole.     On  account  of 


CHRONIC  VALVULAR   DISEASE  OF  THE  HEART  453 

the  consequent  lack  of  resiliency  the  leaflets  do  not  approximate  properly, 
or  on  account  of  shortening,  they  do  not  approximate  at  all,  and  the 
condition  known  as  insufficiency  of  the  valve  ensues.  In  the  case  of 
the  auriculoventricular  (mitral)  valve  this  is  often  due  to  or  augmented 
by  involvement  in  the  sclerotic  and  contracting  process  of  the  chordae 
tendinene  and  tips  of  the  papillary  muscles.  In  the  course  of  time  the 
adjacent  edges  of  the  leaflets  often  become  adherent,  in  consequence  of 
which  their  movement  is  still  further  restricted,  and  not  receding  as  they 
should  normally,  they  oppose  a  barrier  to  the  onward  movement  of 
the  blood^-so-called  stenosis  or  obstruction.  Calcium  salts  frequently 
become  deposited  in  the  sclerotic  and  necrotic  tissues,  and  add  to  the 
already  existing  rigidity  of  the  leaflets.  In  advanced  cases  the  normal 
tissues  of  the  valves  may  be  entirely  replaced  by  a  firm,  fibrous,  resistant 
calcareous  mass  capable  of  scarcely  any  movement,  so  that  the  valves 
are  insufficient  and  the  orifice  stenosed.  The  lesions  sometimes  spread 
from  the  valves  to  the  mural  endocardium ;  rarely  the  mural  endocardium 
alone  is  involved,  a  larger  or  smaller  indurated,  cicatricial,  and  perhaps 
calcareous  patch  being  present.  Superadded  to  the  chronic,  acute 
lesions  are  sometimes  found.  Hypertrophy  and  dilatation  of  the  heart, 
varying  grades  of  myocarditis,  and  coronary  sclerosis  are  almost  constant 
concomitants. 

Pathological  Physiology. — The  heart  and  bloodvessels  are  so  adjusted 
to  the  actual  and  potential  work  required  of  them,  that  in  health  and 
under  the  stress  of  unusual  temporary  functional  demands,  the  required 
work  is  performed  without  discomfort  to  the  patient.  Sudden  increased 
demands,  such,  for  instance,  as  are  developed  during  strenuous  exercise, 
lifting  unusually  heavy  weights,  etc.,  are  met  with  increased  rapidity  of 
the  heart  action;  often  slight  dilatation  of  the  heart  ensues,  but  being 
well  within  the  limits  of  the  so-called  reserve  power  of  the  heart,  no 
serious  consequences  ensue;  with  the  accomplishment  of  the  work  the 
dilatation  subsides  and  the  heart's  action  returns  to  the  normal.  Should 
the  demands  be  more  continuous,  although  perhaps  less  onerous,  the 
heart  responds,  as  does  the  musculature  throughout  the  body,  by  hyper- 
trophy, and  the  persisting  dilatation  that  otherwise  would  ensue  is 
counteracted,  the  equilibrium  of  the  circulation  is  maintained:  the  lesion 
is  said  to  be  compensated.  In  valvular  disease,  in  consequence  either 
of  orificial  obstruction  to  the  onward  flow  of  the  blood  or  of  insufficiency 
of  valves  permitting  regurgitation  of  the  blood,  the  primary  dilatation 
and  consecutive  hypertrophy  involve  first  that  chamber  of  the  heart  im- 
mediately back  of  the  valve  or  orifice  affected — the  auricle  in  mitral  and 
tricuspid  valve  disease,  and  the  ventricle  in  aortic  or  pulmonary  valve 
disease.  Hypertrophy  may  not  develop  when  the  myocardium  lias  be- 
come enfeebled  in  consequence  of  long-continued  fever,  general  debilitat- 
ing conditions,  such  as  marked  anemia,  diabetes,  carcinoma,  amyloidosis, 
flbroid  degeneration,  etc.  The  hypertrophy  when  it  does  occur  is 
sufficient  to  maintain  the  equilibrium  of  the  circulation  for  a  longer  or 
shorter  period,  but  it  is  not  permanently  efficient;  to  the  hypertrophy 


454  DISEASES  OF  THE  ENDOCARDIUM 

dilatation  is  gradually  added,  and  as  the  dilatation^  in  consequence  of 
insufficient  nourishment  and  consecutive  degeneration  of  the  hyper- 
trophied  myocardium,  assumes  the  ascendency,  the  period  of  compensa- 
tion is  supplanted  by  a  period  of  unstable  compensation,  and  finally  by  a 
period  of  failure  or  lack  of  compensation  (decompensation).  During 
the  period  of  compensation  the  valvular  disorder  is  disclosed  only  by  its 
physical  signs  or  by  a  lessened  ability  on  the  part  of  the  heart  to  respond 
to  unusual  demands  without  discomfort  to  the  subject  (dyspnoea,  cyan- 
osis, palpitation  of  the  heart,  etc.) ;  this  the  consequence  of  lessened  reserv^e 
power.  Gradually,  as  the  myocardium  becomes  enfeebled,  it  becomes 
less  able  to  withstand  the  vicissitudes  of  ordinary  life,  and  it  dilates. 
The  ensuing  loss  of  compensation  may  develop  suddenly  and  rapidly 
lead  to  death;  usually  it  is  of  gradual  onset  and  progressive;  it  may  be 
temporary  or  permanent.  For  a  time  the  heart  is  manifestly  adequate 
to  meet  the  demands  of  quiet  life,  but  more  or  less  distress  (dyspnoea, 
cough,  cyanosis,  palpitation  of  the  heart,  precordial  pain,  vertigo,  faint- 
ness,  slight  and  transient  oedema  about  the  ankles,  etc.)  ensues  upon 
exertion,  excitement,  a  full  meal,  etc. ;  but  the  symptoms  subside  upon  the 
restoration  of  quiet:  the  compensation  is  unstable.  Sooner  or  later  the 
heart  becomes  unable  to  maintain  the  equilibrium  of  the  circulation 
even  when  the  body  is  at  rest;  the  aforementioned  symptoms  become 
more  or  less  permanent :  the  compensation  is  lost.  This  condition  may 
eventuate  in  death;  but  in  many  cases  the  symptoms  gradually  subside 
temporarily,  and  are  followed  by  recurring  relapses  and  partial  or  more 
or  less  complete  recoveries. 

The  first  evidences  of  this  failure  of  compensation  are  manifest  in  that 
part  of  the  cardiovascular  system  immediately  back  of  the  chamber 
of  the  heart  primarily  involved :  in  valvular  disease  of  the  left  side  of  the 
heart,  therefore,  in  the  lungs;  but  in  most  cases  the  lungs  have  been  for 
some  time  engorged,  so  that  speedily  the  congestive  and  other  disturb- 
ances become  manifest  in  the  general  venous  system  throughout  the  body. 
At  the  same  time,  failure  of  compensation  becomes  apparent  in  front  of 
the  lesion  in  a  lessened  and  irregular  blood  supply.  The  evidences 
of  lack  of  compensation,  then,  are  disclosed  not  so  much  by  the  physical 
signs  referable  to  the  heart,  although  these  are  important,  as  by  the 
evidences  of  general  venous  and  capillary  stasis  and  a  small,  weak,  fre- 
quent, and  irregular  pulse. 

The  ordinary  mechanism  of  valvular  insufficiency  and  stenosis  is  that 
already  described.  Under  other  circumstances,  however,  the  valvular 
orifices  dilate,  and  normal  leaflets  become,  therefore,  incompetent  to 
close  the  enlarged  orifice — a  condition  spoken  of  as  relative  insufficiency, 
and  very  common  at  the  mitral  and  tricuspid  orifices.  It  doubtless  occurs, 
but  is  very  rare,  at  the  aortic  and  pulmonary  orifices.  Relative  ob- 
struction (or  stenosis)  is  occasionally  produced  by  exuberant  vegetations, 
ball-valve  thrombus,  aneurysmal  dilatation  of  a  leaflet,  etc.;  and  a  condi- 
tion sometimes  spoken  of  as  relative  stenosis  ensues  when  the  cavities 


CHRONIC  VALVULAR  DISEASE  OF  THE  HEART  455 

become  much  dilated  while  the  orificial  ring  remains  normal  or  is  rela- 
tively only  slightly  enlarged. 

Mitral  Insufficiency. — Mitral  insufficiency  is  the  commonest  lesion, 
occurring  alone  in  about  30  per  cent,  or  more  of  the  cases;  mitral  stenosis 
occurs  in  about  16  per  cent.,  and  both  lesions  in  about  12  per  cent. 

Etiology. — Mitral  insufficiency  may  result  from  one  of  three  factors: 
(1)  Acute  or  chronic  endocarditis.  This  is  the  common  cause  of  the 
disorder  in  young  persons;  usually  it  is  a  sequel  of  rheumatism,  "growing 
pains,"  chorea,  scarlatina,  and  other  infections.  The  mitral  leaflets 
may  be  thickened,  indurated,  curled  up  at  the  edge,  or  everted,  and  con- 
tracted or  puckered  (the  contraction  and  thickening  may  also  involve 
the  chordae  tendinese),  so  that  the  leaflets  cannot  be  approximated;  or 
more  or  less  of  one  or  both  leaflets  and  the  adjacent  chordae  tendinese 
may  be  eroded  or  destroyed;  rarely  a  leaflet  may  be  perforated.  In 
some  cases  the  adjacent  margins  of  the  leaflets  become  adherent,  and 
as  the  newly  formed  connective  tissue  contracts,  the  leaflets  are  drawn 
together,  so  that  to  the  insufficiency  obstruction  is  added.  Acute  lesions 
are  not  uncommon  (recurring  or  relapsing  endocarditis).  (2)  Slowly 
progressing  sclerosis,  analogous  to  arteriosclerosis.  This  is  a  less  common 
form;  it  is  due  to  the  ordinary  causes  of  arteriosclerosis,  and  is  found 
in  adults  and  elderly  persons.  The  leaflets  and  the  chordae  tendinea? 
are  usually  thickened  and  contracted,  and  the  seat  of  more  or  less  well- 
marked  atheroma  with  calcification.  Associated  obstruction  is  not 
uncommon  (12  per  cent,  of  the  cases).  Minor  grades  of  atheroma 
of  the  mitral  valve  are  common  in  persons  upward  of  sixty  years  of  age, 
but  usually  do  not  lead  to  valvular  defects.  (3)  Dilatation  of  the  mitral 
ring.  This,  so-called  relative  or  muscular  insufficiency,  is  perhaps  the 
commonest  form.  It  is  found  in  a  wide  variety  of  disorders  in  which 
the  myocardium  becomes  reduced  in  tone  and  permits  of  such  dila- 
tation of  the  mitral  ring,  and  usually  also  of  the  left  ventricle,  that  the 
normal  mitral  leaflets  are  unable  to  close  the  orifice:  anemic  conditions, 
infectious  fevers,  hypertrophy  and  dilatation  of  the  heart,  aortic  valve 
disease,  arteriosclerosis,  chronic  nephritis,  chronic  myocarditis,  nervous 
disorders,  such  as  exophthalmic  goitre,  etc. 

Pathological  Physiology. — In  consequence  of  incompetency  of  the 
mitral  valve,  a  portion  of  the  ventricular  blood,  varying  in  amount  with 
the  degree  of  incompetency,  is  returned  to  the  left  auricle  during  the 
ventricular  systole,  that  is,  at  a  time  when  the  auricle  in  diastole  is 
receiving  blood  normally  from  the  lungs.  The  immediate  result  of  this 
is  an  abnormal  rise  of  the  intra-auricular  pressure  toward  the  end  of 
auricular  diastole  and  consequent  dilatation  of  the  left  auricle.  The 
tension  and  stretching  to  which  the  auricular  musculature  is  thus  sub- 
jected  stimulate  it  to  vigorous  contractions,  in  an  effort  to  expel  the 
augmented  amount  of  blood,  and  the  constant  recurrence  of  the  stimu- 
lus ultimately  induces  more  or  less  hypertrophy.  The  regurgitating 
stream  impedes  the  flow  of  blood  from  the  pulmonary  veins  into  the  left 
auricle  and  leads  immediately  to  stasis  in  the  })ulmonary  circulation — 


456  DISEASES  OF   THE  ENDOCARDIUM 

since  the  pulmonary  veins  are  unprovided  with  valves,  and  the  supposed 
constriction  of  the  musculature  at  the  insertion  of  the  pulmonary  veins 
into  the  auricle  cannot  long  remain  active  or  oppose  an  effective  barrier 
to  back  pressure  into  the  lungs.  The  increased  pulmonary  pressure  acts 
as  an  obstruction  to  the  movement  of  blood  from  the  right  heart  and 
stimulates  the  right  ventricle  to  more  vigorous  contractions  and  soon 
leads  to  hypertrophy — which  is  the  effective  factor  in  maintaining  com- 
pensation. The  increased  volume  of  blood  injected  into  the  left  ventricle 
with  each  auricular  contraction  leads  to  a  corresponding  dilatation  of 
the  left  ventricle;  this,  in  turn,  is  followed  by  more  vigorous  contractions 
in  an  effort  to  discharge  the  augmented  volume  of  blood,  so  that  ulti- 
mately some  hypertrophy  of  the  left  ventricle  ensues,  but  in  uncom- 
plicated mitral  insufficiency  this  is  rarely  marked.  So  long  as  the 
hypertrophy  of  the  right  ventricle  remains  efficient,  the  mitral  lesion  is 
compensated  and  the  patient  may  not  suffer  any  distress.  Sooner  or  later, 
however,  the  musculature  weakens  and  dilates,  either  in  consequence 
of  myocardial  degeneration  or  of  increase  in  the  mitral  lesion;  and 
relative  insufficiency  of  the  tricuspid  valve  ensues.  The  back  pressure 
then  is  communicated  to  the  right  auricle  and  the  liver  and  the  general 
venous  svstem.  In  mitral  insufficiency  the  lungs  are  always  engorged, 
and  ultimately  the  condition  of  cyanotic  induration  develops  (congestion 
and  dilatation  of  the  bloodvessels,  hemorrhages,  pigmentation,  and  fibro- 
sis); the  larger  pulmonary  vessels  may  exhibit  atheromatous  changes. 
When  the  back  pressure  finally  involves  the  general  venous  circulation, 
passive  congestion  ensues,  and  in  the  course  of  time  leads  to  oedema 
of  the  subcutaneous  tissues,  chronic  catarrh  of  mucous  surfaces,  cyanotic 
induration  of  solid  organs,  transudates  in  the  serous  cavities,  etc. 

Symptoms. — -Well-compensated  mitral  insufficiency  may  be  disclosed 
only  by  a  physical  examination  of  the  heart;  there  may  be  no  subjective 
symptoms  whatever,  although  usually  some  little  embarassment  of  respi- 
ration and  hurried  action  of  the  heart  ensue  upon  sudden  or  severe 
exertion,  such  as  hill  climbing,  ascending  stairs,  or  strenuous  exercise. 
In  the  majority  of  cases,  however,  the  patient,  although  not  seriously 
embarassed  during  ordinary  activities,  is  made  aware  of  his  cardiac 
deficiency  upon  any  unusual  exertion;  others  may  lead  a  quiet  life  with 
comfort,  but  even  minor  activities  induce  cardiac  distress-^which  ex- 
erts its  chief  effects  on  the  pulmonary  circulation,  and  becomes  mani- 
fest in  palpitation  of  the  heart,  precordial  distress,  dyspnoea,  and  slight 
cyanosis  of  the  cheeks,  lips,  ears,  and  finger  tips.  The  congestion  of  the 
lungs  disposes  to  attacks  of  bronchitis,  which  are  readily  induced  by 
seasonal  and  climatic  changes,  and  to  attacks  of  hemoptysis  (less  fre- 
quent than  in  mitral  stenosis).  In  long-standing  cases  that  develop  in 
youth,  the  finger  tips  tend  to  become  clubbed. 

Sooner  or  later  the  heart  begins  to  fail,  more  or  less  complete,  temporary 
or  permanent,  loss  of  compensation  ensues;  the  passive  congestion  of  the 
lungs  becomes  more  marked,  and  to  this  is  added  the  evidences  of  general 
venous  and  capillary  stasis.     The  patient  complains  of  palpitation,  and 


CHRONIC   VALVULAR   DISEASE  OF   THE   HEART  457 

the  heart  action  becomes  rapid,  irregular,  and  weak.  ]\Iore  or  less  cyan- 
osis develops.  Dyspnoea,  cough,  and  perhaps  expectoration  are  expres- 
sions of  the  increased  pulmonary  engorgement;  the  expectoration  is 
usually  mucous,  sometimes  watery  or  serous,  occasionally  streaked  with 
blood;  usually  it  contains  pigmented  alveolar  epithelial  cells  (so-called 
heart  disease  cells).  The  congestion  of  the  liver  (enlarged  and  tender)  may 
lead  to  slight  jaundice  or  lend  a  subicteric  hue  to  the  conjunctivte  and  the 
skin.  Dropsical  effusions  supervene,  at  first  in  the  subcutaneous  tissues 
in  the  dependent  portions  of  the  body.  For  a  time  they  are  transitory, 
developing  during  the  day  when  the  patient  is  up  and  about,  and  dis- 
appearing when  he  is  in  bed ;  but  they  soon  become  more  or  less  perma- 
nent, although  fluctuating;  they  may  mvolve  the  general  subcutaneous 
tissues  (anasarca),  and  may  occur  also  in  the  serous  cavities  of  the  body. 
The  right  pleura  is  most  frequently  involved — four  or  five  times  as  fre- 
quently as  the  left,  and  when  there  is  bilateral  involvement,  the  collec- 
tion of  fluid  is  usually  greater  in  the  right  side.  This  was  attributed  by 
Steele  and  Stengel  to  pressure  on  the  azygos  veins  by  the  dilated  right 
auricle;  more  recently  Fetterolf  and  Landis,  stating  their  belief  that  the 
fluid  comes,  not  from  the  parietal,  but  from  the  visceral  pleura,  attribute 
the  pressure  factor  to  compression  and  partial  occlusion  of  the  pulmonary 
veins  by  dilated  portions  of  the  heart — dilatation  of  the  right  auricle  in 
right-sided  transudations,  and  dilatation  of  the  left  auricular  appendix 
and  of  the  left  ventricle,  and  perhaps  also  retrodisplacement  of  the 
ventricular  septum,  in  left-sided  transudations.  The  urine  becomes 
reduced  in  amount  and  contains  a  trace  of  albumin  and  often  erythro- 
cytes and  tube  casts.  Insomnia,  often  distressing,  and  perhaps  slight 
delirium  at  night  may  develop.  Usually  there  are  recurring  attacks 
of  such  failure  of  compensation;  under  appropriate  treatment  the 
patient  recovers  and  may  again  enjoy  good  health.  Eventually,  how- 
ever, compensation  becomes  permanently  lost  and  the  patient  dies  of 
gradually  increasing  cardiac  weakness  and  dilatation;  but  sudden  death 
may  ensue. 

Physical  Signs. — Depending  upon  the  youth  of  the  subject  when  the 
disorder  developed  and  the  degree  of  hypertrophy  of  the  right  ventricle, 
there  is  more  or  less  bulging  of  the  precordium;  the  cardiac  impulse 
is  forcible  and  widespread,  often  especially  conspicuous  toward  the 
sternum  or  in  the  epigastrium;  the  apex  beat  (the  palpable  beat  farthest 
outward  and  downward)  is  displaced  outward  transversely  (usually 
not  downward  in  uncomplicated  mitral  valve  disease);  it  is  of  in- 
creased breadth  and  not  infrequently  somewhat  heaving  in  character. 
A  systolic  thrill  may  be  palpable  at  the  apex,  and  sometimes  the  forcible 
closure  of  the  pulmonary  valve  may  be  palpable  in  the  j^ulmonary  area 
as  a  diastolic  shock.  The  deep  (and  the  superficial)  cardiac  dulness 
is  increased  transversely — somewhat  to  the  left,  but  mostly  to  the  right, 
forming  a  transverse  oval  that  may  extend  one  to  two  inches  or  more  to 
the  right  of  the  sternum.  Sometimes  there  is  an  increase  of  the  (hilness 
upward  and  outward  from  the  left  edge  of  the  sternum — attributable  to 


458  DISEASES  OF  THE  ENDOCARDIUM 

enlargement  of  the  left  auricle  (but  enlargement  of  the  left  auricle  is 
usually  predominantly  fore  and  aft,  and  usually  causes  little  if  any  in- 
crease in  dulness  upward).  At  the  apex  a  systolic  murmur  is  usually 
audible — soft  and  blowing  in  character  and  low  pitched,  but  it  may 
be  harsh  and  high  pitched  or  musical ;  it  may  partly  or  completely  replace 
the  first  sound;  it  may  be  audible  only  in  the  early  part  of  systole  (when 
it  often  progressively  diminishes  in  intensity),  or  it  may  continue  through 
the  entire  systole;  its  point  of  maximum  intensity  is  usually  directly 
over  the  apex  (transmitted  through  the  contracted  left  ventricular 
musculature);  it  is  often  transmitted  to  the  axilla  and  the  angle  of  the 
scapula  (which  is  not  of  much  importance  diagnostically) ;  rarely  it  is 
heard  best  along  or  near  the  left  edge  of  the  sternum,  or  in  the  fourth 
or  the  third,  sometimes  the  second,  interspace  (pulmonary  area) — in 
consequence  of  the  direction  of  the  blood  current  and  of  the  auricle 
being  in  close  contact  with  the  chest;  rarely  it  is  heard  best  in  the  back 
between  the  scapulse;  it  is  often  loudest  when  the  patient  is  recumbent; 
sometimes  it  is  heard  only  when  he  is  recumbent.  The  pulmonic  second 
sound  is  accentuated,  sometimes  reduplicated.  The  pulse  during 
compensation  is  not  characteristic;  it  is  full  and  regular,  although 
perhaps  of  low  tension.  Occasionally  in  extreme  insufficiency  with 
considerable  ventricular  hypertrophy  a  pulmonary  pulsation,  a  diffuse 
systolic  expansion  of  the  lungs  (analogous  to  the  liver  pulsation  of 
tricuspid  insufficiency),  may  be  palpable.  With  failure  of  compensation, 
the  pulse  becomes  small,  frequent,  and  irregular;  the  physical  signs 
of  cardiac  dilatation  assume  the  ascendency;  the  systolic  murmur 
changes  in  character,  lessens  in  intensity  or  disappears  entirely,  or 
perhaps  is  audible  only  during  the  stronger  systoles  that  characterize 
the  arrhythmia;  the  pulmonary  second  sound  loses  its  accentuation, 
and  the  signs  of  relative  tricuspid  insufficiency,  general  venous  engorge- 
ment, and  oedema  develop. 

Diagnosis. — The  characteristic  diagnostic  signs  consist  of  enlarge- 
ment of  the  right  ventricle,  a  systolic  thrill  and  a  systolic  murmur  at  the 
apex,  and  an  accentuated  pulmonic  second  sound.  Relative  mitral 
insufficiency  is  to  be  differentiated  from  organic  insufiiciency,  not  by 
the  physical  signs,  which  may  be  alike  in  both,  but  by  the  antecedent 
conditions  and  associated  phenomena,  by  the  presence  of  an  adequate 
causative  factor  to  give  rise  to  dilatation  of  the  heart  and  a  relative  mitral 
insufficiency,  and  by  the  disappearance  of  the  murmur  with  improve- 
ment in  the  condition  of  the  heart  (lessening  of  the  area  of  dulness,  and  of 
dilatation,  and  increase  of  vigor).  The  systolic  murmur  of  aortic  stenosis 
is  sometimes  very  loud  at  the  apex,  but  it  is  loud  also  at  the  aortic  area 
and  is  propagated  into  the  carotid  artery,  and  it  is  associated  with  the 
other  distinctive  signs  of  aortic  stenosis.  Difficulty  is  not  infrequently 
experienced  in  differentiating  so-called  functional,  inorganic,  accidental, 
or  hemic  murmurs,  as  well  as  certain  exocardial,  cardiorespiratory, 
sounds.  While  it  is  true  that  the  so-called  functional  murmurs  are 
usually  soft  and  blowing  in  character,  are  heard  best,  as  a  rule,  in  the 


CHRONIC  VALVULAR  DISEASE  OF  THE  HEART  459 

pulmonary  area,  and  are  not  far  transmitted,  they  often  of  themselves 
are  not  distinguishable  from  organic  murmurs;  the  diagnosis  is  to  be 
based  less  upon  the  character  of  the  murmur  than  upon  the  concomi- 
tant physical  signs,  such  as  hypertrophy  of  the  heart  and  accentuated 
sounds,  on  the  one  hand,  and  fever,  anemia,  etc.,  on  the  other  hand; 
and  the  disappearance  of  the  murmur  with  the  subsidence  of  the  fever, 
anemia,  etc.  The  cardiorespiratory  murmurs  are  usually  heard  along 
the  left  border  of  the  heart,  are  soft  and  blowing  in  character,  often 
loudest  at  the  height  of  inspiration,  and  disappear  when  the  patient 
stops  breathing.  In  most  cases  of  valvular  lesion,  in  fact,  one  may  elicit 
almost  if  not  quite  conclusive  evidence  of  the  valvular  disorder  without 
any  attention  to  the  presence  or  absence  of  a  murmur  whatever. 

Mitral  Stenosis. — Mitral  stenosis  occurs  in  about  16  per  cent,  of 
the  cases  of  valvular  disease,  and  double  mitral  disease  in  about  12  per 
cent.,  so  that  mitral  obstruction  occurs  in  a  total  of  28  per  cent. 

Etiology. — Mitral  stenosis  may  be  due  to:  (1)  Endocarditis,  in  which 
event  it  is  especially  common  in  adolescents,  and  young  adults,  as  a  sequel 
of  rheumatism,  "growing  pains,"  chorea,  scarlatina,  and  other  infections; 
and  (2)  slowly  progressing  sclerosis,  analogous  to  arteriosclerosis,  a 
form  encountered  in  later  life,  and  in  men  as  well  as  in  women.  In 
many  cases,  especially  in  adult  women,  no  etiological  factor  can  be 
determined  with  certainty — which  has  led  some  observers,  perhaps  too 
frequently,  to  believe  them  congenital.  Two  forms  of  the  disease 
may  be  distinguished:  in  the  one,  found  especially  in  young  persons, 
the  leaflets,  perhaps  only  slightly  thickened,  have  become  adherent 
at  their  edges,  and  the  chordae  tendinese  somewhat  thickened,  short- 
ened and  fused,  so  that  the  valve  viewed  from  the  auricle  seems  to 
have  become  converted  into  a  hollow  cone — the  so-called  funnel-shaped 
mitral  valve.  In  the  second  variety,  more  common  in  adults,  the  leaflets 
are  much  thickened,  indurated,  perhaps  calcified,  and  distorted,  and  are 
represented  by  a  rigid,  often  atheromatous,  mass  of  tissue  exhibiting  a 
central  linear  slit,  admitting  perhaps  only  the  tip  of  the  little  finger — the 
so-called  button-hole  mitral  valve.  The  mitral  ring  is  often  converted 
into  a  fibrous  or  calcareous  ring,  the  chordse  muscles  are  shortened  and 
thickened,  the  papillary  muscles  even  may  be  inserted  directly  into  the 
edge  of  the  leaflets.  In  both  varieties  there  is  practically  always  an 
associated  mitral  insufficiency;  rarely  perhaps  in  the  first-mentioned 
variety,  when  the  leaflets  are  pliable,  there  may  be  a  pure  mitral  stenosis. 
(3)  A  relative  obstruction  (or  stenosis)  is  occasionally  produced  by 
exuberant  vegetations,  ball-valve  thrombus,  aneurysmal  dilatation 
of  the  leaflets,  etc.,  and  a  condition  sometimes  spoken  of  as  relative 
stenosis  ensues  when  the  cavities  become  much  dilated,  while  the  ori- 
ficial  ring  remains  normal  or  is  relatively  slightly  enlarged. 

Pathological  Physiology. — In  mitral  stenosis  the  morbid  phenomena 
are  much  like  those  in  mitral  insufficiency.  There  is  a  similar  increase 
in  the  intra-auricular  pressure  toward  the  end  of  auricular  diastole, 
due  to  the  blood  from  the  lungs  flowing  into  an  insufficiently  emptied 


460  DISEASES  OF  THE  ENDOCARDIUM 

auricle;  the  consequent  dilatation  and  stretching  excite  the  auricle  to 
very  vigorous  contractions,  which  become  augmented  in  consecjuence 
of  the  obstruction  to  the  discharge  of  blood.  The  result  is  an  extraor- 
dinary enlargement  (hypertrophy  and  dilatation)  of  the  left  auricle, 
which  may  attain  dimensions  three  or  four  times  the  normal  (to  200  c.c. 
or  more).  Increased  intrapulmonary  pressure  is  followed  by  hyper- 
trophy and  dilatation  of  the  right  ventricle,  which  as  in  mitral  insuffi- 
ciency is  the  efficient  factor  in  maintaining  compensation.  In  some 
cases,  for  a  time  at  least,  the  increased  power  of  the  left  auricle  serves 
to  supply  a  normal  amount  of  blood  to  the  left  ventricle,  which  in  con- 
sequence presents  no  noteworthy  deviations  from  the  normal.  In  many 
cases,  however,  on  account  of  associated  mitral  insufficiency,  the  left 
ventricle  is  somewhat  enlarged;  in  most  cases  the  amount  of  blood 
supplied  to  the  left  ventricle  is  less  than  normal,  in  consequence  of  which 
it  is  often  said  to  become  reduced  in  size  (this  is  more  apparent  than 
real).  Perhaps  in  primary  or  uncomplicated  mitral  stenosis  the  left 
ventricle  does  lessen  in  size,  but  the  tendency  in  this  direction  is  usually 
counteracted  by  the  primary  and  usually  associated  mitral  insufficiency. 
The  final  breakdown  and  the  visceral  and  other  consecutive  changes 
are  similar  to  those  that  develop  in  mitral  insufficiency. 

Symptoms. — The  disease  is  not  incompatible  with  many  years  of  life 
and  comparative  freedom  from  distress.  Symptoms  when  they  do  de- 
velop are  not  to  be  sharply  differentiated  from  those  of  mitral  insuffi- 
ciency, although  they  are  likely  to  be  more  marked  or  more  readily 
provoked.  Cyanosis  usually  is  of  a  higher  grade,  and  often  gives  rise 
to  a  peculiar  "mitral  facies"  that  of  itself  suggests  the  diagnosis; 
dyspnoea  is  more  readily  induced  by  exertion  and  excitement;  hemopty- 
sis is  more  frequent  and  more  easily  provoked;  and  attacks  of  bronchitis 
are  more  prone  to  develop.  Precordial  pain  and  distress  is  often  an 
obstrusive  and  sometimes  an  intractable  symptom.  Recurring  endo- 
carditis is  quite  common,  and  may  be  the  cause  of  otherwise  inexplicable 
attacks  of  fever  and  leukocytosis.  The  vegetations  disintegrating  are 
often  carried  into  the  circulation  and  set  up  embolism  in  different  parts 
of  the  body,  notably  in  the  brain,  where  they  may  give  rise  to  aphasia, 
hemiphlegia,  etc.;  but  also  elsewhere.  Paralysis  of  the  left  vocal  cord 
(simulating  aneurysm)  occasionally  results  from  pressure  on  the  recur- 
rent laryngeal  nerve  by  the  dilated  left  auricle.  The  disorder  developing 
in  early  life  may  lead  to  stunting  of  the  bodily  growth.  Recurring  attacks 
of  failure  of  compensation  are  perhaps  more  common  than  in  mitral  in- 
sufficiency. Compensation  usually  becomes  reestablished,  but  eventually 
more  or  less  complete  failure  ensues,  and  the  decompensation  phenomena 
mentioned  in  connection  with  mitral  insufficiency  develop. 

Physical  Signs. — The  signs  of  hypertrophy  of  the  right  ventricle  are 
the  same  as  those  in  mitral  insufficiency  (which  is  often  associated  and 
presents  its  own  diagnostic  signs).  In  mitral  stenosis,  perhaps,  there 
is  more  enlargement  of  the  right  ventricle;  the  left  auricle  also  is  usually 
more  enlarged,  and  may  perhaps  present  some  percussion  evidence  of 


CHRONIC   VALVULAR   DISEASE  OF   THE  HEART  461 

this  in  duln-ess  upward  and  to  the  left;  but  commonly  this  is  not  found, 
since  the  increase  in  the  size  of  the  left  auricle  is  usually  predominantly 
anteroposterior.  Occasionally  there  is  impaired  resonance  in  the  left 
infraclavicular  fossa,  due  perhaps  to  compression  of  the  lung  by 
the  dilated  left  auricle;  in  other  cases  the  enlarged  auricle  may  occa- 
sion some  dulness  in  the  left  interscapular  region.  At  the  apex  a 
diastolic  or  presystolic  thrill  is  commonly  palpable,  and  usually  followed 
by,  or  the  thrill  ends  in,  a  quick,  thumping,  or  tapping  apex  beat.  The 
murmur  of  mitral  stenosis,  which  is  often  limited  to  a  small  area  near 
the  apex,' but  is  not  infrequently  audible  over  a  considerable  area  about 
the  apex,  is  diastolic  in  time;  it  may  occur  during  any  part  of  the  diastole 
or  throughout  the  entire  diastole.  Perhaps  the  commonest  is  the 
interrupted  diastolic  murmur  (so-called  Fraentzel  murmur),  a  murmur 
louder  at  the  beginning  and  the  end  of  diastole  than  during  the  mid- 
period  (a  mid-diastolic  diminuendo  and  presystolic  crescendo  murmur); 
this  is  due  doubtless  to  the  greater  quickness  of  the  flow  of  blood  at  the 
beginning  of  diastole  than  during  the  mid-period,  and  an  increased 
acceleration  at  the  end  of  diastole  occasioned  by  the  contraction  of  the 
auricle.  The  next  most  common  murmur  is  the  definitely  late-diastolic 
(or  presystolic)  rough,  rumbling,  crescendo  murmur;  then  a  simple 
diastolic  murmur,  or  a  continuous  murmur  occupying  the  entire  diastole 
and  the  long  pause.  There  may  also  be  a  double  diastolic  tone  at  the 
apex  (bruit  de  rappel,  Bouillard),  which  under  excitement  may  be 
replaced  by  a  double  murmur,  or  a  sound  and  a  murmur.  A  loud, 
sharp,  snappy  first  sound  at  the  apex  is  quite  characteristic  of  mitral 
stenosis,  and  in  the  absence  of  a  murmur  (but  associated  with  the  other 
signs)  suffices  for  the  diagnosis.  It  is  best  explained  as  due  to  differences 
greater  than  the  normal  in  the  tension  of  the  mitral  leaflets  at  the  begin- 
ning and  the  end  of  systole  (closure-time).  These  auscultatory  signs 
vary  much  from  time  to  time,  being  much  influenced  by  quietness  and 
excitement  and  by  strength  and  weakness  of  the  heart  muscle.  The 
pulmonary  second  sound  is  accentuated  or  reduplicated.  The  pulse 
is  small  and  irregular,  due  to  incomplete  filling  of  the  ventricle.  When 
the  heart  fails  the  murmur  may  disappear  (auricular  paralysis)  and 
the  second  sound  at  the  apex  become  inaudible,  so  that  only  the  loud 
first  sound  may  be  heard  at  the  apex;  to  which,  however,  are  usually 
added  the  signs  of  tricuspid  regurgitation,  and  the  general  evidences  of 
failure  of  the  circulation.  With  restoration  of  compensation  the  murmur 
usually  again  becomes  audible,  and  the  pulmonic  second  sound  accent- 
uated. 

Diagnosis. — The  characteristic  diagnostic  signs  consist  of  enlarge- 
ment of  the  right  ventricle  (and  also  of  the  left  auricle,  if  it  can  be 
demonstrated),  a  diastolic  or  presystolic  thrill  and  murmur  at  the 
apex,  a  loud,  snappy,  first  sound  at  the  apex,  an  accentuated  pulmonic 
second  sound,  and  a  small,  weak,  and  irregular  pulse.  Aortic  insuffi- 
ciency acconij)anied  by  a  presystolic  (Flint)  murmur  is  to  l)e  dis- 
tinguished, not  by  the  character  of  the  murmur,  but  by  the  associated 


462  DISEASES  OF  THE  ENDOCARDIUM 

physical  signs.  Adherent  pericardium,  with  dilatation  of  the  heart, 
also  is  sometimes  accompanied  by  a  presystolic  murmur — which,  how- 
ever, rarely  if  ever  has  a  crescendo  character,  and  is  not  accompanied 
by  the  other  physical  signs  of  mitral  stenosis,  but  by  those  of  adherent 
pericardium.  The  presystolic  murmur  of  the  very  rare  tricuspid  steno- 
sis will  scarcely  lead  to  diagnostic  confusion. 

Aortic  Insufficiency. — ^Aortic  insufficiency  occurs  in  about  36  per 
cent,  of  the  cases;  in  about  12  per  cent,  the  lesions  are  described  as 
double  aortic  disease,  and  in  18  per  cent,  there  is  associated  mitral 
valve  disease. 

Etiology. — ^Aortic  insufficiency  may  be  due  to:  (1)  Endocarditis.  This 
occurs  especially  in  adolescents  and  young  adults,  and  although  un- 
common, is  perhaps  more  common  than  is  generally  believed.  It  may 
be  a  sequel  of  rheumatic  fever,  but  is  more  likely  to  result  from  pyococcic, 
pneumococcic,  and  gonococcic  infections.  In  perhaps  a  few  cases  the 
vegetations  disappear  without  permanently  damaging  the  leaflets. 
Usually,  however,  one  or  more  of  the  leaflets  becomes  thickened,  indu- 
rated, and  curled  upon  itself,  so  that  the  normal  approximation  during 
diastole  is  impossible.  In  a  few  cases  the  leaflets  become  adherent 
to  one  another  at  their  adjacent  edges,  so  that  to  insufficiency,  stenosis 
is  added.  Rarely  a  leaflet  may  become  perforated  by  the  necrosing  or 
ulcerative  process.  (2)  Arteriosclerosis.  This  is  the  common  form. 
Although  it  occasionally  occurs  in  women,  it  is  especially  frequent  in 
men  after  the  fortieth  year,  and  is  associated  with  antecedent  alcoholism, 
syphilis,  and  excessive  muscular  strain,  as  well  as  the  causative  factors 
of  arteriosclerosis  and  high  arterial  tension.  Occasionally  following 
syphilis,  the  disorder  may  develop  in  comparatively  young  men — 
several  years  after  the  infection.  In  later  life  a  so-called  parasyphilitic 
form  occurs  and  is  rather  frequently  associated  with  tabes  dorsalis. 
The  lesions  are  those  of  arteriosclerosis  (involving  especially  the  aorta), 
of  which  the  valvular  disorder  constitutes  a  part.  One  or  more  of  the 
valve  segments  lose  their  tonicity  and  plasticity,  become  indurated, 
curled  at  their  edges  and  consequently  shortened,  and  are  then  unable 
to  close  the  orifice.  In  some  cases  calcification  follows  and  the  segments 
become  rigid;  or  they  become  adherent  at  their  adjacent  edges,  so  that 
to  the  insufficiency  stenosis  is  added;  but  stenosis  is  much  less  common 
than  is  usually  thought.  (3)  Rarely  the  disorder  may  be  traumatic, 
developing  in  consequence  of  sudden  undue  muscular  strain,  severe 
contusions  or  compression  of  the  chest,  etc.,  which  lead  directly  to  rup- 
ture of  usually  a  single  leaflet  (normal  or  previously  diseased).  (4) 
Relative  insufficiency  rarely  ensues  in  consequence  of  dilatation  of  the 
aortic  ring,  due  to  loss  of  elasticity,  and  associated  with  considerable 
dilatation  of  the  arch  of  the  aorta.  (5)  In  a  few  cases  the  condition  is 
congenital,  due  to  fusion  or  other  malformation  of  the  leaflets. 

Pathological  Physiology. — In  consequence  of  incompetency  of  the 
aortic  valve  the  left  ventricle  during  diastole  receives  blood  from  two 
sources — the  normal  volume  from  the  Jeft  auricle  and  a  variable  amount, 


CHRONIC   VALVULAR   DISEASE  OF   THE   HEART  4(53 

the  regurgitating  stream,  from  the  aorta.  Whether  the  regurgitating 
stream  is  considerable  in  amount,  and  gradually  increases  with  the 
progress  of  the  disorder,  as  is  generally  believed,  or  is  only  a  relatively 
small  amount  of  the  total  volume  of  ventricular  blood,  as  the  recent 
researches  of  Stewart  suggest,  the  fact  is  that  the  intraventricular  dias- 
tolic pressure  becomes  increased.  The  tension  and  stretching  to  which 
the  ventricular  musculature  is  thus  subjected  stimulate  it  to  vigorous 
contractions,  in  an  effort  to  expel  the  augmented  amount  of  blood,  and 
the  constant  recurrence  of  the  stimulus  ultimately  induces  more  or 
less  hypertrophy.  The  enlargement  of  the  cavity  of  the  ventricle  (dila- 
tation) and  the  concomitant  hypertrophy  may  and  usually  do  counter- 
balance each  other,  so  that  for  a  considerable  period  the  periphery  is 
sufficiently  supplied  with  blood  and  the  patient  suffers  no  noteworthy 
ill  consequences.  Ultimately  the  heart  may  reach  enormous  proportions, 
the  largest  seen  (bovine  heart),  and  may  weigh  1200  grams  or  more. 
In  the  course  of  time  dilatation  assumes  the  ascendency  over  the  hyper- 
trophy in  consequence  of  deficient  blood  supply  through  the  coronary 
circulation  (narrowing  of  the  coronary  orifices  and  sclerosis  of  the  vessels 
in  their  course)  and  concomitant  myocardial  degeneration;  the  equi- 
librium of  the  circulation  is  no  longer  maintained  and  failure  of  compen- 
sation ensues.  The  gradual  enlargement  of  the  ventricular  cavity  leads 
to  relative  mitral  insufficiency,  and  this  in  turn  to  its  own  ill  effects, 
already  mentioned;  organic  mitral  insufficiency  also  may  occur.  The 
aorta,  especially  the  ascending  arch,  is  usually  considerably  dilated 
(so-called  fusiform  aneurysm),  but  it  may  be  only  unusually  distensible; 
that  is,  there  are  signs  of  enlargement  during  life  (expansion  due  to  the 
systolic  output  of  a  large  volume  of  blood),  but  no  material  increase 
in  size  after  death  (so-called  dynamic  dilatation).  The  systolic  output 
of  a  large  volume  of  blood  is  also  apparent  in  the  violent  throbbing  of 
the  superficial  arteries,  which,  as  the  result  of  the  long  continued  strain 
to  which  they  are  subjected,  usually  reveal  more  or  less  sclerosis  (which 
may  be  due  also  to  other  factors — alcoholism,  syphilis,  plumbism,  etc.). 
In  the  acute  cases  that  develop  suddenly  in  consequence  of  rupture  or 
rapid  destruction  of  a  leaflet,  compensation  cannot  be  immediately 
effected,  and  the  patient  suffers  immediate  distress.  An  old  sclerotic 
valve  may  become  the  seat  of  acute  endocarditis. 

Symptoms. — Well  compensated  aortic  insufficiency  may  be  disclosed 
only  by  a  physical  examination  of  the  heart;  indeed,  in  many  cases  the 
disorder  is  for  a  long  time  overlooked  on  account  of  the  absence  of 
subjective  symptoms,  the  slight  degree  of  hypertrophy  of  the  left  ventricle, 
and  the  softness  or  indistinctness  of  the  murmur.  In  many  cases  the 
earliest  symptoms  consist  of  dizziness,  perhaps  amounting  almost  to 
faintness,  throbbing  headache,  flashes  of  light  before  the  eyes,  tinnitus 
aurium,  muscular  weakness,  and  palpitation  of  the  heart  and  dyspnopa 
on  sudden  exertion.  The  phenomena,  which,  as  a  rule,  rapidly  subside 
upon  the  restoration  of  (juiet,  are  attributable  to  cerebral  anemia. 
Marked  pallor  (aortic  facies)  and  a  readily  induced  fhish  are  usually 


464  DISEASES  OF  THE  ENDOCARDIUM 

conspicuous  symptoms;  the  flush  may  be  accompanied  or  followed  by 
sweating,  which  with  occasional  hemoptyses  has  suggested  tubercu- 
losis to  the  unwary;  there  may  also  be  slight  oedema  due  to  the  anemia. 
Precordial  pain  is  often  present  and  sometimes  distressing;  it  is  usually 
dull  and  aching,  but  may  be  severe  and  sharp  and  radiate  to  the  neck 
or  arms  (especially  the  left).  True  angina  pectoris  also  occurs;  more 
frequently  in  aortic  insufficiency  than  in  any  other  form  of  valvular 
disease. 

As  compensation  fails  the  aforementioned  symptoms  become  per- 
sistent and  aggravated:  cough,  dyspnoea,  and  palpitation  of  the  heart 
in  a  rather  pallid  subject  are  quite  characteristic.  With  the  advent 
of  relative  mitral  insufficiency  the  symptoms  of  this  condition  may 
supervene;  but  cyanosis  is  rarely  marked,  hemoptysis  is  not  common, 
and  oedema  is  not  extreme  or  widespread,  being  usually  limited  to  the 
feet  and  ankles  and  other  dependent  parts  of  the  body.  Embolic  phe- 
nomena are  not  uncommon — in  the  brain,  spleen,  kidneys,  etc.  Nervous 
symptoms  are  often  obtrusive — irritability,  restlessness,  insomnia, 
melancholia,  delusions,  suicidal  tendencies,  etc.  For  a  long  time  com- 
pensation may  be  unstable,  and  although  when  more  or  less  lost  it 
may  sometimes  be  restored,  the  restoration  is  much  less  readily  effected 
than  in  any  other  form  of  valvular  disease;  this  decompensation,  espe- 
cially in  elderly  subjects,  often  betokens  the  final  lethal  termination. 
Sudden  death  is  not  uncommon,  being  often  due  to  blockage  of  the 
coronary  arteries. 

In  the  acute  cases  that  develop  from  rupture  (traumatism  or  ulcerative 
processes),  dyspnoea,  precordial  pain,  palpitation  of  the  heart,  some- 
times hemoptysis,  etc.,  often  come  on  immediately  and  may  prove 
extremely  distressing,  until  the  heart  finally  more  or  less  effectually 
compensates  the  lesion. 

Physical  Signs. — Depending  upon  the  youth  of  the  subject  when  the 
disorder  developed  and  the  degree  of  hypertrophy  of  the  left  ventricle, 
there  is  more  or  less  bulging  of  the  precordium;  the  cardiac  impulse 
is  forcible  and  widespread,  and  the  apex  beat  (the  palpable  beat  farthest 
downward  and  outward)  is  displaced  to  the  sixth,  seventh,  or  eighth 
intercostal  space  outside  the  mamillary  line  to  the  anterior  or  mid- 
axillary  line;  it  is  usually  strong  and  forcible  and  heaving  in  character, 
and,  considering  the  size  of  the  heart,  is  rather  pointed  (in  contrast  to  the 
much  wider  and  rounded  apex  of  hypertrophy  of  the  right  ventricle). 
Visible  and  forcible  pulsation  of  the  arteries  is  present  during  compen- 
sation and  is  quite  significant  of  aortic  insufficiency;  it  is  especially  ob- 
vious in  the  aorta  (episternal  notch  and  perhaps  the  second  right  inter- 
costal space),  the  carotids,  temporals,  retinals,  subclavians,  brachials, 
radials,  femorals,  and  often  the  small  arteries  of  the  hands  and  feet.  The 
pulsations  may  be  so  forcible  as  to  occasion  a  visible  nod  of  the  head 
with  each  heart  beat  (Musset's  sign)  and  a  jerk  to  a  leg  crossed  over 
the  other  leg.  In  cases  of  marked  elongation  and  tortuosity  of  the 
arteries,  the  pulsations  are  peculiarly  serpentine,  and  were  interpreted 


CHRONIC   VALVULAR  DISEASE  OF  THE  HEART  465 

by  an  alcoholic  patient  of  mine  as  certain  evidence  of  snake  invasion. 
Usually  the  pulsation  is  transmitted  to  the  capillary  vessels,  and  may  be 
apparent  upon  mere  inspection  of  the  face  or  hands,  or  the  oral  mucous 
membrane  (uvula,  for  instance);  or  it  may  be  readily  brought  in  evidence 
by  rubbing  the  skin  for  a  moment,  or  by  slight  pressure  on  a  finger  nail, 
or  on  the  lip  mucous  membrane  by  a  glass  slide.  This  is  significant 
but  not  diagnostic  of  aortic  insufficiency,  since  it  may  be  found  also  in 
other  conditions  of  relaxation  of  the  peripheral  arteries  (in  health  as 
well  as  in  disease).  In  a  few  cases  there  may  be  an  arterial  pulsation 
in  the  liver.  In  a  few  cases  the  pulsations  are  still  further  transmitted — 
into  the  small  veins,  especially  of  the  back  of  the  hands  (the  penetrating 
or  centripetal  pulse  of  Quincke).  The  arterial  pulse  on  palpation  is 
quite  characteristic — of  increased  volume  and  force,  sudden  of  impact 
and  of  fall,  and  is  empty  between  beats — the  so-called  Corrigan,  water- 
hammer,  pistol,  or  receding  pulse;  pulsus  altus  et  celer.  Usually  it  may 
be  well  perceived  by  grasping  the  muscle  of  the  forearm  in  the  hand. 
The  sudden  collapse  is  usually  attributed  to  diastolic  regurgitation  of 
a  large  volume  of  the  blood  through  the  incompetent  aortic  valve,  but 
it  is  more  likely  due  in  large  measure  to  reflex  dilatation  of  the  peripheral 
arterioles,  induced  by  stimulation  of  the  ventricular  wall  in  consequence 
of  increased  pressure  (Stewart);  and  to  this  also  is  due  the  capillary 
pulse  and  the  penetrating  venous  pulse.  Stewart  interprets  this  periph- 
eral vascular  relaxation  as  a  means  of  preventing  the  ill  effects  of 
undue  pressure  on  the  ventricle.  A  diastolic  thrill  is  sometimes  palpable 
at  the  base,  near  or  beneath  the  sternum;  rarely  it  may  be  felt  also  at 
the  apex;  occasionally  a  thrill  at  the  apex  is  presystolic  (analogous  to 
the  Flint  murmur);  in  many  cases  there  is  a  double  thrill  at  the  base, 
the  systolic  element  being  well  transmitted  into  the  aorta  and  the 
carotids;  this  is  by  no  means  always  due  to  associated  aortic  stenosis. 
On  percussion  there  is  increase  of  the  cardiac  dulness  diagonally,  in 
the  direction  of  the  long  axis  of  the  heart.  The  area  of  dulness  becomes 
diagonally  ovoid,  downward  and  to  the  left;  only  in  advanced  cases 
with  consecutive  dilatation  and  relative  mitral  insufficiency  does  the  dul- 
ness become  much  increased  to  the  right.  The  characteristic  murmur 
is  diastolic  in  time,  soft  and  blowing  in  character,  beginning  with  dias- 
tole and  gradually  decreasing  in  intensity;  it  is  heard  best  usually  (but 
not  always)  over  the  middle  or  at  the  left  edge  of  the  sternum  on  a  level 
with  the  third  rib,  and  it  is  transmitted  down  the  left  edge  of  the  sternum 
to  the  ensiform  cartilage,  or  to  the  apex  (where  it  may  l)e  quite  as  loud 
as  at  the  base  of  the  heart),  or  to  the  axilla  (apart  from  its  transmission 
to  the  apex).  Sometimes  the  murmur  is  so  faint  as  to  be  almost  if  not 
quite  inaudible;  it  may  be  liarsh  and  rasping,  or  musical.  In  most  cases 
there  is  a  double  murmur  in  the  aortic  area  (the  to-and-fi'o  bellows 
murmur  of  Stokes) — the  diastolic  murmur  already  mentioned,  and  a 
systolic  murmur  often  harsh  in  character,  and  transmitted  into  the 
carotids;  it  is  due  to  roughening  of  the  aortic  leaflets,  sclerosis  of  the 
aorta,  dilatation  (fusiform  aneurysm)  of  the  aorta,  aortic  stenosis  (rare), 
3U 


466  DISEASES  OF  THE  ENDOCARDIUM 

true  aneurysm,  or  the  impact  of  the  regurgitating  with  the  outgoing 
stream  of  blood.  In  many  cases  (25  to  50  per  cent.)  a  presvstohc  (Flint) 
murmur,  quite  like  that  of  mitral  stenosis,  is  audible  at  the  apex;  it  is 
probably  due  to  the  regurgitating  stream  of  blood  impinging  upon  and 
actually  driving  the  anterior  mitral  leaflet  toward  the  centre  of  the  ven- 
tricle, thus  interfering  with  the  entrance  of  blood  into  the  ventricle  at  the 
time  of  auricular  systole  by  producing  essentially  a  moderate  mitral 
stenosis  (Guiteras);  or  to  vibrations  of  the  anterior  mitral  leaflet  between 
the  two  streams  of  blood.  The  aortic  second  sound  is  usually  wholly, 
occasionally  only  partly,  replaced  by  the  diastolic  murmur  (perhaps  the 
lesion  is  less  serious  when  the  sound  is  only  partly  replaced).  The 
systolic  murmur  (sometimes  both  murmurs)  is  more  or  less  well  trans- 
mitted to  the  subclavian,  axillary,  and  carotid  arteries.  A  rather  loud, 
sharp,  systolic  (vascular  diastolic)  sound  (pistol-shot  sound)  is  some- 
times audible  over  the  larger  arteries,  especially  the  femorals;  it  is  pro- 
duced locally  and  is  not  transmitted  from  the  heart.  Rarely  two  sounds 
may  be  heard,  the  second  coincident  with  the  collapse  of  the  artery 
(Traube's  sign).  Pressure  with  a  stethoscope  on  the  femoral  artery,  in 
addition  to  a  systolic  murmur  thus  normally  produced,  sometimes  results 
in  the  production  of  a  cardiac  diastolic  murmur  (Durosiez's  sign).  Sys- 
tolic contraction  of  the  pupil  (due  to  elongation  of  the  vessels  of  the 
iris)  and  diastolic  dilatation  (lessened  amount  of  blood)  may  be  observed 
(Landolfi's  sign). 

"With  the  development  of  myocardial  weakness,  dilatation  of  the  heart, 
relative  mitral  insufficiency,  etc.,  the  physical  significance  of  these  dis- 
orders also  develop. 

Diagnosis. — The  characteristic  diagnostic  signs  consist  of  evidences  of 
enlargement  of  the  left  ventricle,  a  diastolic  murmur  at  the  base  of  the 
heart  transmitted  down  the  sternum,  toward  the  apex  beat,  or  into  the 
axilla,  marked  visible  pulsations  of  the  superficial  arteries,  the  Corrigan 
pulse,  a  capillary  pulse,  and  Traube's  and  Durosiez's  signs.  The 
murmur  is  often  very  faint  or  quite  inaudible,  in  which  event  the  diag- 
nosis may  be  quite  apparent  from  the  hypertrophy  of  the  left  ventricle, 
the  collapsing  pulse,  and  the  pallor  of  the  patient.  The  commonly 
associated  systolic  murmur  in  the  aortic  area  should  be  correctly  inter- 
preted; usually  it  does  not  mean  aortic  stenosis.  The  presystolic  (Flint) 
murmur  at  the  apex  is  to  be  distinguished  from  the  similar  murmur  of 
mitral  stenosis  by  the  associated  signs,  especially  the  presence  of  hyper- 
trophy of  the  left  rather  than  the  right  ventricle,  absence  of  accentuation 
of  the  pulmonic  second  sound,  the  presence  of  arteriosclerosis,  and  the 
character  of  the  pulse.  It  is  scarcely  likely  that  the  rare  inorganic 
diastolic  murmurs,  or  those  due  to  pulmonary  insufficiency,  will  lead 
to  diagnostic  confusion.  Evidences  of  fusiform  dilatation  of  the  aorta 
must  not  be  mistaken  for  true  aneurysm. 

Aortic  Stenosis. — Aortic  stenosis  alone  occurs  perhaps  in  1  to  2  per  cent, 
of  the  cases  of  valvular  disease;  in  about  12  per  cent,  of  the  cases  the 
condition  is  described  as  double  aortic  disease  (insufficiency  and  stenosis) . 


CHRONIC  VALVULAR  DISEASE  OF  THE  HEART  467 

Etiology. — xVortic  stenosis  may  be  due  to:  (1)  Endocarditis.  This 
is  quite  rare,  but  may  follow  rheumatism  and  other  infections,  and  occurs 
in  young  subjects.  In  consequence  of  organization  of  the  vegetations, 
the  leaflets  become  thickened,'  indurated,  and  adherent  at  their  adjacent 
margins,  so  that  varying  grades  of  obstruction  ensue.  Later  a  deposit  of 
lime  salts  may  occur,  so  that  the  leaflets  with  the  aortic  ring  may  form 
a  dense  calcified  mass  of  tissue  with  a  variable  sized  and  shaped  opening. 
(2)  Arteriosclerosis.  This  is  the  common  form  of  aortic  stenosis;  but 
in  itself  it  is  rare,  and  is  always  part  of  general  arteriosclerosis,  especially 
of  the  aorta.  It  occurs,  therefore,  especially  in  elderly  subjects.  The 
process  is  slow,  although  usually  progressive,  and  ultimately  leads  to 
thickness  and  marked,  often  cartilaginous,  rigidity  of  the  leaflets, 
with  corresponding  obstruction  to  the  blood  curent.  In  advanced  cases 
there  is  usually  considerable  calcareous  infiltration,  in  which  event  the 
lesions  are  much  like  those  mentioned  in  connection  with  the  endocarditic 
form.  (3)  Relative  aortic  stenosis  (a  misnomer)  is  a  term  sometimes 
used  to  designate  that  condition  in  which,  with  normal  aortic  leaflets 
and  aortic  ring,  the  aorta  just  beyond  is  unusually  dilated.  (4)  There 
are  other  rare  types:  fusion  and  thinning  of  the  leaflets — perhaps  congen- 
ital; fibrocalcareous  thickening  and  induration  of  the  aortic  ring  without 
involvement  of  the  leaflets;  a  subvalvular  constriction  involving  the 
mitrosigmoidian  sinus  and  probably  due  to  foetal  endocarditis,  etc. 

Pathological  Physiology. — On  account  of  obstruction  at  the  aortic  ori- 
fice, the  left  ventricle  is  unable  to  expel  the  normal  amount  of  blood  in 
the  normal  time.  In  consequence,  a  residual  amount  of  blood  is  present 
in  the  ventricle  at  the  beginning  of  diastole,  which,  with  the  normal 
amount  received  from  the  auricle,  leads  to  increased  intraventricular 
pressure;  this,  together  with  stimuli  occasioned  by  resistance  at  the 
aortic  orifice  to  be  overcome,  induces  hypertrophy  of  the  left  ventricle 
- — which  is  the  effective  factor  in  maintaining  compensation,  although 
it  never  attains  the  dimensions  of  that  of  aortic  insufficiency.  This 
hypertrophy  is  often  sufficient  to  enable  the  heart  to  propel  the  normal 
amount  of  blood  into  the  aorta;  no  noteworthy  dilatation  ensues,  and 
the  patient  suffers  no  ill  consequences.  The  systole,  however,  is  pro- 
longed. When  the  stenosis  becomes  greater  than  can  be  compensated 
by  hypertrophy  of  the  left  ventricle,  or  when  the  myocardium  becomes 
enfeebled  in  consequence  of  insufficient  nourishment  (coronary  sclerosis), 
dilatation  ensues,  and  ultimately  perhaps  relative  mitral  insufficiency  and 
its  consequences. 

Symptoms. — Well  compensated  aortic  stenosis  is  often  for  a  long  time 
latent.  Symptoms  when  they  develop  are  much  like  those  of  aortic 
insufficiency,  which  is  usually  associated;  with  absence  of  aortic  insuffi- 
ciency the  symptoms  are  likely  to  be  less  severe,  although  perhaps 
readily  induced  by  exertion.  When  dilatation  ensues,  the  symptoms 
of  failing  compensation  and  relative  mitral  insufficiency  develop. 

Physical  Signs. — In  young  subjects  there  may  be  bulging  of  the  pre- 
cordium  due  to  hypertrophy;  but  since  the  hypertrophy  is  often  slight, 


468  DISEASES  OF  THE  ENDOCARDIUM 

for  a  long  time  it  may  be  overlooked,  especially  in  elderly  emphysematous 
subjects.  The  signs  of  hypertrophy  when  apparent  are  analogous  to 
those  mentioned  in  connection  with  aortic  insufficiency,  although  less 
marked.  Usually  there  is  a  rough  systolic  thrill  at  the  aortic  cartilage 
propagated  into  the  aorta  and  the  carotid,  perhaps  other  nearby  arteries. 
The  pulse  is  quite  characteristic:  it  is  small  or  moderate  in  volume, 
slow  (pulsus  tardus),  and  rises  slowly  (prolonged  systole),  is  well  sus- 
tained (broad  siunmit),  and  falls  slowly.  On  auscultation  there  is  a 
systolic  murmur  at  the  base  of  the  heart,  which  obscures  or  replaces  the 
first  sound  and  is  usually  rough  and  rasping  in  character,  sometimes 
loud  and  musical  (perhaps  audible  at  a  distance),  but  may  be  soft 
(especially  when  the  ventricle  is  weak);  its  point  of  maximum  intensity 
is  at  or  near  the  aortic  cartilage,  and  it  is  usually  transmitted  to  the 
carotid  arteries,  and  sometimes  to  the  descending  aorta  (audible  in  the 
left  interscapular  space),  the  axillary  arteries,  etc.  Occasionally  it  is  very 
loud  at  the  apex  (without  any  associated  mitral  insufficiency).  The 
second  aortic  sound  is  commonly  absent  or  weak,  or  replaced  by  a  dias- 
tolic murmur,  on  account  of  rigidity  of  the  aortic  leaflets  and  commonly 
co-existing  aortic  insufficiency.  With  the  advent  of  myocardial  weakness 
and  dilatation,  relative  mitral  insufficiency  usually  ensues  and  materially 
modifies  the  previously  existing  physical  signs. 

Diagnosis. — The  characteristic  diagnostic  signs  consist  of  evidences 
of  enlargement  of  the  left  ventricle,  a  systolic  thrill  and  a  systolic  murmur 
at  the  base  of  the  heart  and  transmitted  into  the  aorta  and  carotid 
arteries,  a  weak  or  absent  aortic  second  sound,  and  a  slow  (as  distin- 
guished from  an  infrequent)  pulse.  A  basal  systolic  murmur,  upon  which 
the  diagnosis  is  often  based,  is  usually  due  to  some  other  disorder,  such 
as  roughening  of  the  aortic  leaflets,  sclerosis  of  the  aorta,  dilatation  (fusi- 
form aneurysm)  of  the  aorta,  true  aneurysm,  or  the  impact  of  a  regurgi- 
tating with  the  outgoing  stream  of  blood.  Sclerosis  or  atheroma  of  the 
aorta  may  be  differentiated  by  absence  of  the  characteristic  pulse  and 
usually  also  of  a  thrill,  and  the  presence  of  an  accentuated  aortic  second 
sound  and  of  other  signs  of  arteriosclerosis.  Dilatation  of  the  aorta  and 
true  aneurysm  may  be  recognized  by  their  own  diagnostic  signs.  The 
basal  systolic  murmurs  of  anemia,  fever  states,  etc.,  usually  have  an 
obvious  cause,  are  rarely  loudest  in  the  aortic  area,  and  do  not  give 
rise  to  enlargement  of  the  left  ventricle.  Pulmonary  stenosis  and  mitral 
insufficiency,  which  perhaps  might  enter  into  the  diagnosis,  give  rise  to 
enlargement  of  the  right  rather  than  the  left  ventricle,  and  other 
unequivocal  signs. 

Tricuspid  Insufl&ciency. — Etiology. — ^Tricuspid  insufiiciency  rarely 
results  from  acute  or  chronic  endocarditis  (antenatal  or  postnatal). 
Usually  the  condition  is  relative  and  due  to  inability  of  the  muscle  of 
the  right  heart  to  perform  the  work  to  which  it  is  subjected.  This 
insufficiency,  especially  as  a  temporary  disorder,  is  much  more  common 
than  is  suspected;  it  develops  in  health  under  the  stress  of  unusual  or 
sudden  strain  (athletic  exercises,  parturition,  etc.),  and  in  disease  when 


CHRONIC  VALVULAR   DL'iEASE  OF  THE  HEART  469 

the  enfeebled  myocardium  is  suddenly  called  upon  for  some  extra 
work — in  both  of  which  circumstances  the  safety-valve  action  of  the 
right  ventricle  (involving  the  wall  of  the  ventricle,  the  papillary  mus- 
cles, which  readily  become  fatigued  and  act  imperfectly  or  ineffectually, 
and  the  tricuspid  ring)  becomes  operative  and  prevents  serious  and 
lasting  damage  to  the  myocardium.  The  more  obvious  and  clinically 
important  tricuspid  insufficiency  occurs  in  chronic  hypertrophy  with 
consecutive  dilatation  of  the  right  ventricle,  which  in  turn  results  from 
advanced  mitral  valve  disease,  chronic  diseases  of  the  lungs  (emphysema, 
bronchitis,  interstitial  pneumonitis,  pleural  adhesions,  etc.),  pericardial 
adhesions,  and  myocardial  weakening  due  to  any  local  or  general  cause. 
There  is  associated  congestion  of  the  liver,  spleen,  kidneys,  gastro- 
intestinal tract,  etc.,  oedema  of  the  subcutaneous  tissues,  effusions  in  the 
serous  sacs,  etc. 

Symptoms. — ^The  symptoms  are  those  of  failing  cardiac  compensation 
and  are  due  to  the  associated  passive  congestion  and  consequent  func- 
tional inactivity  of  the  organs.  The  embarrassment  of  the  heart  itself  is 
obvious  in  precordial  distress  or  pain  and  palpitation  of  the  heart.  Con- 
gestion of  the  lungs  leads  to  cyanosis,  dyspnoea  (aggravated  upon  exer- 
tion and  excitement),  cough,  expectoration,  hemoptysis,  etc.;  of  the 
liver,  to  local  pain  and  tenderness;  of  the  gastro-intestinal  tract,  to  poor 
appetite,  disordered  digestion,  flatulence,  nausea,  vomiting,  consti- 
pation, etc.;  of  the  kidneys,  to  oliguria,  albuminuria,  cylindruria, 
erythrocyturia,  etc.  Oedema  is  always  present  and  may  become  universal; 
effusions  are  common  in  the  serous  sacs,  especially  the  right  pleura; 
ascites  is  rarely  present  before  general  oedema,  but  it  may  be  dispropor- 
tionately marked. 

Physical  Signs. — ^The  physical  signs  consist  of  dilatation  of  the  heart, 
especially  of  the  right  side  (the  dulness  may  extend  to  the  right  nipple 
line);  a  systolic  murmur  (usually  soft  and  blowing,  but  sometimes  rough) 
in  the  tricuspid  area  (and  especially  significant  if  heard  to  the  right  of 
the  sternum,  where  the  murmur  of  mitral  insuflSciency  is  rarely  heard); 
a  ventricular  systolic  autochthonous  pulsation  in  the  veins  of  the  neck, 
often  especially  marked  in  the  jugular  bulb  and  sometimes  propagated  to 
adjacent  veins  (rarely  a  murmur  may  be  heard);  and  a  ventricular 
systolic  expansile  pulsation  of  the  liver.  The  signs  of  the  antecedent 
disorder,  usually  mitral  valve  disease,  or  chronic  disease  of  the  lungs,  etc., 
are  also  present.  Enfeeblement  of  a  previously  accentuated  pulmonic 
second  sound  is  a  valuable  sign  of  the  development  of  tricuspid  insufli- 
ciency;  as  the  insufficiency  grows  less  (or  the  right  side  of  the  heart 
grows  stronger)  the  pulmonary  second  sound  again  becomes  accentuated. 
The  safety  valve  leakage  usually  occasions  no  noteworthy  symptoms 
and  soon  subsides;  indeed,  the  occurrence  of  the  leakage  probably 
prevents  the  onset  of  more  or  less  serious  symptoms. 

Tricuspid  Stenosis. — Etiology. — Tricuspid  stenosis  is  a  rather  rare 
condition.  It  may  be  due  to  endocarditis,  either  antenatal  or  postnatal 
(usually  rheimiatic);  rarely  it  seems  to  be  primarily  degenerative,  analo- 


470  DISEASES  OF  THE  ENDOCARDIUM 

gous  to  the  arteriosclerotic  process.  It  is  most  common  in  women 
(75  per  cent,  of  the  cases),  and  in  more  than  99  per  cent,  of  the  cases 
is  associated  with  disease. of  one  or  more  of  the  other  valves,  especially 
mitral  stenosis  (56  per  cent,  of  the  cases).  The  characteristic  lesions 
consist  of  hypertrophy  and  dilatation  of  the  right  auricle. 

Symptoms.— The  symptoms  are  virtually  those  of  mitral  stenosis. 
Cyanosis  is  often  the  earliest  obtrusive  symptom,  and  may  be  present 
for  months  before  there  are  other  noteworthy  manifestations  of  de- 
compensation. Polycythemia  is  common  and  the  fingers  may  be  clubbed. 
When  the  heart  begins  to  fail,  the  symptoms  cannot  be  distinguished 
from  those  of  tricuspid  insufficiency.  Dropsy  may  occur  early  and  is 
unusually  persistent. 

Physical  Signs. — The  physical  signs  are  commingled  with  those  of  the 
complicating  lesions;  but  the  significant  signs  consist  of  increase  of  the 
cardiac  dulness  to  the  right  (which  may  extend  to  or  beyond  the  mammil- 
lary  line);  a  presystolic  or  diastolic  thrill,  and  a  usually  rough,  rumbling 
presystolic  or  diastolic  murmur,  sometimes  ending  in  a  rather  sharp 
first  sound,  at  the  end  of  the  sternum;  and  presystolic  (auricular  systolic) 
pulsations  in  the  veins  of  the  neck  and  in  the  liver. 

Pulmonary  Insufficiency. — Etiology. — Pulmonary  insufficiency  is  very 
rare  as  an  acquired  affection,  but  it  sometimes  results  from  acute 
endocarditis  (usually  set  up  by  the  pyococci,  sometimes  by  the  gono- 
coccus).  Occasionally  in  cases  of  long-standing  high  pulmonary  tension 
there  is  some  sclerosis  of  the  leaflets  and  consequent  insufficiency. 
Perhaps  relative  insufficiency  sometimes  results  from  stretching  of  the 
pulmonary  ring  in  conditions  of  high  pulmonary  pressure.  The  lesions 
much  resemble  the  analogous  lesions  of  aortic  insufficiency,  involving, 
however,  the  right  instead  of  the  left  ventricle. 

Symptoms. — Symptoms  are  in  abeyance  until  the  right  heart  begins 
to  fail,  whereupon  the  phenomena  common  in  decompensation  develop. 

Physical  Signs. — The  physical  signs  consist  of  hypertrophy  and  later 
of  dilatation  of  the  right  ventricle,  and  a  diastolic  murmur  at  the  base  of 
the  heart,  usually  loudest  in  the  pulmonary  region  and  transmitted  down 
the  left  edge  of  the  sternum.  Aortic  insufficiency  may  be  excluded  by 
the  absence  of  enlargement  of  the  left  ventricle  and  of  the  characteristic 
vascular  phenomena. 

Pulmonary  Stenosis. — Etiology. — Acquired  pulmonary  stenosis  is 
the  rarest  of  valvular  lesions.  Occasionally  it  follows  acute  endocarditis, 
or  the  endocarditis  may  become  engrafted  upon  an  old,  perhaps  con- 
genital defect;  occasionally  also  the  lesion  may  be  due  to  slow  sclerosis, 
when  it  is  associated  with  pulmonary  endarteritis.  Very  rarely,  perhaps 
trauma  may  lead  to  rupture  of  one  of  the  leaflets.  The  lesions  are  much 
like  the  analogous  aortic  stenosis,  involving,  however,  the  right  instead 
of  the  left  ventricle. 

Symptoms. — Symptoms  are  not  obtrusive  until  the  right  heart  begins 
to  fail,  whereupon  the  symptoms  common  to  decompensation  ensue. 


CHRONIC  VALVULAR   DISEASE  OF  THE  HEART  471 

Physical  Signs. — The  physical  signs  consist  of  hypertrophy  and 
dilatation  of  the  right  ventricle,  a  systolic  thrill  and  murmur  in  the 
pulmonary  area,  and  a  weak  or  absent  pulmonary  second  sound;  or  the 
sound  m^y  be  replaced  by  a  diastolic  murmur.  A  systolic  murmur 
is  very  common  in  the  pulmonary  region,  but  it  is  rarely  due  to  pulmonary 
stenosis:  it  may  occur  in  healthy,  thin-chested  persons,  especially  chil- 
dren, and  is  often  induced  by  exercise ;  it  is  common  in  anemic,  cachectic, 
and  fever  states;  it  may  be  due  to  the  interaction  of  the  heart  and  the 
lung  (cardiopulmonary  murmur);  and  it  may  be  due  to  aortic  stenosis 
(and  the  other  factors  mentioned  as  causative  of  an  aortic  systolic 
murmur),  or  to  mitral  insufficiency.  In  most  of  these  cases  the  diagnostic 
inference  is  obvious:  aortic  stenosis  may  be  excluded  by  absence  of 
hypertrophy  of  the  left  ventricle,  of  propagation  of  the  thrill  and  murmur 
into  the  carotid  arteries,  and  of  the  characteristic  pulse.  Mitral  in- 
sufficiency may  be  excluded  by  the  absence  of  the  common  signs,  espe- 
cially the  accentuated  pulmonary  second  sound. 

Combined  Valvular  Lesions. — In  almost,  if  not  quite,  one  half  of 
the  cases  of  valvular  disease,  there  is  more  than  a  single  lesion;  that  is, 
there  may  be  insufficiency  and  stenosis  at  one  valve,  or  two  or  more 
valves  may  be  diseased.  This  double  or  multiple  involvement  of  the 
valves  may  develop  at  the  one  time,  or,  what  is  more  common,  involve- 
ment of  one  valve  follows  that  of  another;  and  the  lesions  may  be  alike 
in  nature  or  dissimilar.  Thus,  while  rheumatic  and  other  infections 
commonly  involve  only  the  mitral  valve,  they  not  infrequently  at  or 
about  the  same  time,  especially  in  children,  involve  also  the  aortic  valve, 
and  occasionally  also  one  or  both  valves  of  the  right  side  of  the  heart. 
More  commonly,  however,  the  primary  lesion,  usually  insufficiency, 
is  followed  in  the  course  of  time  by  cicatrization  and  consequent  stenosis : 
thus  mitral  insufficiency  often  in  the  course  of  time  becomes  associated 
with  stenosis  (so-called  double  mitral  disease);  mitral  stenosis  is  rare 
as  a  single  lesion,  being  usually  associated  with  insufficiency;  aortic 
insufficiency  is  often  the  primary  and  may  remain  the  only  lesion,  but 
sometimes  becomes  associated  with  stenosis  (double  aortic  disease); 
aortic  stenosis  as  a  single  lesion  is  the  rarest  of  all  in  the  left  side  of  the 
heart.  The  developing  stenosis  may  for  a  time  at  least  prove  beneficial 
in  lessening  the  primary  insufficiency  and  retarding  the  development 
of  its  ill  effects.  Varying  combinations  of  aortic  and  mitral  valve  disease 
also  occur,  especially  aortic  and  mitral  insufficiency,  due  usually  to 
sclerosis  rather  than  to  endocarditis.  The  commonest  combination  of 
valvular  disorders,  however,  is  that  of  an  organic  lesion  at  one  orifice, 
followed  by  relative  insufficiency  at  another:  mitral  insufficiency  or 
stenosis  followed  by  tricuspid  insufficiency,  and  aortic  insufficiency  or 
stenosis  followed  by  relative  mitral  insufficiency  and  later  relative 
tricuspid  insufficiency. 

Physical  Signs. — Associated  valvular  lesions  materially  alter  the 
physical  signs  of  individual  lesions  and  proportionately  increase  the 
diagnostic  difficulties.    In  the  diagnosis  accuracy  will  be  best  achieved  by 


472  DISEASES.  OF  THE  ENDOCARDIUM 

paying  less  attention  to  the  murmurs  than  to  the  other  physical  signs, 
and  by  postulating  the  fewest  defects  compatible  with  an  explanation 
of  the  recognizable  physical  signs.  A  systolic  nmrmur  alone  is  of  no 
value  whatever  in  the  diagnosis;  a  diastolic  murmur  almost  certainly 
means  a  valvular  defect,  but  in  this  event  there  are  always  corroborative 
signs.  The  loudest,  most  obtrusive  murmur  (usually  systolic)  may  be 
due  to  a  secondary  lesion  (relative  insufficiency),  the  murmur  of  the 
primary  lesion  being  soft  or  almost  inaudible,  but  in  this  event  also 
the  concomitant  physical  signs  correctly  determined  point  the  way  to 
the  correct  interpretation  of  the  phenomena. 

Diagnosis. — ^The  diagnostic  criteria  of  the  different  forms  of  valvular 
disease  have  been  sufficiently  dwelt  upon.  But  the  diagnosis  is  by  no 
means  complete  with  the  naming  of  the  valvular  defect;  it  must  be  much 
more  comprehensive,  and  should  include  the  nature  of  the  valvular 
disorder  (whether  endocarditic,  sclerotic,  or  relative;  obsolete  or  active), 
the  degree  and  adequacy  (stability)  of  the  compensating  mechanism, 
and  the  factors  that  tend  to  or  actually  provoke  decompensation  in  the 
individual  case;  in  other  words,  in  addition  to  ascertaining  the  valvular 
defect  one  must  determine  also  the  functional  capacity  of  the  myocardium 
— the  relative  preponderance  of  hypertrophy  or  dilatation,  and  the  ability 
of  the  heart  to  do  a  measured  amount  of  work  without  subjective  or 
objective  distress. 

Prognosis. — The  prognosis  in  valvular  disease  of  the  heart  depends 
in  part  upon  the  nature  and  severity  of  the  valvular  defect,  but  in  large 
measure  upon  the  ability  of  the  myocardium  to  effect  and  maintain 
compensation,  which  in  turn  is  much  dependent  upon  the  patient's 
general  health  and  mode  of  life.  The  anatomical  valvular  defects, 
of  course,  cannot  be  cured,  although  material  benefit  often  follows  the 
supervention  of  stenosis  upon  a  well-marked  insufficiency;  relative 
defects  (insufficiencies)  due  to  stretching  of  orifices  may  entirely  dis- 
appear if  the  affected  orifices  regain  their  normal  tone.  The  anatomical 
defects,  however,  are  not  incompatible  with  long  life  and  more  or  less 
freedom  from  distress.  In  point  of  gravity,  the  mitral  lesions  are  less 
serious  than  the  aortic,  the  order  from  the  least  to  the  most  serious  being, 
mitral  insufficiency,  mitral  stenosis,  aortic  stenosis,  and  aortic  insuffi- 
ciency. The  cases  associated  with  extensive  arteriosclerosis  (usually 
aortic  insufficiency)  are  more  grave  than  those  the  result  of  past  rheu- 
matism, since  there  is  usually  also  sclerosis  of  the  coronary  arteries 
with  its  attendant  danger  of  angina  pectoris,  thrombosis  and  embolism 
of  the  coronary  vessels,  and  consequent  sudden  death,  etc.  In  the  aortic 
cases  also  compensation,  when  once  disturbed,  is  much  less  readily 
restored  than  in  the  mitral  cases,  and  when  restored  it  is  usually  unstable. 
Double  or  triple  valvular  defects,  whether  organic  or  relative,  add 
materially  to  the  gravity  of  the  prognosis.  In  children  the  prognosis  is 
generally  bad;  in  women  it  is  better  than  in  men,  because  of  their  quieter 
life,  the  preponderance  of  mitral  lesions,  and  their  less  addiction  to  tlie 
vices  of  intemperance,  venery,  and  hard  manual  labor.     Pregnancy, 


CHRONIC  VALVULAR  DISEASE  OF  THE  HEART  473 

however,  adds  materially  to  the  gravity  of  the  condition,  although  a 
considerable  number  of  cardiopaths  bear  and  rear  large  families.  In 
mitral  cases  there  is  rarely  associated  pulmonary  tuberculosis  (due  to 
relative  immunity  afforded  by  chronic  passive  congestion). 

Treatment. — It  seems  quite  likely,  although  difficult  to  prove,  that 
chronic  valvular  disease  of  the  heart  may  be  prevented  in  some  cases, 
or  that  its  serious  consequences  may  be  lessened  or  retarded.  Since 
most  of  the  cases  of  the  endocarditic  group  are  due  to  rheumatism,  the 
prompt  and  efficient  jugulation  of  this  infection  should  tend  to  minimize 
its  complications :  that  this  really  occurs  there  can  be  no  doubt,  although 
from  the  nature  of  the  disorder  definite  proof  can  scarcely  be  adduced. 
Since  the  cases  of  the  sclerotic  group  are  associated  with  arteriosclerosis, 
and  since  arteriosclerosis  is  largely  the  penalty  of  unwise  living  and 
divers  sorts  of  indiscretions,  it  is  quite  probable  that  a  rational  and 
hygienic  mode  of  life,  tending  to  retard  the  degenerative  changes  of 
the  arteries,  should  tend  also  to  prevent  the  development  of  many  cases 
of  chronic  degenerative  or  atheromatous  valvular  disease.  In  most  of 
these  cases,  however,  "when  we  have  prescribed  that  continual  temper- 
ance in  all  things  which  is  necessary  to  the  care  of  most  disorders,  how 
often  do  we  find  that  our  patient  reckons  the  loss  of  pain  to  be  purchased 
too  dear  by  the  loss  of  pleasure."    (Gee.) 

The  chronic  valvular  disease  being  a  fact,  the  treatment  varies  with  its 
stage.  During  the  period  of  compensation,  the  one  important  desider- 
atum is  so  to  regulate  the  patient's  life  that  his  activities  may  be  well 
within  the  potentialities  of  his  myocardium.  This  may  be  estimated 
by  determining  the  relative  amount  of  hypertrophy  and  of  dilatation, 
the  reaction  of  the  heart  and  blood  vessels  to  a  measured  amount  of 
work  (such  as  walking,  climbing  stairs,  lifting  weights,  etc.),  and  by 
the  condition  of  the  other  organs  (passive  congestion,  etc.).  In  most 
cases  it  is  wise  to  explain  to  the  patient  the  condition  of  his  heart  and 
blood  vessels;  to  tell  him  that  although  disabled  (impaired),  his  heart 
is  still  capable  of  many  years  of  effective  work,  provided  the  demands 
made  upon  it  are  well  within  its  reserve  power,  but  that  this  reserve 
power  is  less  than  in  normal  subjects.  The  patient's  entire  life,  his  diet, 
his  work,  his  rest,  his  exercise,  must  be  adjusted  to  the  capabilities  of  his 
heart.  The  diet  should  be  nutritious  and  readily  digestible;  the  total 
amount  at  each  meal  should  not  be  voluminous,  fluids  especially  being 
restricted  and  taken  between  meals;  a  large  meal,  as  a  rule,  should  not 
be  taken  in  the  evening;  strict  attention  should  be  paid  to  free  daily 
evacuation  of  the  bowels,  and  to  free  action  of  the  skin  (bathing).  The 
patient  should  have  an  abundance  of  rest,  and  should  be  as  much  as 
possible  in  the  open  air;  his  occupation  should  not  be  too  engrossing 
mentally  nor  too  strenuous  physically;  and  his  exercise  should  be  such  as 
to  afford  pleasure,  but  not  to  provoke  any  manifestations  of  cardiac 
embarrassment.  If,  on  the  one  hand,  the  desirable  life  entails  continued 
repression  of  bodily  spirits  and  intellectual  ambitions,  it  has  its  com- 
pensation in  prolonged  life  and  postponement  of  the  inevitable.     It 


474  DISEASES  OF  THE  ENDOCARDIUM 

is  especially  important  to  bear  constantly  in  mind  that  a  cardiac  murmur 
is  no  indication  whatever  for  the  administration  of  cardiac  tonics  (such 
as  digitalis);  and  that  therapeutically  a  murmur  is  the  least  important  of 
the  physical  signs.  Furthermore,  many  symptoms,  such  as  attacks 
of  precordial  distress,  palpitation  of  the  heart,  dyspnoea,  etc.,  are  due 
to  causes  that  excite  these  s}'mptoms  in  non-cardiac  subjects,  such  as 
dietetic  indiscretions,  the  abuse  of  alcohol,  tea,  coffee,  or  tobacco, 
excessive  venery,  worry,  anxiety,  hill  climbing,  etc.;  and  they  are  to  be 
combated  by  eradication  of  their  cause,  rather  than  by  the  immediate 
resort  to  digitalis  and  similar  drugs.  In  some  cases  subjective  complaints 
of  precordial  distress  and  palpitation  are  found  to  be  associated  with  an 
excited  overhypertrophied  heart;  the  use  of  digitalis  only  adds  to  the 
patient's  discomfort,  which  may  be  materially  lessened  by  minute  doses 
of  aconite,  small  doses  of  the  bromides,  valerian,  regulation  (lessening) 
of  the  diet,  and  free  purgation.  ^'Vhen  the  disease  has  advanced  and 
the  compensation  tends  to  become  somewhat  unstable  (lessened  reserve 
power),  beneficial  results  may  attend  the  judicious  combination  of  rest, 
graduated  exercises,  hydrotherapy,  small  doses  of  digitalis  or  strophanthus 
for  short  periods,  and  free  purgation.  In  other  cases  the  imminence  of 
decompensation  is  suggested  by  anemia  and  general  failure  of  health, 
and  it  often  yields  to  iron,  quinine,  arsenic,  strychnine,  etc. 

Finally,  in  some  cases  suddenly,  in  most  cases  gradually,  more  or 
less  complete  failure  of  compensation  ensues;  the  indications  to  be  met 
are  to  reduce  the  work  demanded  of  the  heart  and  to  increase  the  strength 
and  vigor  of  its  contractions.  The  most  important  is,  temporarily  at 
least,  to  reduce  the  work  demanded  of  the  heart — which  is  best  effected 
by  eradication  of  the  cause  (excessive  mental  or  physical  work,  worry, 
anxiety,  excitement,  dietetic  and  other  indiscretions,  malnutrition,  etc.) 
sometimes  directly  responsible  for  the  breakdown,  by  rest  in  bed,  regu- 
lation of  the  diet,  and  depletion  of  the  engorged  venous  system.  The 
rest  in  bed  should  be  absolute;  nothing  else  is  so  important  or  so  effica- 
cious. Rest  in  bed  for  ten  days  or  two  weeks  of  itself  often  suffices 
to  restore  compensation  so  seriously  disturbed  as  to  lead  to  considerable 
oedema;  with  recurring  breaks  in  compensation  rest  in  bed  may  continue 
to  suffice,  in  which  event  digitalis  and  other  cardiac  tonics  need  not  be 
given;  they  should  be  reserved  until  needed — which  assuredly  tends  to 
prolong  the  patient's  life.  The  diet  should  be  carefully  regulated  to  suit 
each  individual  patient,  the  main  indications  being  to  nourish  the  patient 
(concentrated,  readily  digestible,  solid  and  semisolid  foods),  to  prevent 
flatulence  (avoidance  of  food  likely  to  undergo  fermentation),  and  to 
limit  the  amount  of  fluid  intake  (which  not  only  overloads  the  blood 
and  adds  to  the  work  of  the  heart,  but  also  distends  the  stomach  and 
mechanically  adds  to  the  embarrassment  of  the  heart).  The  digestive 
processes  may  be  much  improved  by  free  purgation  by  blue  mass  (or 
calomel)  and  salines,  which  serve  to  deplete  the  engorged  gastro-intes- 
tinal  and  hepatic  systems. 

In  many  cases  the  foregoing  do  not  suffice,  or,  having  once  or  twice 


CHRONIC   VALVULAR  DISEASE  OF  THE  HEART  475 

proved  efficacious,  they  are  inadequate  in  a  later  recurrence  of  decom- 
pensation; recourse  must  be  had  to  drugs  that  increase  the  strength  and 
vigor  of  the  cardiac  contractions.  Digitahs  is  the  sovereign  remedy. 
Since  it  increases  the  tonicity,  contractihty,  excitability,  and  rhythmi- 
city  of  the  cardiac  muscle,  it  is  indicated  in  the  failure  of  compensation 
that  may  develop  in  any  and  all  forms  of  valvular  disease.  The  special 
indication  for  its  use  is  insufficiency  (dilatation)  of  the  myocardium, 
manifested  by  cyanosis,  dyspnoea,  venous  stasis,  and  oedema,  rather 
than  any  special  valvular  defect  per  se.  The  best  effects  of  the  drug 
are  seen  in  cases  of  dilatation  with  final  tricuspid  insufficiency,  congestion 
of  the  viscera,  and  oedema.  In  appropriate  cases,  its  good  influences  are 
obvious  often  within  tw^enty-four  hours:  the  volume  of  the  heart  lessens; 
the  cardiac  action  becomes  regular  and  vigorous;  the  pulse  becomes 
full,  strong,  and  regular;  dyspnoea,  cyanosis,  and  cardiac  palpitation 
lessen;  the  urine  increases  in  amount;  and  the  oedema  begins  to  be  ab- 
sorbed. It  is  no  less  efficacious  in  aortic  insufficiency  with  dilatation 
and  venous  congestion  than  it  is  in  mitral  valve  disease;  the  theoretical 
objection  to  its  use  in  aortic  insufficiency,  based  upon  its  prolonging  the 
ventricular  diastole,  is  more  than  counterbalanced  by  its  action  in  pro- 
moting a  full,  vigorous,  and  efficient  systole  with  complete  emptying  of 
the  ventricle,  in  raising  the  tension  in  the  systemic  arteries,  and  in 
leading  to  the  establishment  of  circulatory  equilibrium  in  the  capillaries 
and  veins. 

There  are  three  good  preparations — the  powdered  leaves,  the  infusion, 
and  the  tincture;  the  infusion  is  perhaps  the  best,  but  must  always  be 
freshly  prepared  from  the  leaves.  It  may  be  serviceably  combined  with 
alkaline  diuretics: 

I^ — Potassium  acetate, 

Potassium  citrate,  of  each 2  drams  8l0 

Infusion  of  digitalis 6  ounces       200 lo 

M.  S. — One  tablespoonful  (15  c.c.)  every  four  hours  (or  at  longer  intervals,  as  may  be 
required). 

Failure  in  the  use  of  digitalis  is  attributable  to  inefficient  preparations 
made  from  inert  leaves  (or  the  preparation  of  a  supposed  infusion  from 
a  mother  fluid  extract  or  similar  preparation),  insufficient  dosage,  and 
unsuitable  case.  When  the  stomach  is  or  becomes  deranged  (nausea, 
vomiting,  etc.),  a  fat-free  tincture  may  be  employed,  or  the  infusion  may 
be  given  by  the  rectum;  or  digitalin  (germanicum,  y^^  to  ^  grain,  0.0C5 
to  0.01  gram)  or  digalen  (a  soluble  digitoxin)  may  be  given  hypoder- 
mically;  or  in  suitable  cases  digalen  or  digitalone  may  be  given  intra- 
venously. Digitalin  or  digalen  also  may  be  given  by  the  mouth  when 
a  prolonged  mild  effect  is  desired;  but  one  must  remember  that  most 
of  the  commercial  alkaloids  or  so-called  active  principles  are  inert. 

Digitalis,  however,  must  be  employed  with  circumspection;  it  is  not 
indicated  in  any  case  of  cardiac  disease  without  evidence  of  myocar- 
dial insufficiency;  nor  in  cases  of  rapid,  irregular,  or  overacting  heart 


476  DISEASES  OF  THE   ENDOCARDIUM 

unattended  with  the  aforementioned  signs  of  faihng  myocardium ;  nor  in 
cases  of  aortic  insufficiency  manifested  only  by  dyspnoea,  precordial  pain, 
anginoid  attacks,  etc. ;  nor,  as  a  rule,  in  high  arterial  tension,  and  angina 
pectoris,  except  perhaps  in  some  cases  in  elderly  subjects  with  an  asso- 
ciated valvular  lesion  and  failing  compensation,  in  whom  it  often  is  of 
much  service,  and  in  whom  it  may  be  combined  with  vasodilators. 

As  a  rule,  the  drug  should  be  discontinued  as  soon  as  the  desired 
results  have  been  obtained;  it  may  be  resorted  to  again  should  the 
indication  arise.  In  cases  in  which  its  use  has  been  continued  for  some 
time,  toxic  symptoms  may  develop;  but  there  is  little  evidence  of  the 
sudden  development  of  the  much-feared  so-called  cumulative  action. 
Nausea  and  vomiting  are  the  earliest  symptoms;  these  may  be  followed 
by  slowing  and  weakening  of  the  pulse,  lessening  in  the  amount  of  urine, 
and  fall  in  the  blood  pressure.  More  marked  evidences  of  intoxication 
consist  of  the  pulsus  alternans,  the  pulsus  bigeminus,  and  the  develop- 
ment of  a  type  of  heart  block  (toxic  depression  of  conductivity  and 
contractility). 

Of  the  substitutes  for  digitalis,  strophanthus  (or  strophanthin)  is  the 
best,  but  it  is  much  less  efficient;  it  is  said  to  cause  less  vasoconstriction 
than  digitalis,  and  may  be  used  when  a  mild  effect  is  desired,  or  after 
the  use  of  digitalis  for  some  time,  or  in  children  or  elderly  subjects. 
Excellent  results  sometimes  attend  the  intravenous  injection  of  strophan- 
thin {y¥o  gram,  0.0005  grain).  Convallaria,  caffeine,  adonis  venalis, 
sparteine,  cactus  grandiflorus,  squill,  etc.,  occasionally  are  useful  substi- 
tutes, but  they  are  much  less  efficient  than  digitalis,  and  their  preparations 
are  often  inert.  Strychnine,  iron,  arsenic,  and  alcohol  are  often  very  useful 
adjuvants  to  digitalis,  and  may  be  used  as  the  patient  convalesces. 

Attacks  of  acute  heart  failure,  which  sometimes  are  the  initial  mani- 
festations of  final  decompensation,  but  which  also  frequently  develop 
during  the  persistence  of  more  or  less  well-marked  failure  of  compensa- 
tion, often  demand  immediate  and  active  treatment.  Frequently  the 
attacks  are  due  to  obvious  causes  (dietetic  indiscretions,  constipation, 
exertion,  excitement,  etc.) — which  should  be  avoided.  When  developed 
the  attacks  should  be  met  with  diffusible  stimulants  and  carminatives, 
such  as  aromatic  spirit  of  ammonia,  compound  spirit  of  ether,  brandy, 
whiskey,  strong  coffee,  etc.,  by  the  mouth;  or  whiskey,  caffeine,  cam- 
phor in  oil,  strychnine,  digitalin,  strophanthin,  adrenalin  chloride,  etc., 
hypodermically.  In  many  cases  the  most  effective  treatment  consists 
of  prompt  venesection  and  the  abstraction  of  a  pint  or  more  of  blood. 

The  obtrusive  symptoms  of  decompensation  are  usually  relieved  by 
improvement  of  the  condition  of  the  heart,  but  sometimes  they  require 
special  or  additional  treatment.  Dyspnoea  not  improved  by  the  meas- 
ures already  mentioned  is  commonly  due,  in  part  at  least,  to  some  asso- 
ciated condition,  especially  hydrothorax,  chronic  bronchitis,  flatulency, 
dyspepsia,  ascites,  etc.  Hydrothorax  (usually  right  sided)  is  very  com- 
mon and  is  often  overlooked.  It  should  always  be  sought,  and  when 
found,  paracentesis  should  be  immediately  resorted  to.     This  is  an 


CHRONIC  VALVULAR  DISEASE  OF  THE  HEART  477 

exceedingly  important  therapeutic  measure,  and  is  usually  promptly 
followed  by  great  relief  and  improvement  in  the  condition  (removal 
of  one  cause  of  embarrassed  heart  action).  The  dyspnoea  due  to  flatu- 
lent dyspepsia  may  be  controlled  by  regulation  of  the  diet  and  the  use 
of  carminatives,  such  as  brandy,  aromatic  spirit  of  ammonia,  spirit  of  lav- 
ender, resorcin,  charcoal,  sodium  bicarbonate,  and  bismuth.  Nocturnal 
dyspnoea,  especially  the  awakening  with  a  start  and  subsequent  dyspnoea, 
should  be  controlled  with  morphine  hypodermically.  Small  doses  (y y-  to 
■J J  grain,  0.004  to  0.005  gram)  often  suffice;  such  is  the  relief  that  in 
suitable  cases  the  drug  should  not  be  withheld,  but  its  use  should  not 
be  long  continued.  Nitroglycerin  is  sometimes  of  service  in  cases  with 
high  arterial  tension.  Distressing  palpitation  is  usually  associated 
with  dyspnoea,  is  due  to  similar  causes,  and  is  to  be  similarly  treated. 
In  addition,  hot  moist  applications  or  an  ice  bag  to  the  precordium  are 
often  grateful.  The  palpitation  of  excessive  muscular  hypertrophy  is 
often  best  relieved  with  tincture  of  aconite  (1  to  2  minims,  0.06  to  0.12 
c.c,  thrice  daily).  Anginoid  pains  are  often  provoked,  as  are  attacks  of 
palpitation  and  dyspnoea,  and  should  be  similarly  met.  The  anginoid 
pains  of  aortic  lesions  are  often  much  benefited  by  nitroglycerin  and 
potassium  iodide.  Nausea  and  vomiting  require  limitation  of  food,  free 
purgation  (calomel  and  salines),  and  bismuth,  cerium  oxalate,  dilute 
hydrocyanic  acid,  carbolic  acid,  creosote,  etc.,  and  the  non-use  of  digi- 
talis by  the  mouth.  Restlessness  and  insomnia  are  often  distressing  and 
weakening  to  the  patient.  The  bromides,  valerian,  nervines,  whiskey  or 
brandy  in  hot  water,  and  hypnotics,  such  as  chloralamid,  sulphonal, 
veronal,  paraldehyde,  etc.,  are  often  more  or  less  efficacious;  but  in 
many  cases  nothing  is  comparable  to  morphine  (or  codeine  or  heroin) — 
which  in  aggravated  cases  should  not  be  withheld,  although  it  must  be 
used  with  circumspection  and  not  too  long  continued.  Persistence  of 
oliguria  after  several  days  treatment  with  digitalis  calls  for  alkaline  and 
other  diuretics  (caffeine,  sparteine,  theobromine,  etc.).  An  active  pur- 
gation (calomel,  jalap  powder,  etc.)  is  often  followed  by  active  diuresis; 
in  other  cases  the  so-called  Addison's,  Guy's,  or  Niemeyer's  pill  renders 
excellent  service : 

I^ — Powdered  digitalis, 

Powdered  squill,  of  each 20  grains      1  3 

Blue  mass  (or  calomel) 10  grains      01)5 

Mix  and  make  20  pills.  * 

S. — One  pill  four  times  daily. 

The  ascites  and  anarasca  that  do  not  yield  to  several  days  (jf  digitalis 
therapy  should  be  relieved  by  tapping  the  abdomen  and  the  use  of 
Southey's  tubes  or  aseptic  puncture  of  the  legs.  Immediate  benefit 
often  follows,  and,  as  after  tapping  a  hydrothorax,  the  heart,  relieved  of 
much  embarrassment,  is  likely  to  regain  its  tone. 


478  DISEASES  OF  THE  PERICARDIUM 

DISEASES  OF  THE  PERICAKDIUM. 

PERICARDITIS. 

Pericarditis  may  be  variously  classified :  It  may  be  apparently  primary 
(rarely)  or  secondary  (usually);  acute  or  chronic  in  onset  and  course; 
circumscribed  or  diffuse;  fibrinous,  serofibrinous,  purulent,  or  hemor- 
rhagic as  regards  the  character  of  the  exudate;  and  tuberculous,  strep- 
tococcic, staphylococcic,  pneumococcic,  etc.,  as  regards  the  specific 
etiological  factor.  Inasmuch  as  an  etiological  classification  is  scarcely 
feasible  at  the  bedside,  the  following  clinical  classification  will  be  found 
serviceable:  Acute  and  chronic  pericarditis;  of  the  acute,  the  following 
forms:  fibrinous,  serofibrinous,  purulent,  and  hemorrhagic;  and  of  the 
chronic  forms:  serous  and  adhesive. 


FIBRINOUS  PERICARDITIS. 

(Dry,  Plastic,  or  Acute  Adhesive  Pericarditis.) 

Etiology. — Fibrinous  pericarditis  occurs  most  commonly  in  early 
adult  life  (the  eighteenth  to  the  thirty-fifth  year),  but  it  may  be  observed 
also  in  childhood  and  in  advanced  life.  It  is  rare  as  a  primary,  common 
as  a  secondary  disorder,  and  it  results  always  from  infection.  It  is  found 
most  frequently  associated  with  acute  rheumatic  fever,  but  occurs  in 
tuberculous,  pneumococcic,  pyococcic,  gonococcic,  and  influenzal,  as  well 
as  in  other  infections.  It  occurs  also  in  chorea,  chronic  alcoholism,  gout, 
diabetes,  scurvy,  purpura,  anemic  and  cachetic  conditions,  acute  and 
chronic  nephritis  (frequently  as  a  terminal  infection),  etc.  It  is  often 
associated  with  myocarditis  and  endocarditis,  the  disease  in  reality 
being  a  pancarditis;  and  it  frequently  results  from  extension  of  disease 
of  adjacent  structures,  such  as  the  mediastinal  Imyph  nodes  (whence 
the  frequency  of  tuberculous  pericarditis),  the  pleurae,  the  lungs,  the 
oesophagus,  the  vertebrae,  the  peritoneum,  etc.  It  rarely  follows  local 
traumatism. 

Pathology. — ^The  lesions  may  be  circumscribed  or  diffuse.  The 
inflamed  area  becomes  hyperemic,  swollen,  lustreless,  and  finally 
granular  in  appearance;  and  a  more  or  less  abundant,  thick  or  thin, 
usually  slightly  adherent,  flbrinous  exudation  is  poured  out.  In  most 
cases,  in  reality  the  exudation  is  serofibrinous,  that  is,  there  is  always 
some  fluid  exudation,  but  this  may  be  minimal  (dry  pericarditis);  the 
fibrinous  exudation  varies  considerably  in  amount,  from  a  thin  semitrans- 
lucent  layer  to  a  thick  encasement  that  may  completely  envelop  the  heart. 
In  cases  of  moderate  fibrinous  exudation  the  motion  of  the  heart  gradu- 
ally produces  a  honeycomb-like,  or  a  bread-and-butter,  appearance  (cor 


FIBRINOUS  PERICARDITIS  479 

villosiim).  The  exudation  causes  agglutination  of  the  opposed  peri- 
cardial surfaces,  and,  ultimately  undergoing  organization,  may  lead  to 
the  formation  of  permanent  adhesions  and  pericardial  thickening.  The 
inflammatory  lesions  may  extend  a  variable  distance  into  the  myo- 
cardium. 

Symptoms .^As  a  rule,  the  disease  is  entirely  latent,  and  is  discovered 
during  life  only  when  searched  for.  There  may  be  a  little  precordial 
pain  or  distress;  and  some  fever  may  be  present,  but  this  is  usually 
an  antecedent  condition  due  to  the  primary  disorder;  it  may  be  aug- 
mented by  the  pericarditis.  The  disease  is  to  be  recognized  only  by 
the  detection  of  the  pathognomonic  friction  sound.  This  is  a  peculiar 
rubbing,  grating,  or  creaking,  to-and-fro  sound,  corresponding  in  gen- 
eral to  the  systole  and  diastole  of  the  heart,  but  not  occurring  abso- 
lutely synchronously  with  the  cardiac  sounds — lagging  behind  them, 
as  it  were;  this  is  due  to  the  fact  that  the  greatest  systolic  excursion  of  the 
surface  of  the  heart  and  therefore  of  its  pericardium  does  not  occur 
during  the  closure-time,  but  during  the  expulsion-time  of  the  systole, 
especially  at  the  termination  of  this  period  (Geigel).  In  some  cases  the 
sounds  are  systolic  or  diastolic  only;  rarely  they  exhibit  a  triple  rhythm. 
These  frictions,  as  a  rule,  are  best  heard  over  the  normal  area  of  super- 
ficial cardiac  dulness  (where  the  heart  is  closest  to  the  chest  wall)  or 
toward  the  base,  near  the  root  of  the  aorta;  they  are  often  sharply  local- 
ized to  a  small  area,  which,  as  a  rule,  is  not  a  "valve  area,"  and  they  are 
not  transmitted  as  are  endocardial  murmurs;  they  give  the  impression 
of  being  superficial,  close  to  the  surface;  they  vary  in  intensity  and 
are  sometimes  temporarily  absent;  and  they  may  be  intensified  by 
the  pressure  of  a  stethoscope,  a  full  inspiration,  the  patient's  leaning 
forward,  etc. 

Diagnosis. — ^The  diagnosis  rests  solely  upon  the  detection  of  the 
characteristic  pericardial  friction.  Pleuropericardial  frictions  may  be 
differentiated  by  their  common  situation  at  the  left  edge  of  or  beyond 
the  limits  of  the  cardiac  dulness;  by  their  being  much  influenced  by 
the  phases  of  respiration;  that  is,  although  perhaps  systolic  and  dias- 
tolic in  time,  they  are  often  intensified  during  expiration  and  lessened  or 
abolished  at  the  height  of  full  inspiration. 

Prognosis. — In  many  cases  the  prognosis  is  that  of  the  primary  dis- 
ease, the  pericardial  lesions  being  more  or  less  inconsequential.  Slight 
lesions  may  subside,  and  leave  perhaps  only  a  localized  area  of  thick- 
ening of  the  epicardium  (so-called  milk-spots);  usually,  however,  more 
or  less  obliteration  of  the  pericardial  sac  ensues.  If  the  lesions  do  not 
subside,  they  progress  to  serofibrinous  pericarditis. 

Treatment. — The  treatment  is  identical  with  that  of  the  early  stage 
of  serofibrinous  pericarditis. 


480  DISEASES  OF  THE  PERICARDIUM 

SEROFIBRINOUS  PERICARDITIS. 

{Pericarditis  with  Effusion.) 

Etiology. — ^There  is  no  sharp  line  of  demarcation  between  fibrinous 
and  serofibrinous  pericarditis;  in  many  cases  they  represent  different 
stages  of  the  one  process — ahke  etiologically  (bacteriologically)  and 
pathologically.  The  cases  with  much  serous  effusion,  however,  are 
most  common  in  young  male  adults,  and  are  usually  associated  with 
rheumatism,  tuberculosis,  or  mild  pyococcic  infections;  severe  pyo- 
coccic  infections  usually  lead  to  suppurative  pericarditis. 

Pathology. — In  the  early  stage  the  lesions  are  identical  with  those  of 
fibrinous  pericarditis.  Soon,  or  in  some  cases  from  the  beginning, 
a  more  or  less  abundant  fluid  exudate  is  poured  out — thin,  serous, 
yellowish,  alkaline,  albuminous  (3  to  7  per  cent.),  usually  at  least 
slightly  turbid,  and  often  containing  fibrinous  flacculi;  occasionally  the 
fluid  may  have  a  greenish  tint  or  it  may  be  purulent  or  hemorrhagic 
(suppurative  or  hemorrhagic  pericarditis).  The  fluid  varies  in  amount, 
as  a  rule,  from  100  to  2000  c.c.  In  favorable  cases  the  inflammatory 
lesions  subside,  and  are  followed  by  whitish  patches,  so-called  "milk 
spots"  (evidences  of  past  circumscribed  pericarditis),  or  total  oblitera- 
tion of  the  sac  (evidences  of  past  diffuse  pericarditis).  In  some 
cases  the  acute  lesions  become  subacute  and  finally  chronic,  and  lead 
to  partial  obliteration  of  the  pericardial  sac  associated  with  a  small 
amount  of  fluid.  In  these  cases  exacerbations  may  occur.  In  most, 
especially  severe  cases,  the  heart  shows  more  or  less  marked  interstitial 
myocarditis,  and  parenchymatous  and  perhaps  fatty  degeneration  of  the 
muscular  fibers. 

Symptoms. — Serofibrinous  pericarditis,  occurring  in  the  course  of  many 
of  the  infectious  diseases,  frequently  runs  its  course  entirely  unsuspected; 
in  other  cases  extensive  collections  of  fluid  occasion  but  little  distress,  and 
are  only  accidentally  discovered  by  physical  examination  (latent  cases). 
In  some  severe  cases  certain  well-marked  though  non-characteristic 
symptoms  occur. 

The  general  symptoms  are  those  of  the  primary  disease,  and  moderate, 
irregular  fever — 102°  to  103°  F.  The  local  symptoms  consist  of  pain, 
which  is  usually  moderately  distressing,  but  which  may  be  severe  or 
may  be  absent;  and  dyspnoea,  in  some  cases  progressing  with  the  out- 
pouring of  the  exudation  to  orthopnoea,  and  the  other  results  of  pressure 
(such  as,  paroxysmal  cough,  aphonia,  pulsus  parodoxus,  etc.).  Further- 
more, the  accumulating  fluid,  increasing  the  intrapericardial  tension, 
interferes  with  the  diastole  of  the  heart,  and  the  inflammatory  alterations 
(of  the  myocardium  as  well  as  of  the  pericardium)  interfere  with  the 
systole  of  the  heart;  these  lead  to  pallor,  cerebral  anemia,  and  headache, 
and  later  cyanosis  and  aggravation  of  the  dyspnoea  (in  part  due  also  to 
compression  of  the  lungs,  especially  the  left),  and  a  small,  weak,  and 


SEROFIBRINOUS  PERICARDITIS  481 

irregular  pulse.  In  severe  cases  toxic  symptoms  are  marked — vomiting, 
sweats,  mental  hebetude,  coma,  delirium,  etc. 

Physical  Signs. — Physical  signs  are  necessary  to  the  diagnosis.  In 
the  first  stage  there  are  the  usual  signs  of  cardiac  excitement,  such  as 
excitation  and  frequency  of  the  heart  action,  accentuated  sounds,  etc.; 
possibly  a  palpable  friction  fremitus;  sometimes  a  little  increase  in  the 
transverse  cardiac  dulness  (from  dilatation);  and  the  pathognomonic 
friction  sounds  on  auscultation.  As  the  fluid  accumulates,  the  apex 
becomes  weak,  and  ultimately,  as  a  rule,  disappears.  The  maximum 
palpable  impulse  is  often  in  the  fourth  or  the  third  intercostal  space; 
this  is  often  erroneously  interpreted  as  the  apex  beat,  but,  as  a 
matter  of  fact,  in  most  cases  the  position  of  the  heart  is  not  much 
changed;  in  large  effusions  it  often  descends  with  the  descent  of  the 
diaphragm,  being  somewhat  influenced  also  by  the  size  of  the  heart 
(whether  compressed  or  dilated).  Often  the  apex  beat  can  be  palpated 
in  or  near  its  normal  situation  by  having  the  patient  lean  forward. 
Especially  in  young  subjects,  as  the  fluid  increases  the  pericardium 
may  bulge  and  the  interspaces  become  widened;  in  purulent  cases 
there  may  be  some  oedema  of  the  overlying  skin  and  subcutaneous 
tissues. 

The  area  of  cardiac  dulness  becomes  increased  in  all  directions  (lat- 
eral displacement  of  the  pulmonary  margins).  Of  especial  importance 
is  the  fact  that  it  is  no  longer  possible  to  distinguish  an  absolute  (or 
superficial)  and  a  relative  (or  deep)  cardiac  dulness;  the  dulness  is 
absolute  throughout,  and  the  resistance  is  greatly  increased.  The  dul- 
ness varies  much  in  shape  in  different  cases:  it  is  often  described  as 
irregularly  triangular  with  a  blunt  apex  above  on  a  level  with  the  second 
left  rib  or  interspace,  and  a  broad  base  below,  extending  from  near  the 
right  mammillary  line  to  beyond  the  left  (depending  upon  the  amount 
of  fluid).  In  some  cases  the  area  of  dulness  is  distinctly  pear-shaped 
(or  pyriform);  in  others  the  shape  is  that  of  a  truncated  cylinder,  or 
trapezoidal,  or  is  quite  irregular.  The  shape  is  generally  devoid  of  much 
diagnostic  significance.  Important  signs  in  connection  with  the  dulness 
are:  disproportionate  extension  to  the  right  and  upward;  dulness  in  the 
right  fifth  intercostal  space  extending  one  to  two  inches  to  the  right  of 
the  sternum  (Rotch's  sign);  an  obtuse  (rather  than  a  right-angled  or  an 
acute)  cardiohepatic  (Ebstein's)  angle;  extension  of  the  dulness  to  the 
left  beyond  the  still  perceptible  apex  (or  heart)  beat;  change  in  the 
shape  and  extent  of  the  dulness  with  change  in  the  posture  of  the  patient 
— a  larger  area  of  dulness  when  the  patient  leans  forward  than  when  he 
is  erect  or  recumbent,  and  disproportionate  displacement  laterally  toward 
the  lower  side  when  the  patient  is  on  his  side;  dulness  near  the  angle  of 
the  left  scapula,  associated  with  l)ronchial  or  bronchovesicular  breathing, 
bronchophony,  and  increased  vocal  fremitis  (Baml)erger's  sign),  which 
disappear  or  lessen  when  the  patient  leans  forward  (anterior  prone  or 
knee-chest  posture)  and  breathes  deeply.  Similar  phenomena  may  be 
encountered  in  the  left  axilla  and  in  the  right  mammary  region.  These 
31 


482  DISEASES  OF  THE  PERICARDIUM 

signs  are  attributable  to  compression  of  the  lung,  or,  as  suggested  by 
Ewart,  to  an  altered  position  of  the  liver.  The  diaphragm  and  the  left 
lobe  of  the  liver  are  displaced  downward,  and  may  give  rise  to  a  visible 
and  palpable  bulging  of  the  epigastrium.  Compression  of  the  left  lung 
anteriorly  may  cause,  in  the  infraclavicular  region,  a  vesiculotympanitic 
note  (skodaic  resonance)  or  dulness. 

In  most  cases,  as  fluid  accumulates,  the  friction  sounds  lessen  and 
may  entirely  disappear  (especially  in  large  effusions);  often,  however, 
they  merely  become  more  restricted  in  area,  being  still  audible  at  or 
toward  the  base  of  the  heart.  In  the  absence  of  valvular  disease  the 
heart  sounds  are  intact,  although  in  the  early  stages  they  are  more  or 
less  obscured  by  the  frictions,  and  they  become  progressively  less  loud 
(muffled)  as  the  fluid  accumulates,  until  they  may  become  quite  faint 
and  distant.  As  the  fluid  becomes  absorbed,  there  is  a  gradual  disap- 
pearance of  the  abnormal  and  a  gradual  return  of  the  normal  physical 
signs. 

Diagnosis. — ^The  condition  is  frequently  overlooked,  because  of  its 
practically  symptomless  course;  many  cases  are  latent,  and  others  are 
fleeting,  developing  and  disappearing  with  great  rapidity,  especially 
in  the  terminal  stages  of  divers  disorders.  The  diagnosis  must  be  based 
wholly  upon  the  physical  signs.  Less  than  100  c.c.  of  fluid  is  scarcely 
susceptible  of  recognition.  The  nature  of  the  fluid  cannot  be  determined 
by  the  physical  signs,  but  in  rheumatic  and  tuberculous  cases  it  is  usually 
serofibrinous,  but  it  may  be  purulent  in  tuberculosis;  it  is  usually 
purulent  in  pyococcic  infections;  and  hemorrhagic  in  some  tuberculous 
cases,  and  in  purpura,  scurvy,  leukemia,  and  anemic  and  cachectic 
conditions.  It  is  often  difficult  to  distinguish  between  pericardial 
effusion  and  dilated  heart,  but  in  dilated  heart  there  is  usually  a  visible 
wavy  pulsation  over  much  of  the  precordium;  the  superficial  and  the 
deep  cardiac  dulness  may  be  differentiated;  the  dulness  is  more  globular 
in  shape,  and  rarely  reaches  as  high  along  the  right  edge  of  the  sternum, 
or  as  far  out  into  the  fifth  intercostal  space,  and  if  it  does  there  is  usually 
a  visible  and  a  palpable  impulse;  Ebstein's  cardiohepatic  angle  remains 
acute,  or  at  most  is  a  right  angle;  and  the  heart  sounds  are  usually  clear, 
sharp,  and  valvular,  and  a  gallop  rhythm  may  be  audible.  Difficulty 
is  sometimes  experienced  in  differentiating  pleural  effusion,  but  careful 
physical  exploration  should  enable  one  to  make  the  proper  diagnosis. 

Prognosis. — ^The  prognosis  depends  upon  the  nature  of  the  causative 
factors.  Most  cases  due  to  rheumatism  or  tuberculosis  recover  after 
ten  days  or  two  weeks  with  adhesions  (chronic  pericarditis).  In  cases  of 
severe  infection,  with  severe  general  symptoms,  a  large  amount  of  fluid, 
associated  valvular  disease  or  chronic  nephritis,  the  prognosis  is  anxious; 
such  cases  often  terminate  fatally.  Some  cases  become  subacute  and 
chronic. 

Treatment. — ^In  all  eases,  even  the  mildest,  the  patient  must  be  con- 
fined to  bed,  and  he  should  be  given  a  light,  liquid  and  semisolid,  nutri- 
tious diet.     In  general  the  treatment  must  be  based  upon  the  primary 


PURULENT  PERICARDITIS  483 

disorder  (rheumatism,  tuberculosis,  nephritis,  leukemia,  etc.),  if  this 
can  be  determined.  In  many,  especially  rheumatic  cases,  prompt  sub- 
sidence of  the  phenomena  follows  the  administration  of  the  salicylates 
(as  recommended  in  rheumatism).  The  pain  and  discomfort  of  the 
early  stages  not  thus  relieved  may  be  mitigated  by  the  local  application 
of  cold  (dry  or  wet),  cupping,  the  use  of  leeches,  or  by  a  hypodermic 
injection  of  morphine  and  atropine;  or  one  may  use  the  opium  and 
quinine  pill  recommended  for  acute  pleuritis.  A  blister  is  believed  by 
some  observers  to  prevent  or  limit  the  effusion.  When  once  formed,  the 
fluid,  as  a  rule,  tends  to  become  absorbed  spontaneously.  Absorption 
may  be  hastened  by  counterirritation  (blisters  or  iodine  locally),  a  light 
dry  diet  (very  little  fluid),  a  salt-poor  diet,  diuresis  (infusion  of  digitalis 
and  potassium  acetate  and  citrate),  and  catharsis  (concentrated  saline 
cathartics  before  breakfast).  Signs  of  embarrassed  cardiac  action  (fre- 
quent heart  beat,  pulsus  paradoxus,  low  blood  pressure,  pulmonary 
and  general  venous  engorgement)  call  for  withdrawal  of  the  fluid — by 
paracentesis  in  serofibrinous  effusion,  by  incision  and  drainage  in 
purulent  effusion.  For  paracentesis  the  puncture  may  be  made  in  the 
fifth  interspace  in  or  outside  the  midclavicular  line,  depending  upon  the 
distention  of  the  pericardium,  in  the  fifth  or  fourth  intercostal  space 
along  the  left  edge  of  the  sternum,  or  in  the  costoxyphoid  angle  (directing 
the  trocar  upward  and  backward).  Should  serious  cardiac  weakness 
develop  at  any  time,  stimulants,  such  as  alcohol,  camphor,  ether,  digi- 
talis, strophanthus,  etc.,  should  be  resorted  to,  and  withdrawal  of  the 
fluid  should  not  be  delayed. 

PURULENT  PERICARDITIS. 

{Suppurative  Pericarditis;  Empyema  of  the  Pericardium .) 

Etiology. — Suppurative  pericarditis  is  a  secondary  disorder  that  some- 
times occurs  in  the  course  of  various  pyococcic  infections  (pneumonia, 
pleural  empyema,  general  septicopyemia),  tuberculosis,  etc.  It  may 
begin  as  a  serofibrinous  pericarditis,  or  it  may  be  suppurative  from 
the  beginning. 

Pathology. — In  cases  in  which  the  fluid  exudate  is  rather  thin  (sero- 
purulent),  the  changes  are  quite  like  those  of  serofibrinous  pericarditis, 
but  intensified;  the  fluid  is  more  opaque  and  contains  more  cells,  the 
pericardium  is  thickened  and  covered  with  a  thick  fibrinopurulent 
exudate,  and  there  is  a  marked  polynuclear  leukocytic  infiltration  of  the 
pericardium.  In  the  frankly  purulent  cases  the  fluid  is  thicker,  dis- 
tinctly purulent.  The  lesions,  as  a  rule,  extend  a  variable  distance 
into  the  myocardium,  which  may  become  the  seat  of  disseminated 
purulent  foci;  the  lesions  may  even  extend  to  and  involve  the  endo- 
cardium. The  e^xudate  rarely  becomes  in  part  absorbed,  inspissated, 
and  calcified. 

Symptoms. — In  some  cases,  the  onset  and  the  course  of  the  disease 
for  some  time  are  identical  with  those  of  serofibrinous  pericarditis,  of 


484  DISEASES  OF  THE  PERICARDIUM 

which  the  suppurative  process  may  be  an  advanced  stage.  In  other 
cases,  following  antecedent  symptoms  of  the  primary  disorder,  the 
development  of  the  pericarditis  may  be  abrupt,  with  a  cTiill,  high  tempera- 
ture, pain,  or  distress  in  the  precordial  region,  and  general  evidences 
of  toxemia,  notably  delirium  (peculiar  to  pericarditis).  In  many  cases 
the  purulent  character  of  the  exudate  is  not  suspected  for  some  time, 
unless  the  disease  develops  in  a  frank  case  of  septicopyemia.  Con- 
tinuance of  fever  otherwise  explained,  however,  suggests  the  purulent 
character  of  the  exudate,  as  do  also  progressive  pallor,  weakness,  loss 
of  flesh,  and  paroxysms  of  chills  (or  chilliness),  fever,  and  sweats,  and 
polynuclear  leukocytosis.  The  physical  signs  are  identical  with  those 
of  serofibrinous  pericarditis;  that  is,  the  physical  signs  do  not  disclose 
the  character  of  the  exudate.  QEdema  of  the  overlying  skin  and  sub- 
cutaneous tissues  is  quite  significant  of  suppuration. 

Diagnosis. — The  diagnosis  depends  upon  the  physical  signs  of  fluid 
in  the  pericardium,  oedema  of  the  overlying  skin,  general  and  local 
evidences  of  septicopyemia,  and  the  results  of  exploratory  puncture; 
this  should  not  be  neglected  nor  long  postponed  in  doubtful  cases. 

Prognosis. — ^The  prognosis  is  bad,  as  a  rule,  on  account  of  the  process 
itself  and  of  the  usually  pyococcic  infections  of  which  it  is  a  part. 

Treatment. — The  treatment  is  essentially  surgical — incision  and  drain- 
age, which  should  be  instituted  as  soon  as  the  diagnosis  is  made;  and, 
as  stated,  attempts  should  be  made  to  recognize  the  condition  as  soon 
as  possible  by  resort  to  exploratory  puncture.  Otherwise  the  treatment 
is  that  of  pyococcic  infections  in  general. 


CHRONIC  PERICARDITIS. 

Chronic  pericarditis  occurs  in  three  forms: 

1.  White  Patches  or  "Milk  Spots." — These  are  usually  found 
on  the  anterior  surface  of  the  visceral  pericardium.  Usually  they  are 
evidences  of  previous  localized  pericarditis,  although  they  have  been 
attributed  to  a  low  grade  of  chronic  hyperplasia  of  the  connective  tissue, 
the  consequence  of  the  mechanical  irritation  occasioned  by  the  continued 
impact  of  the  heart  against  the  resisting  chest  wall.  Commonly  insus- 
ceptibile  of  diagnosis,  the  condition  is  of  no  clinical  importance,  except 
in  that  it  may  be  the  source  of  frictions,  sometimes  interpreted  as  endo- 
cardial murmurs  in  apparently  healthy  persons. 

2.  Chronic  Pericarditis  with  Effusion. — The  exudate  is  usually 
serofibrinous,  sometimes  hemorrhagic  in  character,  and  not  infrequently 
there  are  some  soft  adhesions  or  partial  obliteration  of  the  sac.  Tuber- 
cles may  be  detected  by  macroscopic  and  microscopic  examination. 
Sometimes  an  apparently  primary  disorder,  it  is  usually  part  and  parcel 
of  a  more  or  less  widespread  tuberculosis.  The  disease  is  suggested  by 
general  and  gradual  failure  of  health,  subacute  onset,  chronic  coiu'se, 
"tuberculous   habitus,"   the   constitutional   symptoms   of  tuberculosis, 


CHRONIC  PERICARDITIS  485 

tuberculosis  in  the  antecedents,  tuberculous  foci  in  other  parts  of  the 
body,  and  the  physical  signs  of  pericardial  exudation,  its  persistence, 
and  the  physical  signs  of  fluid  in  other  serous  cavities.  In  the  absence 
of  clear  evidence  of  tuberculosis  elsewhere  in  the  body,  diagnostic  help 
may  be  found  in  tuberculin  injections,  and  in  the  injection  of  the  fluid 
exudate  into  guinea-pigs.  The  prognosis  is  unfavorable.  The  treat- 
ment is  that  of  tuberculosis  in  general,  and  of  serofibrinous  pericarditis. 

3.  Adhesive  Pericarditis  (Obliterative  Pericarditis;  Adherent 
Pericardium;  Concretio  Cordis  cum  Pericardio;  External  Pericarditis; 
Pleuropericarditis ;  Indurative  Mediastinopericarditis) . — Inasmuch 
as  chronic  obliterative  pericarditis,  external  pericarditis,  pleuroperi- 
carditis, and  indurative  mediastinopericarditis  in  many  cases  represent 
but  stages  of  the  same  disease,  and  can  scarcely  be  dift'erentiated  the 
one  from  the  other,  it  is  the  part  of  wisdom  and  utility  to  discuss  them 
together. 

Etiology. — ^Adhesion  of  the  two  layers  of  the  pericardium  may  be 
the  consequence  of  a  previous  acute  pericarditis,  but  the  absence  of 
symptoms  in  some  cases  leads  to  the  inference  that  the  lesions  were 
chronic  from  the  beginning.  It  is  sometimes  tuberculous  in  nature; 
and  occurs  in  rheumatic,  syphilitic,  and  nephritic  subjects. 

Pathology. — ^The  two  layers  of  the  pericardium  are  usually  intimately 
and  completely  adherent,  and  in  many  cases  also  much  thickened,  in 
consequence  of  hyperplasia  of  the  connective  tissue  and  the  organi- 
zation of  a  fibrous  exudate.  At  times  the  adhesions  being  incomplete, 
the  space  thus  left  may  contain  more  or  less  serofibrinous  or  inspissated 
and  caseous  material.  More  or  less  extensive  calcification  is  not  very 
uncommon.  Associated  with  obliteration  of  the  pericardial  sac  (internal 
pericarditis)  there  is  frequently  external  pericarditis  and  indurative 
mediastinitis  (adhesion  of  the  pericardium  and  the  heart  to  the  chest 
wall,  the  pleurae,  lungs,  and  tissues  of  the  mediastinum);  in  some  cases 
also  obliteration  and  extensive  thickening  of  the  pleurae;  and  in  other 
cases  adhesions  to  the  under  surface  of  the  diaphragm  (perihepatitis,  peri- 
splenitis, and  deforming  peritonitis — multiple  serositis)  may  be  observed. 
If  the  adhesions  are  slight  or  moderate  the  heart  may  show  little  or  no 
change  for  a  long  time.  Usually,  however,  inasmuch  as  the  adhesions 
are  dense  and  extensive,  there  is  more  or  less  extensive  hypertrophy  of 
the  heart  and  fibrous  myocarditis,  which  in  time  are  succeeded  by  dila- 
tation. 

Symptoms. — Clinically  three  classes  of  cases  may  be  distinguished: 
(1)  Cases  in  which  the  pericarditis  runs  its  course  entirely  devoid  of  symp- 
toms, and  constitutes  merely  an  accidental  finding  at  necropsy;  (2)  cases 
in  which,  sooner  or  later,  symptoms  of  disturbed  or  impeded  cardiac 
action  manifest  themselves,  and  in  which  from  the  physical  signs  the 
obliterative  pericarditis  is  more  or  less  susceptible  of  diagnosis;  and 
(3)  cases  characterized  clinically  by  marked  ascites,  with  little  or  no 
cedema  of  the  legs,  cases  in  which  the  diagnosis  of  cirrhosis  of  the  liver 
is  usually  made,  and  which  at  the  necropsy  reveal  chronic  obliterative 


486  DISEASES  OF  THE  PERICARDIUM 

pericarditis  and  certain  morbid  changes  in  other  tissues  and  organs — 
notably  pleuritis,  peritonitis,  perihepatitis,  nutmeg  hver,  red  atrophy 
of  the  Hver,  cirrhosis  of  the  Hver,  etc. 

In  the  majority  of  instances  when  chronic  adhesive  or  obHterative 
pericarditis  gives  rise  to  symptoms,  the  symptoms  that  arise  are  those 
of  faihng  cardiac  compensation — palpitation  of  the  heart,  dyspnoea, 
cough,  cyanosis,  generalized  oedema,  effusions  into  the  several  serous 
cavities  of  the  body,  etc.  On  the  contrary,  in  the  cases  that  simulate  cir- 
rhosis of  the  liver,  clinically,  the  first  symptoms  are  sensations  of  fulness, 
oppression,  and  weight  in  the  upper  abdomen,  or  there  may  be  appar- 
ently a  sudden  onset  with  acute  pain;  the  abdomen  increases  in  size  and 
may  attain  very  large  dimensions — due  evidently  to  ascites  that  may 
necessitate  repeated  tappings  (Rumpf's  patient  was  tapped  301  times). 
With  increase  in  the  amount  of  the  ascites  the  abdominal  walls 
become  tense  and  painful,  and  the  other  subjective  symptoms  become 
markedly  aggravated.  There  may  be  slight  and  transitory  jaundice. 
Later,  oedema  of  the  legs  may  develop.  In  a  few  cases  oedema  of  the 
legs  comes  on  early;  it  may  remain  but  a  short  time,  disappear,  and  not 
recur  until  shortly  before  the  death  of  the  patient.  In  rare  cases  it 
persists;  but  it  is  always  inconspicuous  when  contrasted  with  the  exces- 
sive and  constantly  recurring  ascites,  and  it  scarcely  attracts  attention. 

Physical  Signs. — Physical  signs  are  essential  to  the  diagnosis.  Of 
these  the  most  important  are:  A  weak  or  absent  apex  beat,  especially 
significant  in  cases  in  which  there  is  no  increase  n  the  area  of  cardiac 
dulness;  systolic  retraction  of  a  considerable  area  about  the  apex-beat; 
systolic  retraction  of  the  base  of  the  left  chest  posteriorly,  in  the  region 
of  the  eleventh  or  twelfth  rib  (Broadbent's  sign),  attributable  to  adhesion 
of  the  heart,  pericardium,  and  diaphragm,  and  a  systolic  tug  upon  the 
diaphragm  which  becomes  communicated  to  its  point  of  attachment 
to  the  chest  wall  posteriorly;  arrest  of  the  normal  respiratory  movements 
in  the  epigastric  angle;  a  systolic  tug  in  the  epigastrium  or  in  the  neigh- 
borhood of  the  left  seventh  or  eighth  costal  cartilage;  imperfect  descent 
of  the  apex  beat  during  inspiration;  inadequate  or  entire  absence  of 
shifting  of  the  apex  beat,  with  change  in  the  posture  (lateral  posture) 
of  the  patient;  absence  of  change  in  the  limits  of  cardiac  dulness  during 
the  respiratory  phases;  absence  of  increase  of  the  cardiac  dulness  to  the 
right,  despite  marked  engorgement  of  the  veins  of  the  neck;  a  diastolic 
shock  or  rebound  of  the  heart  and  precordium;  evidences  of  dilatation 
or  hypertrophy  of  the  heart  (which  may  be  marked)  in  the  absence  of 
valvular  or  other  disease  that  might  cause  it;  absence  of  the  character- 
istic changes  in  the  heart  in  the  presence  of  definite  valvular  disease — 
that  is,  absence  of  the  usual  hypertrophy  of  the  right  ventricle  in  mitral 
valve  disease,  and  of  the  left  ventricle  in  aortic  valve  disease;  absence 
of  pericardial  effusion  in  the  presence  of  pleural  and  peritoneal  effusions ; 
paradoxic  pulse — inspiratory  diminution  in  the  force  and  volume  of  the 
arterial  pulse;  diastolic  collapse  of  the  veins  of  the  neck  (Friedreich's 
sign);  inspiratory  swelling  of  the  veins  of  the  neck  (Kussmaul's  sign); 


HBMOPERiCARDiUM  487 

a  presystolic  murmur  (Fisher's  sign)  in  the  absence  of  other  evidences 
of  mitral  stenosis  or  of  aortic  insufficiency  (Flint  murmur);  and,  as 
suggested  by  Musser,  the  non-occurrence  in  young  subjects  with  val- 
vular disease  and  cardiac  insufficiency  of  the  characteristic  improvement 
following  the  administration  of  digitalis.  None  of  these  signs  is  pathog- 
nomonic of  adherent  pericardium;  all  will  not  be  present  in  every  case, 
but  in  many  cases  a  sufficient  number  will  be  present  to  warrant  the 
diagnosis. 

Prognosis. — From  the  nature  of  the  disorder,  restoration  to  the  normal 
is  impossible.  The  outlook  depends  upon  the  establishment  and  main- 
tenance of  an  efficient  hypertrophy  of  the  heart. 

Treatment. — ^The  treatment  is  that  of  myocardial  insufficiency  and 
cardiac  decompensation  in  general.  Brauer  has  suggested  loosening 
the  adhesions  surgically  (cardiolysis),  an  operation  perhaps  permissible 
in  young  subjects  and  in  others  in  whom  the  myocardium  is  in  good 
condition. 

HYDROPERICARDIUM. 

(Dropsy  of  the  Pericardium;  Pericardial  Transudate.) 

Hydropericardium,  the  transudation  of  non-inflammatory  fluid  into  the 
pericardial  sac,  is  a  secondary  process  that  occurs  in  conditions  which 
lead  to  oedema  generally,  such  as  chronic  heart  disease  with  decompen- 
sation, as  well  as  chronic  disease  of  the  lungs  that  induce  myocardial 
disorders;  it  occurs  also  in  the  advanced  stages  of  chronic  nephritis, 
and  in  anemia  and  cachectic  states  generally  (carcinoma,  sarcoma, 
pernicious  anemia,  leukemia,  scurvy,  etc.),  in  consequence  of  hydremia 
and  perhaps  diseases  of  the  capillary  vessel,  and  toxemia.  The  symp- 
toms are  scarcely  suggestive,  and,  as  a  rule,  are  overshadowed  by  those 
of  the  primary  disorder;  dyspnoea,  cyanosis,  and  other  evidences  of 
cardiac  embarrassment,  are  usually  marked.  Hydropericardium  is 
suggested  by  the  primary  causative  factors,  the  physical  signs  of  fluid 
in  the  pericardium,  the  absence  of  friction  sounds  and  of  fever,  and  the 
presence  of  fluid  in  the  other  serous  sacs.  The  prognosis  is  bad.  The 
treaiment  is  that  of  the  primary  cardiac,  renal,  or  other  disorder,  to  which, 
should  the  symptoms  be  urgent,  paracentesis  of  the  pericardium  should 
be  added. 

HEMOPERICARDIUM. 

{Blood  in  the  Pericardium.) 

In  many  cases  of  serofibrinous  pericarditis  the  fluid  exudate  contains 
a  variable  number  of  erythrocytes,  which,  however,  usually  pass  un- 
noticed, unless  the  fluid  is  examined  microscopicly.  Sometimes  the 
erythrocytes  are  present  in  such  numbers  as  to  give  a  more  or  less  well- 
marked  hemorrhagic  tint  to  the  fluid.  This  occurs,  especially  in  certain 
cases  of  tuberculosis,  attended  by  the  eruption  of  miliary  tubercles 


488  DISEASES  OF  THE  PERICARDIUM 

in  the  pericardium  (rupture  of  new-formed  capillaries);  in  primary  and 
secondary  tumors  of  the  pericardium;  in  asthenic  and  cachectic  states, 
such  as  chronic  nephritis,  purpura,  scurvy,  leukemia,  etc.  More  obvious 
blood  in  the  pericardium  may  result  from  perforating  ulcers  of  adjacent 
organs  (oesophagus,  etc.),  and  it  may  be  due  to  rupture  of  the  heart  or 
of  an  aneurysm  of  the  ascending  aorta.  In  the  first-mentioned  cases 
the  symptoms  and  physical  signs  are  those  of  serofibrinous  pericarditis 
with  exudation;  in  the  last  mentioned,  those  of  sudden  heart  failure, 
usually  soon  succeeded  by  death. 


PNEUMOPERICARDIUM;  PYOPNEUMOPERICARDIUM. 

{Ail-  and  Gas  in  the  Pericardium.) 

Pneumopericardium  or  pyopneumopericardium  is  a  rare  condition 
that  may  result  from  trauma  (or  wounds);  from  perforation  from  an 
adjacent  air-containing  organ,  such  as  the  lung,  bronchus,  oesophagus, 
stomach,  or  intestines;  or  from  infection  by  Bacillus  aerogenes  cap- 
sulatus.  Infection  by  Bacillus  aerogenes  capsulatus  usually  occurs 
shortly  before  death,  and  the  lesions  are  those  of  a  pyopneumoperi- 
carditis  without  clear  cause.  Most  cases  result  from  perforation  of  an 
adjacent  air-containing  viscus,  such  as  rupture  into  the  pericardium 
of  a  pulmonary  cavity,  abscess,  or  gangrenous  focus,  or  pyopneumo- 
thorax, or  of  an  esophageal  carcinoma,  or  of  a  gastric  ulcer  or  gastric 
carcinoma.  In  addition  to  the  gas  the  pericardium  may  also  contain  a 
fluid  transudate,  which  in  the  great  majority  of  cases  is  purulent.  In 
rare  and  slightly  advanced  cases  it  may  be  only  serofibrinous. 

Symptoms. — The  symptoms  are  those  of  pericarditis.  The  diagnosis 
rests  entirely  upon  the  result  of  the  physical  examination.  In  the  recum- 
bent posture  the  precordium  is  tympanitic,  partly  or  entirely,  depending 
upon  whether  there  is  little  or  much  fluid.  In  most  cases  the  note  changes 
when  the  patient  assumes  the  upright  posture — the  tympany  low  down 
giving  way  to  dulness  occasioned  by  the  fluid  exudate,  or  the  heart 
itself.  The  dulness  is  still  more  noticeable  in  the  knee-chest  posture. 
The  characteristic  physical  sign  is  a  peculiar  metallic  splashing  sound, 
caused  by  the  heart  churning  up  the  fluid  and  gas;  it  is  often  very  loud, 
and  may  be  heard  at  a  distance  from  the  patient.  A  somewhat  similar 
quality,  however,  may  be  given  to  the  heart  sounds  by  a  distended  sto- 
mach, a  stomach  drawn  up,  or  pushed  up,  or  by  a  pneumothorax. 

The  prognosis  is  hopeless  except  in  a  few  traumatic  cases,  in  which 
appropriate  surgical  treatment,  incision,  and  drainage  are  instituted  early. 


CHYLOPERICARDIUM. 
Chylopericardium  has  been  observed  in  filariasis. 


ARTERIOSCLEROSIS  489 

DISEASES  OF  THE  ARTERIES. 

ACUTE  AORTITIS. 

Acute  aortitis  is  a  rare  and  ill-defined  disorder  that  is  said  to  occur 
in  certain  infections,  especially  those  due  to  the  pyococci  (so-called 
malignant  endocarditis,  puerperal  infection,  etc.),  but  also  in  typhoid 
fever,  pneumonia,  influenza,  tuberculosis,  etc.  The  lesions  are  analogous 
to  those  of  acute  endocarditis.  Acute  lesions  may  be  superadded  to 
chronic,  arteriosclerotic,  or  atheromatous  changes.  The  peripheral 
arteries  also  may  be  involved,  and  it  is  not  unlikely  that  minor  acute 
lesions,  occurring  perhaps  not  uncommonly  in  acute  infections,  are  the 
starting  point  of  the  more  chronic  lesions  of  later  life.  There  are  no 
unequivocal  symptoms,  although  substernal  distress  and  tenderness, 
palpitation  of  the  heart,  dyspnoea,  anginoid  pain,  and  the  physical 
signs  of  dilatation  of  the  arch  of  the  aorta  (without  concomitant  signs 
of  aneurysm)  are  said  to  be  significant  of  acute  aortitis.  There  may  be 
some  fever,  and  signs  of  arterial  embolism.  The  diagnosis  must  be  always 
in  doubt.     The  treatment  is  that  of  acute  endocarditis. 


ARTERIOSCLEROSIS. 

{Arterio-capillary  Fibrosis;  Atheroma;  Angiosclerosis;  Atherosclerosis;  Chronic 
Deforming  Endarteritis.) 

Arteriosclerosis  is  a  term  used  to  denote  the  series  of  changes,  largely 
degenerative  in  nature,  to  which  the  arteries  are  subject,  and  of  which 
the  conspicuous  feature  is  fibrosis. 

Etiology. — Arteriosclerosis  is  a  normal  manifestation  of  advancing 
age,  being  found  in  varying  degrees  after  the  fortieth  year.  It  is  much 
more  common,  and  present  in  higher  grade,  in  men  than  in  women; 
the  onset  in  women  is  commonly  later  in  life  than  in  men.  The  chief 
causes  of  presenile  arteriosclerosis  are  syphilis,  chronic  alcoholism, 
chronic  nephritis,  plumbism,  gout,  diabetes,  excessive  muscular  work, 
excessive  eating  and  drinking,  excessive  and  prolonged  mental  work  and 
worry,  etc.  This  presenile  arteriosclerosis  also  is  much  more  common 
in  men  than  in  women,  largely  on  account  of  the  etiological  factors. 
The  disease  is  rare  in  children,  and  when  occurring  in  them  seems  to  be 
related,  if  not  to  the  ordinary  causes,  to  infections,  such  as  typhoid 
fever,  scarlatina,  influenza,  etc.  This  may  be  the  starting  point  of  an 
arteriosclerosis  that  becomes  more  or  less  obtrusive  in  later  life. 

Pathology. — Adami  points  out  that  in  the  aorta  and  its  main  branches 
three  forms  of  arteriosclerosis  may  be  distinguished:  (1)  Nodose  arterio- 
sclerosis, which  shows  itself  in  the  slightest  cases,  as  a  thickening  and 
sclerosis,  more  particularly  at  or  around  the  origins  of  the  branches 


490  DISEASES  OF  THE  ARTERIES 

of  the  aorta,  as  yellowish-white  thickenings  notably  affecting  the  origins 
of  the  intercostal  arteries.  Later  these  grow  in  size  and  some  of  them 
coalesce,  forming  in  the  opened  aorta  projecting  flattened  nodes;  these 
may  be  scattered  somewhat  irregularly  through  the  aorta,  tending  to  be 
more  abundant  and  more  advanced  in  the  abdominal  region.  This 
is  the  form  especially  that  passes  into  atheromatous  degeneration  and 
softening,  the  breaking  down  of  the  affected  region  into  a  granular 
debris — so-called  atheromatous  abscess;  calcification  may  occur  and 
lead  to  the  formation  of  a  so-called  atheromatous  plaque.  (2)  Senile 
arteriosclerosis,  which  is  characterized  by  the  presence  of  hardened 
and  at  times  pipe-stem  radial  and  other  arteries;  but  in  the  aorta  there 
may  be  a  complete  absence  of  nodose  thickening  of  the  intima.  In  its 
place  there  is  a  diffuse  dilatation  of  the  aorta,  affecting  more  partic- 
ularly the  thoracic  portion;  the  aortic  walls  are  thinned,  instead  of 
thickened,  and  the  increased  volume  of  the  aorta  tends  to  show  itself 
not  only  in  breadth,  but  also  in  length,  the  vessel  being  somewhat 
tortuous;  the  arch  takes  a  wider  sweep,  the  abdominal  section  is  curved. 
In  the  common  iliac  and  the  carotid  arteries  there  are  slight  depressions, 
tending  to  have  their  long  axes  situated  transversely — the  reverse  of  the 
sclerotic  nodosities,  a  giving  way  taking  the  place  of  thickening  of  the 
wall.  Although  there  may  be  a  diffuse  thickening  of  the  intima  of 
moderate  grade  in  these  cases,  it  is  not  the  cause  of  the  hardening  of  the 
arteries,  this  being  due  to  calcification  of  the  media  (Klotz),  which  is 
likely  to  be  preceded  by  marked  hypertrophy  of  the  middle  coat.  This 
Adami  regards  as  the  uncomplicated  type  of  senile  arteriosclerosis 
(Monckeberg's  type),  but  it  is  relatively  uncommon;  the  commonest 
condition  in  elderly  people  being  a  combination  of  the  two  types  men- 
tioned. (3)  Syphilitic  arteriosclerosis,  which  has  its  seat  of  election 
in  the  ascending  aorta  and  the  arch,  where  the  nodes  are  likely  to  lie 
in  groups.  These  in  their  earlier  stage  are  large,  succulent,  and  semi- 
translucent  or  hyaline  in  appearance ;  they  have  little  tendency  to  athero- 
matous or  calcareous  change,  but  exhibit  a  later  scarring  or  central 
depression  with  some  puckering.  Adami  further  states  that  the  primary 
disturbance  in  these  cases  is  a  subacute  mesaortitis,  with  small-celled 
infiltration  around  branches  of  the  vasavasorum  and  absorption  of  the 
elements  proper  of  the  media.  Coincidently  there  is  overgrowth  of  the 
intimal  tissue,  and  when  as  a  result  the  deeper  portions  of  the  over- 
growth exliibit  necrotic  change  and  degeneration,  the  underlying  inflam- 
matory granulation  tissue  advances  new  capillaries  into  the  necrotic 
area.  The  result  is  an  absorption  of  the  degenerated  material,  replace- 
ment by  cicatricial  tissue,  shrinkage,  and  scarring.  There  is  a  lack  of 
this  vascularization  and  replacement  in  the  ordinary  nodose  arterio- 
sclerosis. Adami  speaks  of  the  smaller  arteries  as — the  muscular  arteries 
and  the  arterioles :  the  muscular  arteries  exhibit  changes  similar  to  those 
mentioned  in  the  three  types  of  sclerosis,  but  there  is  less  atheromatous 
and  degenerative  change ;  the  calcification  that  does  occur  in  the  middle- 
sized  arteries  involves  the  media  more  than  the  intima;  and  there  is 


ARTERIOSCLEROSIS  491 

more  or  less  diffuse  thickening  of  the  intima  and  overgrowth  of  the 
intima,  suggesting  a  change  to  compensate  for  thinning  of  the  media; 
the  arterioles  exhibit  in  general  similar  changes,  but  in  one  series  of  cases 
hypertrophy  of  the  muscular  coat  is  the  dominating  change,  in  another 
series  fibrosis  is  the  most  evident  alteration — fibrosis  of  the  intima, 
fibrosis  replacing  largely  the  muscular  tissue  of  the  media,  and  fibrosis 
and  pronounced  overdevelopment  of  the  adventitia. 

Adami  describes  the  following  as  the  effects  of  syphilis  on  the  aorta, 
and  states  that  the  lesions  of  the  other  forms  of  arteriosclerosis  are 
quite  similar:  The  primary  disturbance  is  a  granulomatous  inflam- 
matory degeneration  of  the  media,  which  leads  to  a  local  giving  way 
of  the  media  (fatty  degeneration,  necrosis,  and  calcareous  infiltration 
of  the  muscular  fibers,  and  loss  of  elasticity  of  the  elastica).  If  this 
giving  way  be  moderate,  it  results  in  a  strain  hypertrophy  of  the  intima 
and  the  adventitia,  with  the  development  of  nodose  intimal  sclerosis; 
if  it  be  extreme,  overstrain,  atrophy  of  the  intima,  and  aneurysmal  forma- 
tion ensue.  The  intimal  nodosities  are  not  of  inflammatory  type  and  are 
non-vascular,  although  with  the  progressive  laying  down  of  layer  upon 
layer  of  connective  tissue  on  the  more  internal  aspect  of  the  intima  the 
earlier  and  deeper  placed  layers  of  new  tissue  gain  less  and  less  nourish- 
ment, and  are  likely  to  exhibit  fatty  degeneration  and  necrosis.  These 
products  of  necrosis  exert  a  chemotactic  influence  upon  the  nearby 
vessels  of  the  medial  granulation  tissue,  with,  as  a  result,  a  secondary 
and  later  entrance  of  new  vessels  into  the  early  and  deeply  placed 
atheromatous  area,  absorption  of  the  necrotic  products,  replacement 
by  granulation  tissue,  contraction  of  the  granulation  tissue,  and  depres- 
sion and  scarring  of  the  sclerotic  nodules  so  characteristic  of  syphilitic 
sclerosis.  Strain  and  overstrain  are  believed  to  be  of  the  greatest 
importance.  As  regards  the  significance  of  heightened  blood  pressure 
(hyperpiesis,  Allbutt),  Adami  reaches  the  conclusion  that  like  results 
may  ensue  when,  on  the  one  hand,  the  artery  has  undergone  weakening 
and  the  blood  pressure  is  normal,  and  when,  on  the  other  hand,  the 
artery  has  no  preliminary  degeneration  of  its  media  and  the  blood 
pressure  is  above  the  normal.  The  increased  blood  pressure  may  be 
variously  provoked.  By  some  observers  it  has  been  attributed  to  hyper- 
activity of  the  adrenals,  perhaps  induced  by  divers  toxic  causes. 

Symptoms. — The  symptoms,  like  the  lesions,  as  a  rule,  are  insidious 
in  onset  and  slow  in  progression,  although  rarely  they  seem  to  develop 
with  considerable  celerity.  Even  considerable  degrees  of  arteriosclerosis, 
however,  may  be  present  for  years  without  occasioning  notable  symp- 
toms, and  symptoms  when  they  do  occur  are  most  diverse  in  nature, 
due  to  the  fact  that  although  the  arteriosclerotic  process  may  be  wide- 
spread, the  lesions  are  often  unequally  pronoimced  in  different  parts 
of  the  body. 

In  the  early  stages  there  is  lessened  elasticity  and  contractility  of  the 
vessels  and  consequent  imperfect  and  irregular  distribution  of  the  blood — 
which  may  be  a  more  or  less  permanent  condition  or  only  induced  by 


492  DISEASES  OF  THE  ARTERIES 

exertion,  fatigue,  etc.,  and  the  ensuing  symptoms  are  correspondingly 
variable.  In  general  they  are  those  of  lessened  vigor  and  vitality,  of 
fatigue,  neurasthenia,  etc.  The  patient  readily  becomes  tired,  even 
more  or  less  exhausted ;  he  is  nervous  and  irritable,  unable  to  concentrate 
his  attention  as  formally,  and  suffers  from  headache,  vertigo,  insomnia, 
or  somnolence;  exertion  may  provoke  various  painful  sensations,  such 
as  headache,  paresthesias,  neuralgiform  pains,  or  muscular  cramps; 
the  functional  activity  of  the  special  senses  (especially  hearing  and 
sight)  becomes  impaired;  and  various  other  symptoms  develop,  depend- 
ing upon  the  special  prominence  of  the  lesions  in  the  different  organs. 

Those  referable  to  the  cardiovascular  system  naturally  are  usually  in 
the  ascendency.  The  heart  passes  through  all  the  stages  from  efficient 
hypertrophy  to  final  dilatation  and  decompensation.  More  or  less 
dyspnoea  and  palpitation  of  the  heart  are  usually  present  on  exertion; 
epistaxis  and  other  hemorrhages  are  not  uncommon;  later,  oedema  and 
other  signs  of  cardiac  failure  supervene.  In  general  appearance  the 
patient  may  be  ruddy,  full-blooded,  or  he  may  be  pale  and  anemic 
looking — which  is  due  to  imperfect  distribution  of  the  blood,  and  not 
to  poor  blood,  at  least  in  the  beginning.  In  the  early  stages  major 
diagnostic  importance  attaches  to  visible  and  palpable  evidence  of 
thickening  and  tortuosity  of  the  superficial  arteries,  to  increased  blood 
pressure  (160  to  180  mm.  Hg.  or  more),  to  the  physical  signs  of  hyper- 
trophy of  the  left  ventricle,  a  dull,  prolonged,  somewhat  muflBed  first 
sound  at  the  apex  of  the  heart  (augmented  muscular  element),  an 
accentuated  aortic  second  sound,  and  a  sloping  ascent,  broad  apex, 
and  slow  decline  of  the  pulse  wave,  especially  apparent  in  tracings. 
Ultimately  the  common  signs  of  dilatation  ensue;  "indeed,  these  may  be 
the  symptoms  presented  by  the  patient  when  he  first  comes  under 
observation.  Involvement  of  the  coronary  arteries  may  lead  to  angina 
pectoris,  the  fibroid  heart,  aneurysm  of  the  heart,  thrombosis  with 
sudden  death,  etc. 

Renal  symptoms  are  often  quite  conspicuous — those  of  chronic  dif- 
fuse indurative  (interstitial)  nephritis;  indeed,  in  most  cases,  the  disor- 
der is  correctly  described  as  cardiovascular-renal  disease.  Symptoms 
referable  to  the  nervous  system  are  often  prominent;  of  these,  the 
most  important  are  headache,  vertigo,  tinnitus  aurium,  incapacity  for 
work,  and  irritability;  transitory  attacks  of  hemiplegia,  monoplegia, 
or  aphasia  (sometimes  attributed  to  arterial  spasm  and  consequent 
temporary  anemia);  cerebral  hemorrhage  (often  the  immediate  cause 
of  the  fatal  issue). 

Gastro-intestinal  symptoms — that  is,  so-called  indigestion,  but  also 
some  cases  of  gastric  ulcer,  are  sometimes  attributed  to  special  in- 
volvement of  the  supplying  vessels.  Special  interest  attaches  to 
attacks  of  severe  abdominal  pain  (abdominal  angina)  that  come  on 
several  hours  after  eating,  and  may  be  associated  with  other  anginoid 
phenomena,  such  as  angina  pectoris;  they  are  attributed  to  spasm  of 
the  gastric  and  mesenteric  vessels.     Severe  painful  cramps  in  the  legs 


ANGINA  PECTORIS  493 

induced  by  walking  are  not  infrequent  (intermittent  claudication  or 
lameness);  the  disorder  is  due  to  temporary  anemia  of  the  affected 
parts,  and  is  characterized  by  the  absence  of  symptoms  when  at  rest, 
by  their  provocation  by  walking,  by  their  cessation  upon  resting,  and 
often  by  the  absence  of  a  palpable  pulsation  in  the  pedal  arteries. 

Obstruction  to  arteries  elsewhere  may  give  rise  also  to  local  pain,  and 
if  the  obstruction  become  complete  gangrene  may  follow. 

Diagnosis. — ^The  diagnosis  may  be  suggested  by  the  known  hal)its 
of  the  patient,  his  general  appearance  (full-blooded  or  anemic  looking), 
and  gradual  impairment  of  vigor  and  vitality;  confirmation  of  the 
diagnosis  is  found  in  the  obvious  condition  of  the  peripheral  arteries, 
the  hypertrophy  of  the  left  ventricle,  an  accentuated  aortic  second 
sound,  and  the  pulse.  In  most  cases  also  the  blood  pressure  will  be 
found  high,  but  in  many  quite  advanced  cases,  the  blood  pressure  is 
low,  perhaps  normal  or  less.  All  early  diagnoses  may  sometimes  be 
made  by  ophthalmoscopic  examination  of  the  retinal  vessels. 

Prognosis. — ^The  outlook  in  general  is  unfavorable,  but  it  should  not 
be  exaggerated,  since  the  disorder  is  one  evidence  of  advancing  age, 
Occurring  in  young  subjects,  however,  arteriosclerosis  usually  shortens 
life,  and  is  dangerous  on  account  of  the  possibility  of  apoplexy,  uremic 
manifestations,  heart  failure,  etc.  In  many  cases  the  progress  of  the 
disease  may  be  stayed  by  appropriate  treatment. 

Treatment. — The  disorder  can  be  more  readily  prevented  than  cured. 
All  the  known  causative  factors  should  be  avoided,  especially  excessive 
eating  and  drinking,  alcohol,  tobacco,  tea  and  coffee,  excessive  mental 
and  bodily  work,  etc.,  and  the  patient  should  be  instructed  to  lead  a 
quiet  life  free  from  unnecessary  cares  and  excesses  of  all  kinds.  Dis- 
eases known  to  lead  to  arteriosclerosis  should  be  efficiently  treated, 
especially  syphilis,  gout,  diabetes,  lead  poisoning,  chronic  nephritis,  etc. 
In  many  even  non-syphilitic  cases  the  iodides  seem  to  do  good,  and  may 
be  given  (30  grains,  2  grams,  daily)  for  a  month  at  a  time  and  then  dis- 
continued for  a  month.  Excessive  blood  pressure  should  be  reduced  by 
nitroglycerin  (not  longer  than  three  or  four  weeks  at  a  time),  sodium 
nitrite,  erythrol  tetra-nitrate,  free  catharsis,  a  low  diet,  and  rest;  but 
one  must  remember  that  some  of  the  increased  pressure  is  a  conserva- 
tive process,  and  an  attempt  to  reduce  the  pressure  to  normal  should 
not  be  made.  Much  benefit  often  attends  a  course  of  treatment  at  one 
of  the  well-known  spas,  or  a  course  of  massage,  passive  exercise,  and 
warm  baths.  When  the  heart  begins  to  fail,  the  treatment  is  that  of 
the  fibroid  heart. 

ANGINA  PECTORIS. 

(Stenocardia;  Heart-pa  ncj;  Breast -pang.) 

Angina  pectoris  is  a  disorder  usually  associated  with  sclerosis  of  the 
first  portion  of  the  aorta  and  the  coronary  arteries,  and  characterized 
by  paroxysmal  attacks  of  excruciating  pain  in  the  region  of  the  heart, 


494  DISEASES  OF  THE  ARTERIES 

a  sensation  of  constriction  of  the  chest,  and  a  feeling  or  fear  of  impending 
death,  and  sometimes  sudden  death. 

Etiology. — Angina  pectoris  is  a  disease  of  adult  life  (after  the  fortieth 
year)  and  of  the  male  sex;  women  are  very  rarely  affected.  The  etio- 
logical factors  are  those  of  arteriosclerosis,  especially  alcoholism,  syphilis, 
chronic  nephritis,  gout,  excessive  muscular  and  mental  work,  etc. 

Pathology. — ^The  lesions  found  in  fatal  cases  consist  of  sclerosis  and 
atheroma  of  the  first  part  of  the  aorta,  of  the  coronary  vessels  (especially 
their  mouths),  and  of  degenerative  (fibroid  and  fatty)  changes  of  the 
myocardium.  Often  there  is  associated  disease  of  the  aortic  valve  and 
orifice,  or  aneurysm  of  the  aorta.  In  some  cases  degenerative  changes 
have  been  found  in  the  cardiac  ganglia.  Rarely  the  disorder  is  found 
in  association  with  mitral  disease.  In  a  few  cases  no  noteworthy  lesions 
have  been  found  (perhaps  they  have  been  overlooked). 

The  nature  of  the  disease  has  not  been  fully  elucidated.  It  is  assuredly 
absurd  to  describe  it  as  a  neurosis,  as  is  commonly  done.  Clifford 
Allbutt,  with  much  reason,  regards  the  disorder  as  a  painful  lesion  of 
the  first  part  of  the  arch  of  the  aorta:  an  aortitis,  rheumatic  or  influ- 
enzal, etc.  (in  which  cases  the  tensile  stresses  may  be  about  or  even  below 
normal),  or  atheroma  of  the  aorta  (in  which  cases  the  tensile  stresses 
may  be  normal  or  excessive).  He  believes  that  sometimes  the  disorder 
is  produced  by  stretching  of  the  pericardium,  as  in  aneurysm  of  the 
left  ventricle,  or  by  inflammation  of  that  part  of  the  tunic  which  invests 
the  root  of  the  aorta,  and  that  very  rarely  it  may  depend  on  some  extraor- 
dinary kind  of  disturbance  in  the  mitral  area.  Mackenzie  points  out 
that  the  symptoms  occur  in  patients  with  the  most  diverse  forms  of 
lesions,  even  in  the  absence  of  any  evidence  of  cardiac  disease:  the  most 
common  conditions  are  aortic  aneurysm,  aortic  valvular  disease,  atheroma 
of  the  coronary  arteries,  myocardial  degeneration  or  enfeeblement  from 
poor  nourishment  or  overexertion,  and  increased  arterial  pressure 
usually  associated  with  coronary  sclerosis  and  myocardial  degeneration 
in  elderly  subjects.  He  further  points  out  that  in  these  conditions  angina 
pectoris  is  a  late  symptom,  developing  after  the  heart  has  been  struggling 
for  a  long  time  against  obstacles  opposed  to  an  efficient  action,  or  after 
the  nutrition  of  the  muscle  has  been  impaired  by  gross  pathological 
changes  in  the  coronary  artery,  or  when  the  myocardium  has  become 
impaired  through  slowly  advancing  degeneration  of  the  muscle  fibers; 
that  many  patients  when  at  rest  do  not  suffer  from  pain,  but  that  any 
cause  inducing  increased  work  in  the  heart  provokes  an  attack.  He 
concludes  that  angina  pectoris  is  an  evidence  of  exhaustion  of  contrac- 
tility, and  occurs  when  the  contraction  meets  a  greater  resistance  than  it 
can  easily  and  efficiently  overcome,  whether  a  fairly  strong  muscle 
struggles  against  an  increased  resistance,  or  when  a  weak  or  degenerated 
muscle  has  opposed  to  its  contraction  a  normal  or  even  lowered  pressure, 
but  a  pressure  greater  than  the  weakened  muscle  can  readily  overcome. 
Huchard  attributes  the  attack  to  anemia  of  the  heart  muscle  the  result 


ANGINA  PECTORIS  495 

of  disease  or  spasm  of  the  coronary  arteries,  and  compares  it  to  inter- 
mittent lameness  or  claudication. 

Symptoms. — ^The  chief  manifestation  of  angina  pectoris  is  paroxysmal 
pain;  but  excluding  the  rare  cases  of  sudden  embolic  plugging  of  the 
coronary  artery,  this  paroxysmal  pain  occurs  only  after  a  long  period 
of  gradual  enfeeblement  of  the  myocardium,  and  it  is  almost  always 
induced  by  some  extra  demand  upon  the  heart,  such  as  muscular  effort, 
mental  excitement,  increased  peripheral  resistance  (chilling  of  the 
surface,  etc.),  flatulence,  etc.  The  paroxysms  may  vary  considerably 
in  severity,  from  slight  precordial  pain  or  constriction  of  the  chest  to 
the  most  severe  attacks.  These  consist  of  paroxysms  of  excruciating 
pain  in  the  region  of  the  heart,  a  sensation  of  constriction  of  the  chest, 
especially  in  front,  and  a  feeling  of  exhaustion  and  mental  anguish 
amounting  to  an  apprehension  of  impending  death.  The  pain  is  usually 
of  the  most  excruciating  character;  it  irradiates  from  the  cardiac  plexus 
behind  the  aorta  along  the  distribution  of  the  first  four  thoracic  and  the 
seventh  and  eighth  cervical  nerves,  that  is,  to  the  left  shoulder,  arm, 
and  neck;  rarely  also  to  the  right  side,  or  the  abdomen.  The  associated 
sensation  of  tightness  or  constriction  of  the  front  of  the  chest  is  attrib- 
uted by  Mackenzie  to  spasm  of  the  intercostal  muscles  induced  by  reflex 
stimulation.  Phenomena  of  vasomotor  disturbance  are  usually  present, 
such  as  pallor  (occasionally  flushing)  of  the  face,  profuse  perspiration, 
etc.  The  patient  may  be  absolutely  immobile,  with  a  staring  countenance, 
completely  conscious,  but  unable  to  articulate;  or  he  may  be  restless 
and  anxious;  in  either  event  he  is  usually  overcome  emotionally  by  the 
greatest  mental  anguish.  During  the  attack  the  heart  is  variable;  often 
it  reveals  no  changes  aside  from  the  phenomena  of  arteriosclerosis,  being 
quite  normal  in  rate,  rhythm  and  strength;  but  the  pulse  may  become 
soft,  compressible,  and  scarcely  perceptible  (weak  heart),  or  extra- 
systoles  and  the  alternating  pulse  may  occur.  Mackenzie  states  that  the 
blood  pressure  may  not  be  increased.  Dyspnoea  is  not  a  phenomenon 
of  angina  pectoris  per  se,  although  it  may  be  induced  by  associated 
conditions.  The  attack  lasts  from  a  few  seconds  to  a  minute  or  there- 
al)outs;  rarely,  however,  severe  pain  or  a  succession  of  attacks  may  con- 
tinue for  an  hour  or  more.  The  paroxysm  may  lead  to  immediate 
death  (even  the  first  paroxysm),  or  it  may  subside  as  suddenly  as  it 
began,  or  at  its  height  the  patient  may  pass  into  syncope.  The  end 
of  the  paroxysm  may  be  associated  with  the  eructation  of  gas  (uncon- 
sciously sucked  in  during  the  attack),  the  passage  of  a  large  amount  of 
urine,  etc.  After  the  attack  the  patient  feels  exhausted  for  several  hours 
or  several  days,  and  some  substernal  distress  may  persist  for  a  short  time. 

Recurrences  may  ensue  for  several  days  in  succession  with  increasing 
weakness  of  the  myocardium;  or  at  irregular,  more  or  less  long,  intervals, 
over  a  period  of  years;  or  the  first  may  prove  to  be  the  only  attack. 
Cessation  of  the  attacks  may  follow  dilatation  of  the  heart  and  relative 
mitral  insufficiency  (Musser),  but  the  ordinary  signs  of  decompensation 
are  likely  soon  to  supervene. 


496  DISEASES  OF  THE  ARTERIES 

Diagnosis. — ^The  severe  paroxysms  are  sufficiently  characteristic  as 
scarcely  to  be  mistaken.  Slight  attacks  are  often  overlooked  or  mis- 
interpreted, but  it  is  significant  if  they  are  provoked  by  exertion,  excite- 
ment, etc.,  and  if  they  are  associated  with  anginoid  attacks  in  the  legs 
(intermittent  lameness),  or  in  the  gastro-intestinal  tract  (abdominal 
angina)  etc.  The  so-called  pseudo-angina  that  occurs  in  hysterical, 
neurasthenic,  and  other  nervous  disorders  must  be  excluded.  Huchard 
points  out  that  it  is  most  common  in  women  of  all  ages;  the  attacks 
are  spontaneous,  and  often  periodical  and  nocturnal;  the  pain  is  less 
severe,  lasts  a  long  time,  and  is  associated  with  other  nervous  phenom- 
ena— ^vasomotor  and  neuralgiform;  it  is  not  fatal;  and  it  is  improved 
by  medication  directed  to  the  nervous  system.  A  toxic  angina  is  some- 
times set  up  by  tobacco,  coffee,  etc.  Nothnagel  described  a  vasomotor 
angina,  characterized  by  coldness  and  numbness  (vasomotor  spasm) 
of  the  extremities,  faintness,  and  precordial  pain. 

Prognosis. — ^The  condition,  of  course,  is  grave,  but  not  so  apprehen- 
sively so  as  is  often  maintained;  it  depends  upon  the  efficiency  of  the 
heart  muscle,  and  the  care  with  which  the  patient  regulates  his  Mfe. 
^^^lile  the  first  attack  may  be,  it  is  usually  not,  fatal,  and  proper  treat- 
ment may  lead  to  cessation  of  the  attacks. 

Treatment. — The  treatment  in  general  is  that  of  arteriosclerosis 
and  the  fibroid  heart,  the  chief  indications  being  to  reduce  the  pressure ' 
against  which  the  more  or  less  exhausted  myocardium  must  contend, 
or  the  stress  or  tension  to  which  the  sore  aorta  (Allbutt)  is  subjected, 
and  to  avoid  all  the  factors  that  may  provoke  an  attack.  Underlying 
conditions  such  as  rheumatism,  gout,  syphilis,  diabetes,  flatulence,  etc. 
must  receive  appropriate  treatment.  The  patient  must  bring  his  daily 
work  well  within  the  capabilities  of  his  heart;  he  must  avoid  all  over- 
exertion, and  lead  a  quiet  life.  A  prolonged  holiday  or  a  course  of 
treatment  at  some  one  of  the  well-known  spas  is  often  very  efficacious. 
In  some  cases  rest  in  bed  for  a  time  is  essential.  The  diet  must  be 
restricted  and  carefully  regulated,  an  excess  of  meats  and  especially  of 
carbohydrates  being  avoided,  especially  at  the  evening  meal;  and  cardiac 
excitements,  such  as  alcohol,  coffee,  tea,  tobacco,  must  be  prohibited. 
The  frequent  use  of  mercurial  and  saline  laxatives  is  very  valuable. 
The  iodides  seem  to  be  of  unquestionable  service;  potassium,  sodium, 
or  ammonium  iodide  should  be  given  in  small  (3  to  5  grain,  0.2  to  0.3 
gram)  doses  for  a  long  time,  with  short  periods  of  intermission  (one  week 
in  four);  or  one  may  use  nitroglycerin  for  the  physiological  eft'ect,  in  fre- 
quently repeated  doses  (since  the  effect  of  each  dose  does  not  last  more 
than  an  hour);  or  one  may  give  erythrol  tetranitrate  (^  grain,  0.03 
gram,  three  or  four  times  daily),  or  the  nitrites — which  have  a  more 
lasting  effect. 

The  paroxysms  are  best  treated  with  amyl  nitrite,  of  which  3  to  5 
minims  (0.2  to  0.3  gram)  should  be  given  by  inhalation.  A  subject  of 
angina  pectoris  should  carry  glass  capsules  or  perles  containing  the  men- 
tioned dose,  and  immediately  upon  the  onset  of  the  paroxysm  break  one 


ANEURYSM  497 

in  his  handkerchief  and  inhale  it;  rehef  is  usually  prompt  and  complete. 
In  some  cases  benefit  does  not  ensue,  in  which  event  resort  should  be 
had  to  morphine  {\  grain,  0.015  gram)  and  atropine  (y^o-  grain,  0.CC06 
gram)  hypodermicly ;  or,  as  recommended  by  Osier,  a  few  whiffs  of 
chloroform  (it  must  be  used  with  caution,  since  it  may  prove  a  dangerous 
remedy).  Recurring  nocturnal  attacks  may  be  sometimes  prevented  by 
chloral,  the  bromides,  valerian,  etc.  Allbutt  recommends  the  continuous 
use  of  atropine,  in  increasing  doses  as  tolerance  is  established,  with  a 
view  to  blocking  the  impulse  by  which  the  heart  is  inhibited.  The 
treatment  of  the  eventual  failure  of  the  heart  is  that  of  the  fibroid 
heart;  digitalis,  however,  as  a  rule,  and  similar  cardiac  tonics  are  dis- 
tinctly contra-indicated, 

ANEURYSM. 

An  aneurysm  is  a  circumscribed  tumor  containing  fluid  or  solid  blood, 
communicating  directly  with  the  canal  of  an  artery,  and  limited  by  the 
tunic  which  is  called  the  sac  (Hilton  Fagge). 

Etiology. — The  causative  factors  in  general  are  those  of  arteriosclerosis, 
of  which  aneurysm  is  a  result.  Major  significance  attaches  to  syphilis 
and  excessive  muscular  strain,  whence  aneurysms  are  most  common 
in  the  male  sex  (86  per  cent,  of  the  cases).  They  develop  most  commonly 
between  the  thirtieth  and  the  fortieth  year,  that  is,  they  "coincide  with 
that  time  of  life  when  the  period  of  greatest  bodily  vigor  overlaps  the 
beginnings  of  the  period  of  the  occurrence  of  atheroma"  (Coats). 

Pathology. — True  and  false  aneurysms  may  be  distinguished,  the  true 
aneurysm  being  one  in  which  the  aneurysmal  sac  consists  in  whole 
or  in  part  of  the  wall  of  the  bloodvessel,  the  false  being  one  in  which 
the  aneurysmal  sac  consists  of  connective  tissue,  the  wall  of  the  blood- 
vessel having  ruptured  and  permitted  the  extravasation  of  blood  into  the 
surrounding  connective  tissue;  but  one  must  bear  in  mind  that  the  sacs 
of  many  so-called  true  aneurysms  in  their  later  stages,  at  least,  are  com- 
posed largely  of  connective  tissue,  the  walls  of  the  bloodvessel  originally 
constituting  the  sac  having  become  atrophic,  degenerated,  and  replaced 
by  newly  formed  connective  tissue.  A  true  aneurysm  may  be,  and 
usually  is,  circumscribed  and  saccular,  that  is,  it  communicates  with 
the  lumen  of  the  vessel  by  a  narrow  opening  called  the  neck;  or  it 
may  be  ectatic,  that  is,  merely  a  dilatation  of  the  vessel,  and  fusiform, 
cylindrical,  or  cirsoid  in  shape;  or  it  may  be  dissecting,  that  is,  the 
result  of  rupture  of  the  intima  and  consequent  infiltration  of  the 
blood  between  the  coats  of  the  vessel,  whence  it  may  find  its  way  into 
the  lumen  of  the  vessel  again  or  outward  into  the  adjacent  connective 
tissues.  Quoting  Coats,  an  aneurysm  may  be  said  to  be  the  result  of 
"a  local  disproportion  in  the  normal  balance  between  the  amount  of 
lateral  pressure  inside  the  artei-y  and  the  elastic  resistance  of  the  vas- 
cular walls,  arising  either  from  abnormal  increase  of  the  former  or 
diminution  of  the  latter;  most  frequently,  indeed,  from  both  these  causes 
32 


498  DISEASES  OF  THE  ARTERIES 

combined."  The  increased  pressure  is  a  concomitant  and  causative 
factor  of  the  arteriosclerotic  process;  the  diminution  in  the  elastic 
resistance  of  the  vessel  is  also  part  of  the  arteriosclerotic  process,  but  the 
local  predisposition  that  determines  the  site  of  the  aneurysm  is  a  con- 
genital inherent  localized  weakness  of  the  vessel  wall,  or  an  acquired 
deficiency  of  vitality  that  may  be  only  a  special  localization  of  the 
sclerotic  process  or  the  result  perhaps  of  some  infection  passed  through 
in  early  life. 

Saccular  aneurysms  may  be  single  or  double  (rarely  multiple);  and 
very  small,  scarcely  more  than  a  slight  bulging  or  pouching  of  the  vessel, 
or  they  may  attain  the  size  of  a  child's  head.  Seventy-five  per  cent,  of  all 
aneurysms  involve  the  thoracic  aorta,  and  of  these,  59  per  cent,  the 
ascending  portion  of  the  arch,  29  per  cent,  the  transverse  portion  of  the 
arch,  and  12  per  cent,  the  descending  portion  (Crisp). 

Rarely  other  types  of  aneurysms  occur,  such  as :  embolic  and  mycotic 
aneurysms  due  to  mechanical  or  infected  emboli  (they  are  usually  mul- 
tiple); a  traction  aneurysm  on  the  under  surface  of  the  aortic  arch,  at 
the  site  of  the  insertion  of  the  remnant  of  the  ductus  Botalli;  an  arterio- 
venous aneurysm,  in  which  a  communication  is  established  between  an 
artery  and  a  vein;  should  the  communication  be  direct  the  condition 
is  spoken  of  as  an  aneurysmal  varix ;  should  a  sac  intervene,  it  is  termed 
a  varicose  aneurysm. 

Symptoms. — ^An  aneurysm  may  be  for  a  long  time  latent;  indeed,  the 
first  manifestations  may  be  the  fatal  rupture  and  hemorrhage.  In  most 
cases,  however,  sooner  or  later,  manifestations  develop,  in  the  one  case 
subjective,  the  aneurysm  of  symptoms;  in  the  other  case  objective,  the 
aneurysm  of  physical  signs.  The  symptoms  are  all  pressure  effects. 
Pain  is  most  significant;  although  absent  in  some  cases,  it  may  be  the 
most  obtrusive  manifestation  of  the  disease.  It  is  most  likely  to  be  pres- 
ent in  deep-seated  aneurysms,  and  is  usually  described  as  sharp  and  par- 
oxysmal, or  dull  and  boring.  Persistent  pain  beneath  the  sternum,  or 
in  the  region  of  the  fourth,  fifth,  or  sixth  thoracic  vertebrae,  is  extremely 
significant,  especially  if  it  be  unrelieved  by  medication.  Pressure  on 
the  intercostal  nerves  may  give  rise  to  the  most  intractable  neuralgiform 
pain,  which  may  be  referred  to  the  front  of  the  chest,  and  be  for  some 
time  the  only  symptom. 

In  a  majority  of  the  cases  the  most  noteworthy  pressure  signs  are 
connected  with  the  respiratory  tract,  of  which  the  most  important 
are  a  characteristic  cough,  alterations  in  the  voice,  and  dyspnoea, 
due  to  paralysis  or  spasm  of  one  or  both  vocal  cords,  occasioned 
by  pressure  on  the  recurrent  laryngeal  nerve  or  nerves,  generally 
the  left.  The  cough  is  brassy,  metallic,  clanging,  or  ringing  in  char- 
acter— a  laryngeal  cough,  and  of  itself  often  permits  a  presumptive 
diagnosis.  The  alterations  in  the  voice  have  been  well  described  by 
Walshe,  who  says  that  "the  speaking  voice  may  be  husky,  muffled, 
cracked,  and  hoarse,  or  simply  weakened,  or  tremulous  and  variable 
in  pitch,  or  actually  lowered  in  register."     In  some  cases  complete 


ANEURYSM  499 

aphonia  results.  Laryngoscopic  examination  frequently  reveals  the 
larynx  normal  except  in  one  respect — the  cadaveric  position  of  the  vocal 
cord  corresponding  to  the  recurrent  laryngeal  that  is  paralyzed.  In  these 
cases  the  other  vocal  cord  crosses  the  median  line  and  renders  phonation 
possible,  but  in  consequence  of  unequal  tension,  unequal  vibrations, 
and  hoarseness,  or  a  peculiar  monotone  and  inability  to  reach  a  high 
note,  a  falsetto  voice  develops.  Dyspnoea,  which  is  often  associated 
with  marked  stridor  that  may  be  inspiratory,  or  inspiratory  and  expira- 
tory, and  which  like  the  cough  is  often  paroxysmal,  is  an  extremely 
characteristic  sign.  Sometimes  the  narrow  glottis  is  still  sufficient 
for  easy  respiration  during  quiescence,  but  exertion  produces  increased 
respiratory  demand,  and  during  the  effort  the  paralyzed  cords  are 
violently  drawn  downward  and  inward,  with  resulting  apnoea.  In  some 
cases  the  trachea,  or  more  commonly  one  of  the  bronchi,  usually  the 
left,  becomes  compressed,  and  gives  rise  to  paroxysms  of  dyspnoea,  to 
lessening  of  the  respiratory  murmur  over  a  part  or  the  whole  of  the 
corresponding  lung,  and  perhaps  also  other  signs  of  compression  and 
atelectasis  of  the  lung  (diminished  expansion,  dulness  on  percussion, 
indefinite  signs  of  solidification,  etc.).  If  the  pressure  be  long  continued, 
retention  of  secretion,  fetid  bronchitis,  and  bronchiectasis  may  result; 
and  pressure  on  the  bronchial  arteries  may  lead  to  gangrene  of  the  lung 
or  indirectly  to  tuberculosis  (a  not  uncommon  complication).  Aside 
from  large  and  often  fatal  hemorrhages,  small  hemorrhages  (so-called 
weeping  of  the  aneurysm)  may  occur,  being  due  to  rupture  of  inflam- 
matory capillaries  in  the  trachea  or  bronchus  at  the  point  of  compression, 
or  to  leakage  through  the  sac  that  has  ulcerated  into  the  trachea  or 
bronchus  or  lung.  The  trachea  may  be  displaced  laterally  as  well  as 
anteroposteriorly,  and  the  normal  up  and  down  movements  during 
deglutition  may  be  restricted.  Tracheal  tugging  may  be  elicited — a 
distinct  tug  or  downward  traction  on  the  trachea  occurring  synchron- 
ously with  the  systole  of  the  heart  (Oliver's  sign) ;  a  lateral  rather  than 
a  downward  traction  is  sometimes  apparent  (Cardarelli's  sign).  Both 
are  most  common  in  aneurysms  of  the  transverse  or  descending  arch  of 
the  aorta  that  impinge  on  the  bifurcation  of  the  trachea  or  the  left  bronchus. 
A  tracheal  diastolic  shock  also  may  sometimes  be  detected  (Hall's  sign). 
Pressure  on  the  oesophagus  occasions  dysphagia;  but  it  is  remarkable 
that  in  some  cases  of  even  large  aneurysms  the  oesophagus  escapes. 
Dysphagia  may  also  be  due  to  pressure  on  the  vagus  or  its  oesophageal 
branches,  in  which  event  there  may  be  also  other  manifestations  of 
gastro-intestinal  disorder — vomiting  and  diarrhoea,  but  these  are  unusual. 
The  dysphagia  is  due  to  an  oesophageal  stricture  (which  it  virtually 
amounts  to);  and  it  is  important  to  bear  in  mind  that  in  the  event  of 
suspected  oesophageal  stricture  a  bougie  or  stomach  tube  should  not  be 
passed  until  the  possibility  of  aneurysm  has  been  excluded;  on  more  than 
one  occasion  a  stomach  tube  has  been  inadvertently  introduced  into  an 
unsuspected  aneurysm.  Pressure  on  the  thoracic  duct  may  occur,  and 
lead  to  emaciation;  whence  it  may  be  difficult  to  determine  whether 


500  DISEASES  OF  THE  ARTERIES 

emaciation  is  due  to  such  pressure  or  to  oesophageal  obstruction  and 
the  ingestion  of  insufficient  food. 

The  aneurysm  may  be  so  situated  as  to  interfere  with  the  blood 
supply  to  one  arm  or  one  side  of  the  neck  and  head.  At  times  this 
results  from  direct  pressure  on  the  supplying  artery;  in  other  cases 
it  results  from  the  artery  springing  from  the  aneurysmal  sac,  the 
blood  supply  of  the  part  in  question  being  compromised  by  the  blood 
being  obliged  to  pass  through  a  sac  more  or  less  filled  with  blood  clot. 
Examination  of  the  corresponding  arteries  of  the  two  sides  of  the  arm, 
head,  and  neck  may  disclose  retardation  and  weakness  or  lessened 
volume  of  the  pulse  on  the  affected  side;  but  one  must  bear  in  mind 
anatomical  differences  in  corresponding  arteries.  As  pointed  out  by 
Osier,  in  some  cases  of  large  saccular  aneurysm  the  normal  pulse  in  the 
abdominal  aorta  and  its  branches  (femorals,  etc.)  may  be  obliterated. 
At  times,  although  scarcely  as  frequently  as  in  intrathoracic  tumor, 
obstruction  to  the  venous  circulation  occurs — congestion  and  swelling 
of  the  veins,  cyanosis,  and  sometimes  oedema,  corresponding  in  situation 
and  extent  to  the  situation  and  degree  of  the  venous  obstruction.  In 
some  cases  more  or  less  well-marked  evidences  of  a  vicarious  collateral 
circulation  appear  in  the  normally  small  veins  beneath  the  skin.  Club- 
bing of  the  finger  ends  and  incurving  of  the  nails,  usually  unilateral  and 
corresponding  with  that  toward  which  the  pressure  of  the  aneurysmal 
sac  is  directed,  have  been  observed  in  some  cases. 

Pressure  on  the  ciliospinal  branches  of  the  sympathetic  nerve  is  by  no 
means  uncommon.  Should  it  be  moderate,  sufficient  only  to  irritate  or 
stimulate  the  vasodilator  fibers,  dilatation  of  the  pupil  and  pallor  of  the  cor- 
responding half  of  the  face  result;  should  the  pressure  be  sufficient  to  para- 
lyze or  destroy  the  vasodilator  fibers,  the  pupil  becomes  contracted,  and  the 
half  of  the  face  hyperemic  and  the  seat  of  increased  perspiration.  In  some 
cases  there  may  be  narrowing  of  the  palpebral  fissure  and  enophthalmos. 
Exophthalmos  has  been  observed;  it  has  been  attributed  to  retrobulbar 
venous  engorgement,  but  it  is  inexplicable  in  some  cases  (perhaps  stimu- 
lation of  the  unstriped  orbital  muscle  attached  to  the  eye  ball). 

Physical  Signs, — ^The  important  physical  signs  consist  of  a  visible 
and  palpable  abnormal  expansile  pulsation,  usually  to  one  side  of  or 
beneath  the  sternum,  or  in  the  episternal  notch,  or  in  the  left  back  or 
axilla.  Over  the  pulsation  a  thrill,  usually  systolic,  occasionally  also 
diastolic,  may  be  palpable;  a  diastolic  shock  is  common,  and  is  due 
sometimes  to  augmented  recoil  of  the  aortic  leaflets  (when  the  valve 
is  competent),  sometimes  to  recoil  of  the  aneurysmal  sac  or  the  aorta 
between  the  sac  and  the  aortic  valve.  The  aneurysm  occasions  an  area 
of  dulness  which  usually  merges  with  the  cardiac  dulness;  this  dulness 
is  of  the  greater  significance  the  farther  it  extends  from  beneath  to  either 
side  of  the  sternum  in  the  first,  second,  or  third  intercostal  space.  Dul- 
ness may  be  found  also  posteriorly,  usually  beneath  or  to  the  left  of  the 
vertebrae.  In  deep-seated  aneurysms  no  dulness  may  be  elicited;  and 
in  other  cases  the  dulness  may  be  obscured  by  co-existing  emphysema. 


ANEURYSM  501 

Auscultation  may  reveal  no  abnormalities.  In  the  majority  of  cases, 
in  the  early  stages  at  least,  two  sounds  are  audible  over  the  aneurysm 
— the  two  sounds  heard  normally  in  the  aortic  area.  Some  ol^servers 
attribute  the  second  sound  to  the  aneurysm  itself,  which  perhaps  may  be 
the  case  in  associated  aortic  insufficiency,  in  which,  however,  a  second 
sound  may  not  be  heard  either  at  the  aortic  area  or  over  the  aneurysm. 
In  some  cases  a  systolic  murmur  is  audible  over  the  sac;  in  other  cases 
a  double,  systolic  and  diastolic,  murmur;  the  diastolic  murmur  may  be 
produced  in  the  aneurysm  or  it  may  be  due  to  a  commonly  associated 
aortic  insufficiency.  The  murmur  may  be  audible  in  the  trachea  or  in 
the  open  mouth  of  the  patient.  The  heart  is,  as  a  rule,  more  or  less 
displaced,  and  commonly  reveals  the  physical  signs  of  more  or  less 
hypertrophy,  which  is  due  to  the  associated  arteriosclerosis,  aortic  valve 
disease,  etc. ;  the  aneurysm  as  such  produces  little  if  any  hypertrophy. 

Diagnosis. — ^The  diagnosis  depends  in  part  upon  the  symptoms,  and 
in  part  upon  the  physical  signs.  The  association  of  an  otherwise  in- 
explicable cough,  dyspnoea,  and  interthoracic  pain  should  always 
awaken  the  suspicion  of  deep-seated  aneurysm.  Percussion  and  palpa- 
tion of  a  localized  area  of  the  anterior  chest  may  provoke  paroxysms 
of  severe  pain  and  coughing,  which  Eichhorst  believes  significant  of 
aneurysm.  Aneurysms  of  the  ascending  aorta  usually  grow  from  the 
anterior  surface  forward  and  to  the  right,  and  present  in  the  first,  second, 
or  third  right  intercostal  space,  and  produce,  as  a  rule,  obtrusive  physical 
signs.  Aneurysms  of  the  transverse  arch  usually  grow  from  the  con- 
cavity of  the  arch  downward  and  backward;  symptoms  rather  than 
physical  signs  are  likely  to  be  obtrusive,  although  dulness  may  be  found 
beneath  and  to  the  left  of  the  sternum,  or  in  the  back.  Aneurysms 
of  the  descending  arch  are  likely  to  grow  from  the  posterior  surface, 
and  to  be  for  a  long  time  latent  or  to  produce  indefinite  or  ill-defined 
symptoms.  In  all  cases  of  aneurysm,  the  most  conclusive  diagnostic 
aid  is  furnished  by  the  use  of  the  a;-rays. 

In  the  differential  diagnosis  one  must  exclude  other  forms  of  pulsation, 
such  as  the  so-called  dynamic  pulsation,  which  is  common  in  the  aorta 
in  cases  of  aortic  insufficiency,  and  in  the  abdominal  aorta;  even  wide- 
spread and  forcible  pulsations  of  this  sort  often  subside  remarkably 
under  the  influence  of  rest.  The  palpable  pulsation  of  the  abdominal 
aorta  common  in  thin  and  neurotic  individuals  is  all  too  commonly 
interpreted  as  an  abdominal  aneurysm.  The  diagnosis  of  an  aneurysm 
of  the  abdominal  aorta  depends  upon  the  detection  of  a  definite  palpable 
expansile  tumor.  Pulsating  empema  in  the  neighborhood  of  the  heart 
should  not  occasion  any  diagnostic  difficulty.  Most  difficulty  is  experi- 
enced in  distinguishing  between  an  aneurysm  of  the  aorta  and  a  solid 
mediastinal  tumor;  but  aneurysm  is  most  common  in  males,  between 
the  ages  of  thirty-five  and  fifty-five,  especially  those  who  have  been 
engaged  in  laborious  occupations,  who  have  become  infected  with 
sypliilis,  and  who  have  used  alcohol  to  excess;  intrathoracic  growths 
exhibit  no  special  predilection   for  either  sex;   they  occur  at  any  age 


502  DISEASES  OF  THE  ARTERIES 

if  secondary,  but  usually  before  the  age  of  thirty-five  if  primary,  and 
occupation,  alcohol,  and  syphilis  (except  in  cases  of  gumma)  are  without 
etiological  significance.  A  bulging  expansile  tumor  is  pathognomonic 
of  aneurysm;  in  the  case  of  intrathoracic  tumor,  a  primary  growth 
elsewhere  in  the  body  or  the  development  of  a  mass  of  enlarged  lymph 
nodes  above  the  clavicle  is  likewise  practically  pathognomonic.  OEdema 
of  one  side  of  the  chest,  especially  if  unassociated  with  oedema  of  the 
corresponding  arm,  is  suggestive  of  tumor.  A  systolic  or  a  double 
murmur,  if  unassociated  with  other  evidence  of  valvular  disease,  is 
suggestive  of  aneurysm;  murmurs,  as  such,  have  no  relation  to  intra- 
thoracic growths,  but  they  may  develop  if  the  heart  be  displaced  or  the 
bloodvessels  be  encroached  upon  or  distorted.  A  palpable  diastolic 
shock  and  a  marked  accentuation  of  the  aortic  second  sound  is  quite 
common  in  aneurysm,  but  usually  absent  in  tumor.  Tracheal  tugging 
does  not  occur  in  tumor,  although  a  slight  systolic  movement  of  the 
trachea  (observable  even  in  some  healthy  persons)  may  be  detected.  The 
effects  of  aneurysm  on  the  lung  are  usually  those  of  compression  only, 
whereas  the  effects  of  tumor  growth  may  be  manifest  by  solidification, 
the  growth  invading  the  lung  tissue  and  in  some  cases  giving  rise  to 
metastatic  nodules.  In  the  case  of  tumor  a  clear,  or  probably  more 
likely  a  blood-stained,  fluid  is  common  when  the  growth  has  reached 
and  invaded  the  pleura;  should  an  aneurysm  give  rise  to  alterations  in 
the  pleura,  acute  pleuritis  usually  results.  Pain  is  usually  less  severe, 
and  is  certainly  less  characteristic  in  tumor  formation  than  it  is  in  aneu- 
rysm, although  it  may  be  entirely  absent  in  some  cases  of  aneurysm. 
Pressure  effects  on  the  recurrent  laryngeal  nerve  are  more  suggestive 
of  aneurysm  than  of  tumor.  Under  the  influence  of  rest,  potassium 
iodide,  and  other  treatment,  the  symptoms  of  aneurysm  usually,  for 
a  time  at  least,  show  amelioration,  whereas  almost  without  exception  the 
symptoms  of  tumor  are  continuously  progressive.  The  course  of  aneu- 
rysm is  very  variable  and  it  may  last  for  years,  whereas  intrathoracic 
growths  almost  certainly  result  fatally  within  a  year  from  the  onset  of 
symptoms. 

Prognosis. — ^The  outlook  in  aneurysm  is  bad,  since  from  the  nature  of 
the  disease  the  outcome  is  necessarily  fatal;  occasionally  a  spontaneous 
cure  results.  The  usual  duration  of  life  after  the  diagnosis  has  been 
made  is  from  two  to  three  years,  although  it  may  be  prolonged 
by  appropriate  treatment.  Death  usually  (75  per  cent,  of  the  cases) 
results  from  rupture  and  hemorrhage  into  the  pleura,  the  pericardium, 
the  trachea,  a  bronchus,  the  oesophagus,  or  externally  after  erosion 
and  perforation  of  the  sternum  and  the  adjacent  costal  cartilages  or 
ribs.  Death  may  be  due  also  to  asphyxia  from  compression  of  the  trachea 
or  a  main  bronchus,  to  inanition  from  compression  of  the  oesophagus 
of  the  thoracic  duct,  to  embolism  especially  of  the  brain,  etc. 

Treatment. — ^The  main  object  of  treatment  is  to  promote  clotting 
within  the  sac  and  consequent  cicatrization.  These  are  best  achieved 
by  rest  and  a  restricted  diet  (so-called  Tufnell  treatment),  which  reduce 


ANEURYSM  503 

the  force  and  frequency  of  the  heart  beat.  The  rest  should  be  absolute 
in  bed  for  two  or  three  months,  and  should  be  combined  with  mental 
quietude  and  freedom  from  excitement  and  worry.  The  diet  should 
be  reduced  to  a  minimum :  Tufnell  advised  only  ten  ounces  of  solids  and 
eight  ounces  of  fluids — a  regimen  which  is  scarcely  necessary,  and  if 
rigidly  insisted  upon  usually  induces  the  patient  to  seek  another  physi- 
cian. After  the  early  rest  in  bed,  if  the  patient  has  submitted  to  it, 
he  should  be  directed  to  lead  an  orderly  and  quiet  life,  the  danger  that 
threatens,  on  excitement,  exertion,  and  augmented  blood  pressure  being 
pointed  out  to  him.  His  bowels  should  be  moved  freely  daily  with  laxa- 
tives, so  as  to  avoid  the  straining  inevitable  in  constipation.  The  iodides 
(30  to  60  grains,  2  to  4  grams,  daily),  continued  for  a  long  time,  unques- 
tionably do  good  in  many  cases,  the  s}'philitic  as  well  as  the  non- 
syphilitic;  usually  they  notably  mitigate  the  pain,  and  in  some  cases 
they  seem  to  promote  clotting  within  the  sac.  Calcium  lactate  (40  to  60 
grains,  2  to  4  grams,  daily)  may  be  given  for  four  or  five  days  from 
time  to  time  with  the  same  object  in  view.  Gelatin  is  thought  also  to 
promote  clotting,  and  may  be  given  with  the  food,  but  its  value,  aside 
from  the  contained  calcium,  is  doubtful.  Pain  may  be  somewhat  relieved 
by  hot  or  cold  applications,  counterirritation,  etc.,  but  it  is  sometimes 
so  severe  as  to  demand  morphine,  which  from  the  nature  of  the  disease 
need  not  be  withheld  from  time  to  time,  although  it  should  be  used 
with  circumspection.  Aconite  is  sometimes  of  service  in  quieting  an 
overactive  heart.  The  introduction  of  gold  wire  and  electrolysis  to 
promote  rapid  clotting  has  been  successfully  performed  in  a  number  of 
cases,  with  relief  to  the  patient's  suffering  and  prolongation  of  his  life. 
Obviously  it  should  be  employed  only  in  sacculated  aneurysms. 


SECTION   VII. 
DISEASES  OF  THE  RESPIRATOEY  SYSTEM. 


Pathological  Physiology. — The  respiratory  system  is  designed  to  sub- 
serve the  function  of  gaseous  exchange  between  the  body  and  its  environ- 
ment; that  is,  the  absorption  by  the  blood  circulating  in  the  pulmonary 
capillaries  of  oxygen  from  the  air  contained  within  the  ]  ulmonary  alveoli, 
and  the  giving  up  by  the  blood  to  the  air  of  carbon  dioxide.  This,  the 
so-called  external  respiration,  is  much  related  to  and  upon  it  depends  the 
so-called  internal  respiration — that  is,  the  gaseous  exchange  that  takes 
place  between  the  blood  and  the  tissues,  the  absorption  by  the  tissues 
of  oxygen  essential  to  their  vital,  or  metabolic,  activities,  and  the  giving 
oflF  into  the  blood  of  carbon  dioxide,  one  of  the  end-products  of  katabo- 
lism.  The  lungs,  therefore,  are  primarily  concerned  in  the  oxidative 
processes,  of  which  the  metabolic  and  nutritive  processes  largely  consist; 
and  the  life  history  of  the  oxygen  taken  into  the  body  by  way  of  the 
lungs  (to  a  limited  extent  also  by  the  skin)  soon  becomes  associated 
with  that  of  the  food  taken  in  by  way  of  the  digestive  system;  but  this  is 
a  subject  that  pertains  more  to  disturbances  of  nutrition  than  of  res- 
piration. 

The  lungs  are  prevented  from  collapsing  by  the  pressure  of  the  atmos- 
phere (15  pounds  to  the  square  inch)  which  reaches  the  lungs  by  way 
of  the  air  passages  and  cannot  exert  a  compressing  force  on  the  lungs 
from  without,  on  account  of  the  resistance  of  the  bony  and  muscular 
framework  of  the  thorax.  In  conditions  of  deficient  entrance  of  air  into 
the  lungs  considerable  depression  of  the  intercostal  spaces  may  occur 
(especially  noticeable  in  children  with  laryngeal  or  tracheal  obstruction); 
and  should  the  l)ony  framework  of  the  chest  become  softened  (as  in  rickets) 
notable  deformity  may  and  usually  does  ensue.  In  the  event  of  perfor- 
ation of  the  chest  wall  and  the  conseriuent  access  of  the  air  to  the  ])leural 
sac,  the  lung  collapses,  usually  to  about  one-fifth  it.s  normal  volume;  this 
is  due  not  only  to  the  atmospheric  pressure  as  such,  but  also  to  over- 
coming of  the  normal  negative  intrapleural  pressure  (4  to  6  nnn.  Hg.), 
and  to  the  activity  of  the  contractility  of  the  lungs.  The  contractility 
of  the  lung.s  is  the  resultant  of  the  large  amount  of  ehistic  tissue  in  the 
pulmonary  parenchyma  and  of  the  musculature  of  the  bronchi;  (liese, 
when  normal,  give  the  huigs  their  normal  tone  and  ;ir(>  the  basis  upon 


506  Diseases  of  the  respiratory  system 

which  normal  pulmonary  percussion  resonance  depends.  This  con- 
tractility of  the  lungs,  as  well  as  the  negative  intrapleural  pressure  that 
it  occasions,  is  of  much  importance  in  disease;  it  may  become  impaired 
from  overstrain  by  increased  intrapulmonary  pressure  (blowing  wind 
instruments,  etc.)  and  by  disease  of  the  elastica,  as  happens  in  emphysema, 
as  well  as  by  compression  of  the  lung  by  a  collection  of  fluid  in  the 
pleura,  or  extensive  disease  (such  as  pneumonia)  of  one  lobe;  in  all  of  these 
conditions  the  percussion  note  becomes  vesiculotympanitic  in  character. 
The  contractility  of  the  lung  on  the  non-diseased  side  also  is  a  factor  in 
causing  displacement  of  the  heart  and  mediastinum  in  conditions,  such 
as  pleural  effusion  or  transudation  and  pneumonothorax,  in  which  the 
one  lung  becomes  more  or  less  collapsed;  and  the  negative  intrapleural 
pressure  is  doubtless  a  factor  in  inducing  hydrothorax  when  the  pleural 
vessels  become  passively  congested  (chronic  cardiac  and  pulmonary 
disease). 

Both  phases  of  respiration,  inspiration  and  expiration,  result  from 
muscular  activity,  notably  of  the  scaleni  and  intercostal  muscles  and  the 
diaphragm;  both  are  due  to  the  rhythmically  recurring  activity  and  relax- 
ation of  the  opposing  sets  of  muscles.  While  expiration  is  almost  unop- 
posed, during  inspiration  the  contractility  of  the  lungs,  the  elastic  resist- 
ance of  the  chest  wall,  and  the  force  of  gravity  (represented  largely  in  the 
bony  framework  of  the  thorax)  must  be  overcome.  How  irrational,  then, 
in  diseased  states  to  add  to  the  embarrassment  of  an  already  embarrassed 
respiration  by  the  use  of  heavy  bedclothes,  a  heavy  poultice  to  the  front 
of  the  chest,  etc.  During  inspiration  the  lungs  expand  downw^ard, 
forward,  and  laterally,  the  greatest  excursion  occurring  downward  and 
laterally,  whence  the  friction  sound  of  pleuritis  is  usually  best  heard  in 
the  anterolateral  aspect  of  the  chest.  Comparatively  little  expansion 
occurs  upward  or  backward;  such  expansion  upward  as  does  occur 
is  due  largely  to  descent  of  the  lungs  as  a  whole,  a  fact  in  part,  at  least, 
answerable  for  the  common  localization  of  tuberculosis  at  the  apices. 

The  normal  vital  capacity  of  the  lungs,  that  is,  the  greatest  volume 
of  air  that  can  be  expired  after  the  fullest  possible  inspiration,  varies 
between  3500  and  4000  c.c,  averaging  in  the  adult  male  about  3700  c.c. 
(Howell).  It  varies  somewhat  with  the  size  of  the  chest,  the  age  and 
height  of  the  individual  (being  greater  in  tall  than  in  short  subjects); 
it  is  less  in  the  prone  than  in  the  sitting  or  upright  posture  (whence  the 
exaggerated  dyspnoea  of  the  prone  posture).  It  diminishes  in  old  age, 
in  part  on  account  of  ossification  of  the  costal  cartilages  and  rigidity  of  the 
thorax,  and  it  is  reduced  in  diseases  of  the  lungs,  especially  tuberculosis. 

The  tidal  air,  the  air  breathed  in  and  out  during  ordinary  quiet 
respiration,  averages  about  500  c.c;  the  complemental  air,  the  amount, 
in  addition  to  the  tidal  air,  that  can  be  breathed  in  by  the  fullest  possible 
inspiration,  averages  about  1600  c.c;  and  the  supplemental  air,  the 
amount  which  by  a  forced  expiration  can  be  breathed  out  after  an  ordi- 
nary quiet  expiration,  averages  also  about  1600  c.c  The  tidal  air,  the 
complemental   air,   and  the  supplemental   air  together  make  up   the 


PATHOLOGICAL  PHYSIOLOGY  507 

vital  capacity.  The  residual  air,  the  amount  of  air  that  remains  in  the 
lungs  after  a  forced  expiration,  averages  about  1000  c.c;  it  becomes 
much  increased  in  emphysema.  In  health  and  during  normal  breathing 
the  reserve  supply  of  air  amounts  to  about  2600  c.c,  that  is  the  supple- 
mental air  plus  the  residual  air.  Of  the  500  c.c.  of  air  regularly  inspired 
during  quiet  breathing,  about  360  c.c.  (Howell)  reaches  the  pulmonary 
alveoli  by  a  process  of  diffusion ;  this  bears  a  relation  to  the  reserve  supply 
of  air  about  as  1  to  7,  so  that  one  may  assume  a  renewal  of  the  air 
contained  within  thelungsonce  during  each  seven  or  eight  respiratory  acts. 

The  tidal  air  suffices  for  the  ordinary  requirements  of  life,  but  the 
increased  demand  for  oxygen  entailed  by  muscular  exercise  is  met  by 
deep  breaths  (supplemental  air)  and  increased  frequency  of  breathing. 
Similarly  in  diseased  states,  when  the  available  breathing  surface  of  the 
lungs  becomes  lessened  or  the  blood  surcharged  with  carbon  dioxide, 
deep  and  frequent  respirations  (dyspnoea)  are  obvious  efforts  on  the 
part  of  the  body  to  supply  a  sufficiency  of  oxygen;  this  is  not  always 
successful,  so  that  to  the  dyspnoea,  cyanosis  is  added.  In  a  healthy  man 
weighing  70  kilograms  (150  pounds)  the  average  daily  intake  of  oxygen 
is  about  700  grams,  and  the  average  daily  output  of  carbon  dioxide  is 
about  800  grams.  This  may  be  increased  by  excessive  muscular  activity 
and  other  factors. 

The  composition  of  the  inspired  air  averages,  in  volume  per  cent., 
nitrogen,  79;  oxygen,  20.96;  and  carbon  dioxide,  0.04;  and  the  expired 
air,  nitrogen,  79;  oxygen,  16.02,  and  carbon  dioxide,  4.38  (Howell). 
This  gain  of  4.34  volumes  per  hundred  of  carbon  dioxide  and  loss  of  4.94 
volumes  of  oxygen  does  not  accurately  represent  the  change  in  the 
composition  of  the  air  in  the  alveoli,  since  during  ordinary  quiet  respira- 
ation  only  72  per  cent,  of  the  tidal  air  reaches  the  alveoli.  In  the  alveoli 
the  carbon  dioxide  reaches  5  to  6  volumes  per  cent.,  and  the  oxygen 
falls  to  13  to  14  per  cent.  Furthermore,  the  air  as  expired  has  been 
warmed  almost,  if  not  quite,  to  the  body  temperature,  whereby  the 
body  loses  daily  from  50  to  100  calories;  and  the  expired  air  is  also  almost 
saturated  with  aqueous  vapor,  from  250  to  500  grams  of  water  being 
thus  lost,  and  in  consequence  of  the  evaporation  entailing  a  daily  loss  of 
from  145  to  290  calories.  In  addition,  the  expired  air  is  often  said  to 
contain  a  poisonous,  volatile,  organic  substance  to  which  the  ill  effects 
(headache,  depression,  etc.)  of  the  vitiated  atmosphere  of  badly  ventilated 
rooms,  churches,  schools,  and  other  places  where  large  numbers  of 
people  congregate,  are  attributed.  The  results  of  investigations  of  this 
subject  are  not  entirely  conclusive,  but  there  is  no  definite  proof  of  the 
existence  of  such  a  poisonous  organic  substance.  The  unquestionable 
ill  effects  of  bad  ventilation  are  with  more  propriety  attributed  to  decrease 
of  oxygen,  increase  of  carbon  dioxide,  augmented  temperature  of  the  air 
and  its  saturation  with  aqueous  vapor,  and  exhalations  from  unclean 
bodies,  perspiration,  excretions  from  the  sebaceous  glands,  and  odors 
from  clothes. 

The  normal  body  is  able  to  withstand  the  effects  of  considerable 


508  DISEASES  OF   THE  RESPIRATORY  SYSTEM 

variations  in  atmospheric  pressure  without  ill  consequences;  but  this 
varies  much  in  different  individuals,  and  is  considerably  reduced  in 
diseases  of  the  lungs  and  the  heart  and  bloodvessels.  Notable  reduction 
in  atmospheric  pressure,  such  as  obtains  at  high  altitudes  (mountain 
climbing,  balloon  and  aeroplane  ascents,  etc.),  often  results  in  so-called 
mountain  sickness  (weakness,  faintness,  syncope,  epistaxis,  etc.);  and 
the  results  of  increase  in  atmospheric  pressure  are  well  exemplified  in 
caisson  disease.  Compressed  air,  however,  may  be  resorted  to  with 
benefit  in  many  cases  of  diseases  of  the  lungs. 

The  chief  results  of  disease  of  the  respiratory  system,  in  so  far  as  this 
system  itself  is  directly  concerned,  consist  of  diminution  of  the  external 
gaseous  exchange.  This  is,  in  part,  a  passive,  physical  process;  in  part, 
an  active  vital  process,  the  result  of  a  specific  functional  activity  of 
the  alveolar  epithelium — which  may  become  deranged  or  abolished  in 
disease.  Speaking  generally,  this  diminished  gaseous  exchange  may  be 
due  to  impeded  entrance  of  air  into  the  lungs  or  to  inability  on  the  part 
of  the  lungs  to  utilize  an  adequate  supply  of  air.  In  either  event  the 
obtrusive  clinical  manifestations  consist  of:  (1)  Disturbances  in  the 
rate  and  rhythm  of  respiration,  and  (2)  of  cyanosis;  but  both  of  these 
phenomena  may  be  due  also  to  disorder  of  the  heart,  as  well  as  to  other 
factors. 

Disturbances  in  the  Rate  and  Rhythm  of  Respiration  com- 
prise : 

1.  Dyspnwa.  The  term  dyspnoea  is  generally  applied  to  any  note- 
worthy increase  in  the  force,  rate,  or  depth  of  the  respirations;  some- 
times it  is  restricted  to  labored  breathing,  being  thus  distinguished  from 
merely  quickened  breathing  (hyperpnoea,  polypnoea,  tachypnoea),  a 
condition  that  may  be  observed  after  muscular  exercise,  during  nervous 
excitement  or  perturbation,  in  cerebral  disorders,  in  hysteria,  etc.  Dysp- 
noea is  a  provision  of  nature  designed  to  subserve  the  function  of 
breathing,  that  is,  the  proper  oxygenation  of  the  blood,  and  it  is  the 
consequence  of  obstacles  to  the  ready  performance  of  this  function  or 
of  increased  demands  for  oxygenation  (deficiency  of  oxygen  or  increase 
of  carbon  dioxide,  which  is  a  direct  stimulant  to  the  respiratory  centre). 
It  varies  in  degree  in  different  cases — from  slight  breathlessness  on  exer- 
tion or  excitement  to  orthopnoea  even  when  the  patient  is  at  rest  in  bed. 
It  may  be  objective  or  subjective,  or  both;  that  is,  it  may  or  may  not  be 
accompanied  by  subjective  sensations  of  substernal  or  thoracic  distress 
or  actual  pain,  oppressed  breathing,  lack  of  air,  and  more  or  less  anxiety 
and  apprehension;  in  some  cases  the  subjective  sensations  (so-called 
air-hunger)  may  entirely  overshadow  the  objective  dyspnoea.  Although 
increased  frequency  of  the  respirations  is  usually  an  obtrusive  feature, 
increased  respirations  are  not  always  dyspnoeic,  and  notable  dyspnoea 
may  be  associated  with  oligopnoea.  Dyspnoea  may  occur  in  the  following 
conditions:  (a)  All  painful  affections  of  the  respiratory  tract  (including 
the  pleura),  the  thoracic  wall,  the  diaphragm,  etc.  The  respirations  are 
likely  to  be  superficial  and  of  increased  frequency,     (b)  Obstruction  of 


PATHOLOGICAL  PHYSIOLOGY  509 

the  upper  air  passages:  obstructions  within  the  kimen,  disease  of  the 
passages  themselves  constricting  the  hniien,  or  compression  from  without. 
The  respirations  are  Hkely  to  be  deep,  they  are  often  infrequent,  there  is 
usually  an  associated  inspiratory  stridor,  and  the  expiration,  as  a  rule,  is 
not  prolonged,  (c)  Obstruction  of  the  lower  air  passages — the  smaller 
bronchi  and  bronchioles,  such  as  occurs  in  the  several  types  of  bronchitis, 
in  bronchial  asthma,  etc.  The  respirations  are  likely  to  be  increased  in 
frequency,  and  there  is  usually  prolonged  expiration  and  expiratory 
stridor,  (d.)  Disorders  of  the  pulmonary  alveoli,  in  which  the  available 
breathing  surface  becomes  restricted,  such  as  pulmonary  congestion  and 
oedema  (of  which  unstable  or  non-compensated  cardiac  disease  is 
usually  the  primary  factor),  emphysema,  inflammatory  conditions 
(pneumonia,  bronchopneumonia,  abscess,  etc.),  as  well  as  conditions 
that  lead  to  compression  of  the  lungs  (pleural  and  pericardial  collections 
of  fluid,  pneumothorax,  mediastinal  tumors,  distortion  of  the  vertebrae, 
displacement  upward  of  the  diaphragm,  etc.).  The  respirations  are 
usually  of  increased  rate,  force,  and  depth,  {e)  Infectious  febrile  con- 
ditions generally.  The  increased  respirations  are  due  to  a  direct  action 
of  the  bacterial  toxins  and  the  augmented  temperature  on  the  respiratory 
centre  and  to  surcharging  the  blood  with  carbon  dioxide,  a  consequence 
of  increased  metabolism.  (/)  Intoxications,  such  as  uremia  and  diabetic 
coma,  in  which  Kussmaul's  dyspnoea,  or  air-hunger  (deep,  energetic, 
long-drawn  inspirations  contrasting  with  short,  sighing  expirations), 
may  be  observed,  {g)  Anemic  conditions,  in  which  the  available  hemo- 
globin may  be  so  small  that  even  frequent  and  deep  respirations  do  not 
suffice  to  satisfy  the  demand  for  oxygen. 

2.  Oligopnoea.  Infrequent  breathing  may  be  regular  or  irregular 
(arrhythmic).  It  results  from  depression  of  the  respiratory  centre,  and 
may  be  encountered  in — some  severe  infections;  exogenous  poisonings, 
such  as  opium  and  chloral  poisoning;  autogenous  intoxications,  such  as 
uremic  and  diabetic  coma;  nervous  disorders,  such  as  meningitis,  hemor- 
rhage and  tumor  of  the  brain;  and  the  death  agony. 

3.  Arrhythmic  Breathing.  There  are  two  chief  types  of  peculiarly 
arrhythmic  breathing:  (a)  Cheyne-Stokes  breathing,  which  occurs  in 
arteriosclerotic  subjects  (cardiovascular-renal  disease),  uremia,  myocar- 
dial degeneration,  conditions  of  increased  intracranial  pressure,  etc.,  and 
is  characterized  by  longer  or  shorter  periods  of  apnoea  (cessation  of 
breathing)  alternating  with  periods  of  breathing,  at  first  slow  and  shal- 
low, but  gradually  becoming  deeper  and  more  rapid  until  they  reach  a 
maximum,  whereupon  they  gradually  decrease  and  finally  again  cease; 
and  (6)  Boit's,  or  meningeal,  breathing  (which,  however,  occurs  in  condi- 
tions other  than  meningitis) ;  it  is  characterized  by  more  or  less  periodic, 
but  sometimes  irregularly  recurring,  pauses  in  breathing  lasting  from  a 
few  to  thirty  or  more  seconds,  and  is  unattended  by  the  characteristic 
increase  and  decline  of  the  respirations  of  the  Cheyne-Stokes  breathing. 
The  causes  of  the  periodicity  of  these  types  of  breathing  are  not  well 
understood.     Both  are  of  serious  prognostic  significance. 


510  DISEASES  OF  THE  RESPIRATORY  SYSTEM 

4.  Asphyxia  or  Suffocation.  Complete  obstruction  of  respiration 
and  final  cessation  of  breathing  may  result  from:  (a)  Subjection  to  an 
inert  or  irrespirable  atmosphere;  (b)  obstruction  of  the  larynx  or  trachea 
by  an  impacted  foreign  body,  false  membrane,  tumor,  etc.,  or  by  com- 
pression from  without,  as  by  an  aneurysm,  mediastinal  tumor,  goitre, 
etc.,  or  by  hanging  or  strangulation;  (c)  laryngeal  spasm  or  oedema  or 
paralysis  of  the  vocal  cords;  [d)  drowning;  (e)  inundation  of  the  lungs 
by  fluid  from  within  the  body — blood  (ruptured  pulmonary  bloodvessel 
or  aneurysm),  serous  fluid  (severe,  especially  acute,  pulmonary  oedema), 
pus  (retropharyngeal  abscess,  etc.);  (/)  intoxications,  such  as  accom- 
pany chronic  passive  congestion  from  decompensated  cardiac  disease, 
in  which  the  excess  of  carbon  dioxide  poisons  the  respiratory  centre; 
morphine,  chloral,  or  chloroform,  which  poison  the  respiratory  centre 
directly;  and  coal-gas  poisoning,  in  which  carbon  monoxide  replaces 
the  oxygen  from  the  hemoglobin;  and  (g)  severe  and  prolonged  tetanic 
convulsions  (strychnine  poisoning,  tetanus,  status  epilepticus). 

Cyanosis.  Cyanosis  commonly  attends  dyspnoea  and  is  due  to 
like  causes,  to  a  deficiency  of  oxygen  and  an  excess  of  carbon  dioxide  in 
the  blood.  Dyspnoea,  however,  may  occur  without  cyanosis,  as  in  uremia, 
and  cyanosis  may  be  present  without  dyspnoea,  as  in  congenital  heart 
disease.  Cyanosis  is  common  in  diseases  of  the  lungs  interfering  with 
proper  oxygenation  of  the  blood,  and  may  result  from  obstruction  to 
the  entrance  of  air  into  the  lungs,  to  restriction  of  the  available  breathing 
surface  of  the  lungs,  and  to  weakness  of  the  respiratory  muscles  and 
nerves.  It  occurs  also  in  disease  of  the  heart,  in  erythremia  (page  385), 
in  chronic  acetanilide  and  other  coal-tar  poisonings,  and  in  so-called 
enterogenous  cyanosis  (page  414). 

There  are  a  number  of  acts,  such  as  coughing,  sneezing,  sighing, 
yawning,  sobbing,  hiccough,  etc.,  that  may  be  looked  upon  as  modified 
respiratory  movements.  Coughing,  the  most  important  of  these,  is 
primarily  and  essentially  protective  in  character,  being  designed  to  rid 
the  upper  air  passages  of  irritating  bodies  or  particles  or  fluid  secretions; 
it  may  also  be  produced  by  irritating  vapors,  and  by  stimuli  originating 
in  various  parts  of  the  body  and  communicated  to  the  pneumogastric 
nerve.  The  chief  sources  of  such  stimuli  comprise  the  larynx,  the 
posterior  aspect  and  the  bifurcation  of  the  trachea,  and  the  pleura.  So- 
called  gastric,  hepatic,  splenic,  and  uterine  coughs  are  sometimes 
described,  but  there  is  no  proof  whatever  of  their  acutal  occurrence.  In 
the  event  of  pathological  secretions  being  present  in  the  air  passages, 
coughing  subserves  the  useful  purpose  of  their  elimination;  it  should  not, 
therefore,  be  unwisely  suppressed  at  all  hazards,  since  retained  secretions 
are  likely  to  undergo  decomposition  and  may  bring  in  their  wake  con- 
ditions other  than  those  to  which  they  owe  their  origin.  Often,  however, 
it  is  excessive  and  disadvantageous,  distending  the  lungs  unduly  in  con- 
sequence of  increased  intrapuhnonary  pressure,  increasing  the  intra- 
thoracic pressure  and  impeding  the  flow  of  blood  to  the  heart,  and 
subjecting  the  patient  to  the  danger  of  rupturing  a  bloodvessel;  in  these 


DISEASES  OF  THE  NOSE  511 

cases  the  cough  per  se  should  be  kept  in  control.  On  the  other  hand, 
weak  or  ineffectual  coughing  or  the  inability  to  cough  may  prove  a 
source  of  danger  to  the  subject,  leading  to  retention  of  foreign  bodies, 
pathological  secretions,  etc.;  this  occurs  especially  in  aged  and  infirm 
persons,  in  those  debilitated  from  any  cause,  in  muscular  asthenia, 
especially  of  the  respiratory  muscles,  in  diabetic,  uremic,  and  other 
forms  of  coma,  in  anesthetization,  and  in  grave  disorders  of  the  nervous 
system.  The  retained  secretions,  being  usually  infected,  commonly  lead 
to  bronchopneumonia  and  often  a  fatal  termination. 


DISEASES  OF  THE  NOSE. 


EPISTAXIS. 

( Nose-bleeding . ) 

Etiology. — Epistaxis,  the  most  common  mucous-membrane  hemorrhage, 
may  be  due  to  general  or  local  causes.  The  general  causes  are  those  that 
determine  hemorrhage  in  other  parts  of  the  body,  such  as:  (1)  The  acute 
infectious  diseases,  especially  typhoid  fever  (being  characteristic  of  the 
onset),  diphtheria,  scarlatina,  measles,  pneumonia,  influenza,  etc.; 
(2)  blood  dyscrasias,  such  as  purpura,  scurvy,  hemophilia,  leukemia, 
pernicious  anemia,  etc.;  (3)  conditions  of  increased  arterial  tension, 
such  as  plethora  (especially  after  unusual  exertion  and  suddenly  increased 
blood  pressure),  arteriosclerosis  (nose-bleeding  of  the  aged),  chronic 
interstitial  nephritis,  etc.;  (4)  chronic  venous  congestion — that  of  ad- 
vanced cardiac  and  pulmonary  disease,  as  well  as  the  more  local  conges- 
tion produced  by  tumors  of  the  neck,  etc. ;  (5)  certain  poisonings  (phos- 
phorus, salicylic  acid,  etc.);  (6)  ascent  to  high  altitudes  (mountain 
climbing,  balloon  ascensions);  and  (7)  it  may  occur  as  a  manifestation 
of  vicarious  menstruation.  The  local  causes  of  epistaxis  are  commonly 
traumatic — injuries  to  the  nose  (fracture  of  the  nasal  or  cranial  bones), 
the  presence  of  foreign  bodies,  the  violent  use  of  instruments,  excessive 
"nose  blowing,"  and  ''nose  picking"  of  children;  and  local  diseases, 
such  as  acute  and  chronic  rhinitis;  diphtheria,  tuberculosis,  syphilis, 
glanders,  and  other  ulcerative  processes;  benign  and  malignant  tumors, 
etc.  Osier  has  described  a  multiple  telangiectasis  of  the  skin  and  mucous 
membrane  with  recurring  epistaxis. 

Pathology. — ^The  bleeding  may  result  from  capillary  oozing  or  from 
rupture  of  the  vessel  wall  (traumatism  or  ulceration).  The  frequency 
of  this  nasal  hemorrhage  is  due  to  the  abundant  vascular  supply  and  the 
absence  of  adequate  support  to  the  vessels,  which  conditions  are  most 
marked  over  the  middle  and  inferior  turbinate  bones,  where  the  veins 
form  a  well-marked  venous  plexus.  When  bleeding  is  the  result  of 
local  ulceration,  it  generally  comes  from  an  area  on  the  cartilaginous 


512  DISEASES  OF  THE  NOSE 

septum  about  half  an  inch  from  its  anterior  end.  This  has  sometimes 
been  described  as  the  site  of  predilection.  In  most  cases  the  hemorrhage 
takes  place  from  only  one  nostril. 

Symptoms. — Following  traumatism  the  hemorrhage  is  sudden  and 
may  persist  for  some  time,  or  it  may  cease  suddenly.  AVhen  due  to 
fracture  of  the  anterior  fossa  of  the  base  of  the  skull,  it  is  usually  con- 
tinuous though  slight,  and  is  generally  mixed  with  cerebrospinal  fluid. 
Wlien  due  to  local  causes,  it  may  be  sudden,  severe,  and  often  very  diffi- 
cult to  control.  When  due  to  general  diseases,  it  may  take  place  on 
the  slightest  provocation  and  varies  in  severity.  The  blood  may  be 
arterial  or  venous.  The  quantity  may  vary  from  a  few  drops  to  several 
pounds.    It  is  rarely  dangerous  to  life. 

Diagnosis. — The  diagnosis  is  usually  quite  evident;  but  occasionally 
the  source  of  the  bleeding  may  not  be  immediately  apparent.  Blood 
from  the  nasal  mucous  membrane  may  be  swallowed  (especially  during 
sleep),  and  being  later  vomited,  may  simulate  true  hematemesis;  or  it 
may  enter  the  pharynx  and,  being  expectorated,  simulate  true  hemoptysis. 
Examination  of  the  nasal  mucosa  and  attention  to  the  associated  phe- 
nomena should  prevent  diagnostic  errors. 

Prognosis. — The  prognosis  depends  altogether  upon  the  cause  of  the 
bleeding  and  the  general  condition  of  the  patient. 

Treatment. — In  most  cases  the  hemorrhage  ceases  spontaneously. 
Should  this  not  occur,  the  nasal  cavities  should  be  examined  to  determine 
the  seat  of  the  bleeding.  Divers  sorts  of  local  applications  are  often 
effectual — adrenalin  chloride,  hot  water,  ice  water,  cocaine,  alum,  zinc, 
hamamelis,  tannin,  iron  perchloride,  etc.  Persisting  hemorrhage  from 
a  ruptured  vessel  may  sometimes  be  stilled  by  the  direct  application  of 
chromic  acid,  the  Paquelin  cautery,  etc.  Should  these  measures  prove 
ineffectual,  the  nares  should  be  plugged  (anteriorly,  posteriorly,  or  both) 
with  cotton  or  similar  material,  or  a  thin  rubber  finger  cot  may  be 
introduced  into  the  nares  and  then  distended  with  air  or  water.  Internal 
remedies  are  of  little  value,  except  perhaps  calcium  lactate  in  certain 
general  disorders  associated  with  lessened  coagulability  of  the  blood. 


ACUTE  RHINITIS. 

{Acute  Coryza;  Acute  Nasal  Catarrh;  Common  Cold.) 

Etiology. — A  "cold  in  the  head"  is  really  an  acute  infection  of  the  upper 
air  passages;  it  may  be  merely  an  acute  rhinitis,  or  the  catarrhal  inflam- 
mation may  extend  to  the  pharynx  and  perhaps  involve  the  entire  upper 
respiratory  tract.  It  may  occur  as  an  independent  disorder,  involving 
persons  of  all  ages,  especially  during  the  changeable  weather  of  the  late 
fall  and  early  spring.  It  is  commonly  attributed  to  exposure  to  cold  and 
damp,  but  these,  as  well  as  divers  local  disorders  (chronic  rhinitis,  nasal 
polyps,  etc.)  and  general  debilitating  conditions,  act  as  predisposing 
factors;  the  exciting  cause  is  doubdess  some  bacterium.    Micrococcus 


ACUTE  RHINITIS  513 

catarrhal  is  is  believed  to  be  the  cause  of  most  of  the  cases  that  exhibit 
infectious  (epidemic)  characteristics;  other  cases  seem  to  be  due  to  the 
pneumococcus,  the  bacillus  of  Friedlander,  Micrococcus  paratetragenus, 
Bacillus  septus  (Bacillus  coryzse  segmentosus),  etc.  In  some  cases  acute 
coryza  is  merely  symptomatic — of  certain  acute  general  infections, 
such  as  measles,  influenza,  pertussis,  syphilis,  etc.,  or  drug  intoxications, 
such  as  the  iodides,  the  bromides,  etc.;  or  it  may  result  from  the  inhala- 
tion of  irritating  dust  or  vapors  (acids,  ammonia,  etc.). 

Pathology. — The  nasal  mucosa  is  swollen,  congested,  oedematous, 
and  covered  with  a  profuse,  clear,  alkaline,  mucous  secretion — which  is 
also  abundantly  discharged  through  the  nares.  The  lesions  may  extend 
to  the  pharynx  and  the  upper  respiratory  tract  generally,  the  Eustachian 
tubes,  the  accessory  nasal  sinuses,  etc.  After  the  lapse  of  several  days 
the  swelling  and  oedema  subside  somewhat,  the  secretion  lessens  and 
becomes  mucopurulent  in  character,  and  gradually  ceases  entirely. 
Occasionally  the  nares  may  be  more  or  less  filled  and  obstructed  by  a 
fibrinous  exudation  (fibrinous  rhinitis);  this  is  usually  due  to  the  diph- 
theria bacillus,  but  may  also  be  caused  by  streptococci,  staphylococci, 
and  pneumococci. 

Symptoms. — The  onset,  as  a  rule,  is  sudden;  not  infrequently  there  is 
initial  headache  and  chilliness  (rarely  a  distinct  chill),  which  are  soon 
followed  by  sneezing,  a  sense  of  fulness  in  the  nose,  embarrassed  breath- 
ing (nasal  obstruction,  often  necessitating  mouth  breathing),  general 
malaise,  neuromuscular  pains  in  the  neck,  back,  and  extremities,  fever 
(100°  to  101°  F.),  rapid  pulse,  and  other  fever  phenomena.  At  first  there 
is  very  little  nasal  discharge,  but  this  soon  sets  in,  and  usually  becomes 
abundant,  clear,  and  watery.  The  sense  of  smell  and  of  taste  are  usually 
obtunded.  The  inflammatory  lesions  may  extend  to  the  frontal  sinuses, 
and  occasion  severe  frontal  headache  (at  the  base  of  the  nose);  to  the 
lacrymal  duct,  and  lead  to  conjunctivitis  and  epiphora;  to  the  Eus- 
tachian tube,  and  cause  temporary  deafness  and  tinnitus  aurium;  to  the 
pharynx  and  induce  local  pain  and  soreness  and  dysphagia;  to  the  larynx 
and  trcichea,  and  cause  hoarseness,  difficult  phonation,  and  bronchial 
cough,  etc.  At  the  end  of  thirty-six  to  forty-eight  hours,  the  swelling 
and  congestion  of  the  nasal  mucosa  begin  to  subside,  nasal  breathing 
becomes  less  embarrassed,  the  discharge  becomes  lessened  in  amount 
and   mucopurulent  in  character,  and  convalescence  is  established. 

Diagnosis. — The  diagnosis,  as  a  rule,  is  quite  obvious.  Care  should 
be  taken  to  avoid  confounding  a  simple  acute  rhinitis  with  the  cases 
symptomatic  of  one  of  the  general  infections,  such  as  measles,  influenza 
pertussis,  diphtheria,  etc. 

Prognosis. — The  disease  usually  runs  a  course  of  from  three  to  seven 
days,  and  is  usually  free  from  complications.  Rarely  the  accessory 
sinuses,  the  P^ustachian  tube,  etc.,  may  become  seriously  aft'ected;  or  the 
condition  (usually  from  rej)eatcd  attacks)  tends  to  become  chronic. 

Treatment. — Jn  those  subject  to  repeated  attacks,  local  disease  of  the 
nose  should  receive  attention.     A  hygenic  mode  of  life  may  prevent 


514  DISEASES  OF  THE  NOSE 

attacks  or  mitigate  their  severity — that  is,  suitable  clothing  during 
changeable  weather,  the  avoidance  of  draughts  and  exposure  to  wet 
and  damp,  good  ventilation  in  working  rooms  and  sleeping  rooms, 
frequent  bathing,  exercise,  etc. 

Many  attacks  are  mild,  do  not  occasion  much  distress  or  incapacitate 
the  patient,  and  soon  subside.  But  if  the  attack  is  at  all  severe,  and  if 
there  is  fever,  the  patient  should  go  to  bed  for  the  first  twenty-four  hours 
at  least.  The  time-honored  purge  (calomel  or  blue  mass  followed  by  a 
saline),  10  grains  (0.6  gram)  of  Dover's  powder,  and  hot  whiskey  and 
water  (or  hot  lemonade)  still  find  justification  in  frequent  abortion  of 
the  attack;  it  is  really  good  and  effective  treatment  if  the  patient  sweats; 
but  he  may  be  made  to  sweat  otherwise,  as,  for  instance,  by  a  Turkish 
bath,  which  is  often  very  beneficial.  The  "fulness  in  the  head"  and  the 
embarrassed  nasal  breathing  may  be  relieved  by  preliminary  cleansing  of 
the  nares  with  an  alkaline  solution  (Dobell's  solution)  and  the  use  of 
adrenalin  chloride  (1  to  1000)  or  cocaine  (1  per  cent,  in  liquid  albolene), 
or  thymol  and  camphor  (each  0.5  per  cent,  in  liquid  albolene).  The 
adrenalin  and  cocaine  may  be  followed  by  unpleasant  after-effects  (vas- 
cular relaxation  and  oedema);  they  should  not  be  used  too  frequently, 
and  assuredly  not  given  to  the  patient  for  self  medication.  The  inhala- 
tion of  menthol  sometimes  lessens  the  local  discomfort.  In  addition, 
relief  may  be  afforded  by  the  following,  in  a  capsule  or  tablet,  every 
two  or  three  hours: 

I^ — Quinine  sulphate 2  grains  0]l3 

Aspirin  (or  salol) 3  grains  0  20 

Atropine  sulphate y^o^  grain  0|0006 

Camphor  monobromate 1  grain  0  065 — M. 

If  there  is  much  fever,  a  mixture  such  as  the  following,  is  often  of  much 
service : 

I^ — Spirit  of  nitrous  ether 

Spirit  of  camphor,  of  each         .     ^ 3  drams  12|00 

Camphorated  tincture  of  opium 2  drams  8  00 

Solution  of  ammonium  acetate,  sufficient  to  make  .  3  ounces       100  00 — M. 

S. — Two  teaspoonfuls  (10  c.c.)  every  three  hours. 

A  minute  dose  of  tincture  of  aconite  may  be  added  to  this  mixture  if 
the  fever  is  high  and  there  is  much  vascular  throbbing.  During  con- 
valescence from  severe  attacks  the  patient  should  be  careful  not  to 
expose  himself  to  inclemencies  of  the  weather,  and  he  should  take  a 
tonic. 

CHRONIC  RHINITIS. 

(Chronic  Nasal  Catarrh.) 

Etiology. — Chronic  nasal  catarrh  may  be  due  to  repeated  attacks  of 
acute  rhinitis;  some  cases  seem  to  be  chronic  from  the  beginning,  that  is, 
the  acute  passes  into  the  chronic  form;  other  cases  are  due  to  specific 
infections,  such  as  tuberculosis,  syphilis,  etc.    Certain  of  the  atrophic  cases 


HAY  FEVER  515 

(ozoena)  are  attributed  to  microorganisms,  such  as  Bacillus  mucosus 
ozoenae,  Bacillus  foetidus,  etc.  Anemia  and  conditions  of  general  debility 
predispose  to  the  disorder. 

Pathology. — Simple,  hypertrophic,  and  atrophic  cases  may  be  dis- 
tinguished. In  the  simple  cases  the  nasal  mucosa  is  swollen  and  con- 
gested and  covered  with  more  or  less  thinnish  mucous  or  mucopurulent 
exudate.  The  erectile  tissue,  especially  of  the  turbinate  bones  and  the 
septum,  is  especially  susceptible  to  the  action  of  irritants,  including  cold, 
and,  becoming  swollen,  may  occasion  more  or  less  nasal  obstruction, 
embarrassed  nasal  breathing,  and  consequent  mouth  breathing.  In  the 
hypertrophic  cases,  in  addition  to  the  foregoing,  there  is  more  or  less 
marked  and  permanent  hypertrophy  of  the  nasal  mucosa,  the  forma- 
tion of  so-called  polyps,  and  sometimes  involvement  of  the  turbinate 
bones,  leading  to  partial  or  complete  obstruction  of  the  nasal  passages. 
There  is  usually  also  moije  or  less  catarrh  of  the  pharynx,  with  adenoid 
vegetations,  and  consequent  mouth  breathing,  nasal  voice,  deafness 
(Eustachian  tube  involvement),  flattened  face,  peculiar  expression,  and 
defective  mentality  (especially  when  occurring  in  young  subjects); 
perhaps  also  asthma,  bronchitis,  etc.  The  atrophic  cases  perhaps  some- 
times develop  out  of  the  hypertrophic,  but  often  they  seem  to  be  atrophic 
from  the  beginning.  The  mucosa  is  pale  and  thin,  the  erectile  tissue 
is  atrophic,  and  both  in  many  places  are  replaced  by  ulcerating  or  scar 
tissue;  the  nasal  passages  are  widened;  there  is  a  little  mucopurulent 
secretion,  which,  drying,  forms  crusts  and  occasions  an  extremely  offensive 
odor  (ozoena). 

Symptoms. — ^The  chief  symptom  in  the  hypertrophic  form  is  embar- 
rassed nasal  respiration,  which  is  usually  associated  with  a  sense  of 
fulness  in  the  nasopharynx,  and  a  more  or  less  abundant  mucous  or 
mucopurulent  excretion,  which  gives  rise  to  the  so-called  "hawking" 
and  spitting.  The  atrophic  form  is  especially  characterized  by  the  foetid 
odor  and  more  or  less  local  distress. 

Diagnosis. — ^The  diagnosis  suggested  by  the  symptoms,  is  to  be  made  by 
rhinopharyngeal  examination. 

Treatment. — The  treatment  consists  of  mild  antiseptic  douches,  such 
as  Dobell's  solution,  etc.,  to  insure  cleanliness  and  remove  secretions; 
the  local  use  of  iodine,  potassium  iodide,  etc.,  in  the  hypertrophic  form, 
with  eventual  removal  of  the  enlarged  turbinates,  and  of  various  anti- 
septics and  deodorants  in  the  atrophic  forms.  For  details  of  the  treat- 
ment one  should  refer  to  special  treatises  on  rhinology. 

HAY  FEVER. 

(Hay  Asthma;  June  Cold;  Rose  Cold;  Autumnal  Catarrh.) 

Hay  fever  is  a  disease  provoked  by  the  pollen  of  certain  grains  and 
plants,  and  is  characterized  by  catarrhal  inflammation  of  the  conjunc- 
tiva and  the  upper  respiratory  tract,  embarrassed  respiration  (asthma), 
and  general  depression. 


516  DISEASES  OF  THE  NOSE 

Etiology. — Hay  fever  is  most  common  in  adult  males,  but  it  occurs 
in  both  sexes,  especially  in  those  engaged  in  intellectual  as  contrasted 
with  manual  pursuits.  Individual  sufferers  exhibit  a  special  suscepti- 
bility, which  it  seems  may  be  inherited  (familial  predisposition),  but 
which  usually  is  an  acquired  general  nervous  instability  or  a  local 
disorder  (hypersensitiveness)  of  the  nerve  endings  of  the  nasal  mucosa. 
In  this  country,  as  well  as  in  England  and  Germany,  the  disease  begins 
toward  the  end  of  ]\Iay  and  lasts  five  to  eight  weeks;  and,  especially  in 
this  country,  it  appears  again  about  the  middle  of  August  and  lasts  again 
six  or  eight  weeks  or  until  the  first  frost  (which  it  does  not  survive). 
Many  subjects  escape  the  first,  but  succumb  to  the  second  visitation. 
The  exciting  cause  appears  undoubtedly  to  be  the  pollen  of  certain 
grains  and  plants.  Ragweed  (ambrosia)  and,  to  a  less  degree,  goldenrod 
(salidago)  are  the  main  causes  in  this  country;  but  grains  such  as  rye, 
(especially  in  England),  corn,  etc.,  and  other  plants  (chrysanthemums, 
asters,  etc.)  are  also  of  etiological  significance.  All  cases  are  not  pro- 
voked by  the  one  cause;  the  American  disorder,  for  instance,  seems  to 
differ  etiologically  from  the  English,  the  German,  etc.  Dunbar  has 
isolated  from  the  pollen  a  toxalbumin  which  he  believes  to  be  the  specific 
cause  of  the  disease;  it  is  pathogenic  in  susceptible  individuals  in  doses 
of  4  Q  Q  Q  Q  milligram.  The  disease  itself  is  believed  to  be  an  expression 
of  hypersusceptibility  to  this  toxin,  which  exerts  a  specific  action  on  the 
terminal  nerve  fibers  of  predisposed  persons,  and  has  some  influence 
also  on  the  erythrocytes,  which  it  lakes. 

Pathology. — The  lesions  consist  of  catarrhal  changes  in  the  conjunc- 
tivae and  the  upper  respiratory  tract.  The  asthma  and  general  depression 
are  attributable  to  the  general  influence  of  the  toxin. 

Symptoms. — The  onset,  as  a  rule,  is  abrupt,  and  in  susceptible  subjects 
develops  about  the  same  time  each  year.  In  many  instances  the  attack 
resembles  an  ordinary  acute  coryza,  in  others,  an  attack  of  bronchial 
asthma;  or  the  one  may  alternate  with  the  other.  At  the  onset,  in  most 
cases,  to  the  more  common  manifestations  of  coryza,  there  are  added 
considerable  sneezing,  obstructed  nasal  passages,  conjunctivitis  with 
marked  itching  of  the  eyelids  and  lacrymation,  and  severe  itching 
sensations  of  the  soft  palate  and  pharynx;  the  nasal  discharge  is  usually 
copious,  thin,  and  watery — rarely  mucopurulent.  The  catarrhal  pro- 
cess may  extend  to  the  larynx,  bronchi,  and  lungs,  with  accompanying 
cough  and  asthmatic  seizures;  these  may  even  predominate,  and  not 
infrequently  prevent  sleep.  Headache,  malaise,  exhaustion,  fugitive 
pains,  mental  depression,  and  other  general  symptoms  occur,  and  there 
may  be  gastro-intestinal  disturbances.  Variability  in  the  severity  of  the 
symptoms  may  develop  from  day  to  day — mitigation  due  perhaps  to 
staying  indoors  or  to  rain  which  precipitates  the  pollen,  and  augmenta- 
tion due  to  going  outdoors,  especially  in  the  sunshine  which  dries  and 
permits  dift'usion  of  the  pollen  (which  may  be  increased  ])y  high  winds). 

Diagnosis. — The  disease  is  readily  recognized  from  the  rather  sudden 
development  annually,  in  the  .spring,  or  more  commonly  in  August  in 


DISEASES   OF   THE  LARYNX  517 

this  country,  of  severe  coryza,  accompanied  bv  conjunctival,  pharyngeal, 
and  bronchial  (asthmatic)  symptoms,  and  general  depression. 

Prognosis. — The  disease  usually  lasts  five  to  eight  weeks  and  subsides 
spontaneously — the  autumnal  catarrh  with  the  first  frost.  Rarely 
a  person  attacked  in  the  spring  suft'ers  more  or  less  throughout  the 
summer  and  until  October.  Those  once  attacked  are  likely  to  suffer 
again,  but  spontaneous  abatement  of  the  symptoms  is  sometimes  ob- 
served after  the  age  of  about  sixty  years. 

Treatment. — The  only  certain  means  of  relief  is  a  sojourn,  during  the 
hay-fever  season,  at  a  high  altitude  in  a  region  free  from  the  ragweed, 
etc.  The  White  Mountains,  the  Adirondack^,  as  well  as  certain  moun- 
tainous regions  of  the  South  and  West  and  Canada,  afford  complete 
immunity.  Some  subjects  do  well  at  the  seashore.  Dunbar  has  intro- 
duced a  pollen  antitoxin,  under  the  name  of  pollantin  (marketed  in  a 
dry  and  in  a  liquid  form),  which  is  to  be  used  locally  in  the  nose  (and 
not  injected  hypodermicly) ;  he  asserts  that  he  has  employed  it  with 
excellent  results  or  partial  success  in  87  per  cent,  of  1240  cases.  Tem- 
porary relief  is  afforded  by  the  local  use  of  adrenalin  chloride  (1  to  1000), 
cocaine  (whence  the  habit  has  often  been  acquired),  menthol,  morphine, 
etc.,  and  by  the  internal  use  of  atropine,  which  usually  produces  the 
greatest  relief.  S.  Solis-Cohen  recommends  the  local  and  hypodermic 
use  of  pituitary  extracts  (posterior  lobe).  Obvious  diseases  of  the  nasal 
passages  should  be  treated  appropriately  (see  special  treatises) ;  and  the 
general  neurotic  basis  of  the  subject  should  be  improved  by  the  avoid- 
ance of  mental  and  bodily  overwork,  and  the  use  of  iron,  arsenic, 
phosphorus,  strychnine,  etc. 


DISEASES  OF  THE  LAEYNX. 


ACUTE  CATARRHAL  LARYNGITIS. 

Etiology. — iVcute  catarrhal  laryngitis  may  occur  at  any  age,  but  it 
is  most  common  in  adolescents  and  adults,  especially  in  those  debili- 
tated from  any  cause.  The  exciting  causes  are  infectious,  toxic, 
mechanical,  or  thermic  irritants.  The  infectious  form  of  the  disease 
may  be  primary  or  secondary.  Most  primary  cases  are  related  eti- 
ologically  to  exposure,  or  "catching  cold,"  and  they  are  provoked 
by  streptococci,  staphylococci,  pneumococci,  influenza  bacilli,  Micro- 
coccus catarrhalis,  etc.  Secondarily,  the  disease  may  follow  disease 
of  the  nose,  throat,  or  bronchi,  or  it  may  occur  as  a  manifestation  or 
complication  of  certain  infectious  diseases  (measles,  scarlatina,  infiuenza, 
typhoid  fever,  diphtheria,  syphilis,  tuberculosis,  etc.).  The  toxic 
factors  comprise  the  inhalation  of  irritant  vapors  (acids  and  alkalies); 
the  excessive  and  prolonged  use  of  tobacco,  alcohol,  etc.;  gout,  and 


5i8  DISEASES  OF  THE  LARYNX 

sometimes  the  use  of  drugs,  such  as  mercury,  the  iodides,  etc.  The 
mechanical  factors  comprise  traumatism,  inhalation  of  dust,  the  action 
of  foreign  bodies,  overuse  of  the  voice,  etc.  The  thermal  factors  com- 
prise the  action  of  very  hot  liquids,  steam,  etc. 

Pathology. — The  lesions  consist  of  swelling  and  redness  of  the  mucous 
membrane,  especially  in  the  aryepiglottidean  folds.  The  mobility  of 
the  vocal  cords  is  impaired;  sometimes  there  is  considerable  oedema; 
and  there  is  more  or  less  mucous  or  mucopurulent  secretion.  Occasion- 
ally there  are  minute  submucous  hemorrhages,  and  rarely  superficial 
erosion  of  the  mucous  membrane  (catarrhal  ulcers),  especially  on  the 
cords,  the  anterior  commissure,  or  the  interarytenoid  fold.  Inspissation 
of  the  secretion  gives  rise  to  a  condition  called  laryngitis  sicca. 

Symptoms. — At  first  there  is  a  sensation  of  soreness  or  irritation  and 
tickling  or  burning  in  the  throat,  a  harsh,  dry,  sometimes  spasmodic 
cough,  and  more  or  less  alteration  of  the  voice  that  may  amount  to 
complete  aphonia.  Phonation,  deglutition,  and  inspiration  (especially 
of  cold  air)  are  painful;  dyspnea  may  be  marked,  especially  in  children, 
in  whom  it  may  be  spasmodic  and  quite  urgent  (oedema).  Expectora- 
tion at  first  is  slight,  but  it  soon  becomes  more  abundant  and  mucous, 
or  mucopurulent,  occasionally  blood-streaked.  The  general  phenomena 
are  usually  slight — moderate  fever  for  several  days,  headache,  and 
malaise.  Occasionally,  especially  in  children  and  when  the  inflamma- 
tory phenomena  are  marked  below  the  vocal  cords,  such  narrowing  of 
the  lumen  of  the  larynx  may  be  produced  that  the  symptoms  resemble 
what  have  been  ascribed  to  "croup" — crowing  cough,  stridor,  and 
attacks  of  suffocation.  These  attacks  often  come  on  at  night — due 
to  accumulation  of  secretion  and  aspiration  of  the  tongue. 

Diagnosis. — The  diagnosis  is  usually  easy,  even  without  laryngo- 
scopic  examination,  which,  however,  may  be  required  in  doubtful 
cases.  Laryngismus  stridulus  may  be  distinguished  by  the  mode  of 
onset,  neurotic  temperament,  associated  rickets,  and  the  absence  of  fever, 
of  coryza,  of  hoarseness,  and  of  aphonia.  Diphtheria  may  be  dis- 
tinguished by  the  more  severe  local  and  general  symptoms,  the  presence 
of  membrane  on  the  tonsils  or  fauces,  and  early  swelling  of  the  cervical 
lymph  nodes.  Hysterical  aphonia  may  be  distinguished  by  the  absence 
of  fever  and  the  results  of  the  laryngoscopic  examination. 

Prognosis. — The  prognosis  in  adults  is  good,  as  a  rule,  the  disorder 
ending  in  recovery  in  from  three  or  four  days  to  a  week  or  more.  In 
children  a  fatal  termination  may  be  induced  by  suffocation  or  a  consecu- 
tive bronchitis  or  bronchopneumonia. 

Treatment. — Confinement  of  the  room  (the  bed,  in  severe  cases), 
rest  to  the  larynx  by  the  non-use  of  the  voice,  a  mercurial  purge,  a 
diaphoretic  febrifuge  mixture  (mentioned  under  coryza),  and  the  in- 
halation of  steam  impregnated  with  menthol,  compound  tincture  of 
benzoin,  etc.,  suffice  to  bring  about  recovery  in  the  majority  of  cases. 
Cold  moist  applications  to  the  neck  are  often  grateful  to  the  patient. 
If  the  cough  is  very  irritating,  the  throat  may  be  sprayed  with  menthol, 


(EDEMATOUS  LARYNGITIS  519 

cocaine,  etc.,  or  a  Dover's  powder  or  other  sedative  may  be  administered 
at  night.  The  severe  nocturnal  attacks  common  in  children  are  usually 
promptly  relieved  by  an  emetic  and  hot  compresses  to  the  neck. 


(EDEMATOUS  LARYNGITIS. 

((Edema  of  the  Larynx;  (Edema  of  the  Glottis;  Phlegmonous  Laryngitis.) 

Etiology." — Q^ldematous  laryngitis  is  peculiarly  a  disease  of  adult  life, 
being  uncommon  in  childhood.  It  may  be  primary  or  secondary.  As  a 
primary  disorder  it  may  be  due  to:  (1)  Infectious  agents — whence  it' 
occurs  (a)  during  the  course  of  certain  infectious  diseases  (smallpox, 
measles,  scarlatina,  typhoid  fever,  diphtheria,  tuberculosis,  syphilis, 
etc.);  (6)  as  a  concomitant  of  acute  catarrhal  laryngitis,  laryngeal  peri- 
chondritis, etc. ;  and  (c)  as  an  extension  of  the  inflammatory  oedema  of 
Ludwig's  angina,  parotitis,  tonsillitis,  etc.  (2)  Toxic  agents — inhalation 
of  irritant  vapors,  the  medicinal  or  other  use  of  mercury,  the  iodides, 
etc.  (3)  Mechanical  agents — foreign  bodies  impacted  in  the  larynx. 
(4)  Thermal  agents — inhalation  of  steam.  (5)  Angioneurotic  factors — 
angioneurotic  oedema.  As  a  secondary  disorder  it  may  occur  (1)  as  a 
complication  of  general  oedema  (in  heart  disease,  kidney  disease,  and 
lung  disease),  and  (2)  in  consequence  of  pressure  on  the  jugular  veins 
(as  by  aneurysm  of  the  aorta,  tumors  of  the  thyroid,  mediastinum,  etc.). 

Pathology." — ^The  lesions  consist  of  an  inflammatory  oedema,  involving 
especially  the  aryepiglottic  ligaments,  the  epiglottis,  and  the  false  vocal 
cords.  The  swelling  is  sometimes  unilateral,  sometimes  subglottic,  and 
may  be  so  extreme  as  entirely  to  close  the  glottis.  The  mucous  mem- 
brane is  swollen,  pale,  grayish,  and  semitranslucent,  or  dull  reddish  in 
color.     Rarely  the  exudation  is  purulent. 

Symptoms. — -The  symptoms  are  those  of  severe  laryngitis,  together 
with  urgent  dyspnoea — at  first  inspiratory  and  later  expiratory  stridor, 
inspiratory  depression  of  the  intercostal  spaces,  scorbiculus  cordis, 
etc.  Suffocation,  that  may  lead  almost  immediately  to  a  fatal  issue, 
may  be  the  first  manifestation  of  the  disease.  The  oedema  is  quite 
apparent  on  laryngoscopic  examination;  the  swelling  of  the  epiglottis 
may  be  detected  by  the  finger  or  seen  when  the  tongue  is  depressed. 

Diagnosis. — ^The  diagnosis  is  easy  from  the  symptoms  and  the  results 
of  laryngoscopic  examination  or  palpation  by  the  finger. 

Prognosis. — The  prognosis  depends  upon  the  basic  condition  and 
the  promptness  with  which  treatment  is  instituted.  The  disease  is 
often  fatal. 

Treatment. — The  patient  should  be  given  ice  to  suck,  an  ice  collar 
should  be  applied  externally,  the  throat  and  larynx  should  be  sprayed 
with  cocaine  and  adrenalin  chloride,  and  the  swollen  areas  should  be 
scarified.  If  the  symptoms  are  urgent,  tracheotomy  should  be  performed 
immediately,  since  the  high  mortality  is  due  to  delay. 


520  DISEASES   OF   THE  L ART XX 

SPASMODIC  LARYNGITIS. 

(Laryngismus  Stridulus:  Stridulous  Laryngitis;  Spasmodic  Croup:  False  Croup.) 

Etiology. — Spasm  of  the  larynx  occurs  in  association  with  divers  dis- 
eases of  the  larynx,  but  it  is  a  dominant  feature  of  the  disorder  known  as 
spasmodic  laryngitis  or  laryngismus  stridulus.  Probably  these  are  dis- 
tinct disorders,  the  one  an  acute  catarrhal  laryngitis  with  spasm,  the  other 
a  pure  neurosis.  The  disorder  is  peculiar  to  children,  especially  rickety 
children,  between  the  ages  of  six  montlis  and  six  years,  and  is  said  to  be 
more  common  in  boys.  It  is  closely  related  to  tetany,  and  may  be  one 
of  its  manifestations.  In  some  cases  it  is  related  to  enlargement  of 
the  thymus  and  receives  the  name  thymic  asthma  (page  403).  The 
attacks  are  often  provoked  by  passion  or  emotional  disturbances- 
so-called  "passion  fits"  and  "attacks  of  holding  the  breath."  AMiether 
the  exciting  cause  acts  centrally,  as  is  supposed  in  rickets,  or  peripherally, 
has  not  been  determined.  Among  the  causes  believed  to  act  reflexly  are 
adenoids,  teething,  indigestion,  preputial  irritation,  intestinal  parasites,  etc. 

Pathology. — The  lesions  consist  of  paroxysmal  tonic  spasms  of  the 
adductor  muscles  of  the  glottis,  in  consequence  of  which  the  glottis 
is  closed  and  breathing  rendered  impossible.  There  may  or  may  not 
be  an  associated  catarrhal  laryngitis. 

Symptoms. — The  attacks  usually  come  on  at  night,  the  child  having 
gone  to  bed  well  and  being  awakened  out  of  a  sound  sleep.  As  a  rule, 
there  are  no  premonitory  symptoms,  no  cough,  no  hoarseness.  The 
attack  begins  with  a  forced  inspiration,  followed  by  complete  cessation 
of  respiration.  The  face,  at  first  pale,  becomes  cyanotic  and  anxious, 
the  eyes  protrude  and  are  rolled  about,  violent  inspiratory  efforts  are 
made,  the  intercostal  spaces  and  the  abdomen  become  retracted,  and 
profuse  perspiration  breaks  out.  The  attack  may  last  for  from  several 
seconds  to  several  minutes,  when  suddenly  with  relaxation  of  the  con- 
tracted adductors,  a  deep  labored,  noisy  inspiration  ("child-crowing") 
occurs,  the  cyanosis  and  anxious  expression  disappear,  and  the  child 
becomes  comfortable.  In  some  cases  there  is  loss  of  consciousness 
and  tonic  and  clonic  spasms  of  the  trunk  and  extremities  (carpopedal 
spasms).  Rarely  the  attack  leads  immediately  to  death.  Attacks 
vary  much  in  severity,  and  they  may  occur  singly  or  be  frequently 
repeated — during  the  day  as  well  as  at  night. 

Diagnosis. — The  diagnosis  is  quite  apparent  from  the  symptomatology 
and  the  etiological  factors.  ]\Iembranous,  or  diphtheritic,  laryngitis 
(true  croup)  may  be  distinguished  by  the  presence  of  fever,  the  gradual 
development  of  the  dyspnoea,  and  presence  of  a  false  membrane  in  the 
fauces  or  in  the  larynx  on  laryngoscopic  examination. 

Prognosis. — The  prognosis  is  good,  since  despite  its  alarming  aspects, 
the  disease  is  rarely  fatal. 

Treatment.- — During  the  paroxysm  cold  water  should  be  dashed  in 
the  child's  face,  or  the  child  should  be  placed  in  a  warm  bath  (100°  to 


CHRONIC  LARYNGITIS  521 

105°)  and  cold  water  applied  to  its  back  and  chest.  Recourse  may 
be  had  to  a  few  whiffs  of  chloroform,  or  an  emetic,  such  as  ipecac. 
Recurrence  of  the  attaclvs  may  be  obviated  by  cold  or  counterirritation 
to  the  neck,  and  the  internal  use  of  bromides,  chloral,  belladonna,  etc. 
All  possible  sources  of  peripheral  irritation  must  be  corrected.  Since 
the  children  are  anemic  and  rachitic,  tonics  containing  iron,  arsenic, 
phosphorus,  strychnine,  cod-liver  oil,  etc.,  and  nutritious  diet  must  be 
e'iven  for  a  lono-  time. 


CHRONIC   LARYNGITIS. 

{Chronic  Laryngeal  Catarrh:  Preachers  Sore  Throat.) 

Etiology. — Chronic  laryngitis  results  from  repeated  attacks  of  acute 
laryngitis;  the  long  continued  and  ill  use  of  the  voice  (public  speakers, 
preachers,  singers,  etc);  the  continued  action  of  injurious  agents  upon 
the  larynx,  such  as  tobacco  smoke,  dust  (stone  cutters,  etc.),  alcohol 
(inebriates),  etc. 

Pathology. — The  lesions,  as  a  rule,  consist  of  swelling,  thickening, 
and  pale  grayish  or  bluish-red  discoloration  of  the  mucous  membrane, 
especially  of  the  epiglottis,  the  interarytenoid  folds,  and  about  the 
vocal  cords.  Rarely  superficial  erosions  or  ulcerations  occur.  Special 
types  of  the  disease  are  described:  Laryngitis  hypertrophica,  or  ver- 
rucosa— verrucous  projections  or  swellings  the  result  of  hyperplasia 
of  the  epithelium  and  the  papillae;  laryngitis  atrophica — pallor  and 
thinness  of  the  mucous  membrane  the  consequence  of  atrophy;  and 
laryngitis  hypoglottica  chronica  hypertrophica,  or  chorditis  vocalis 
inferior  chronica — hyperplasia  of  the  subchordal  mucous  membrane, 
leading  to  marked  constriction  of  the  laryngeal  lumen. 

Symptoms. — The  symptoms  consist  of  irritation  in  the  throat,  cough, 
hoarseness,  and  expectoration — varying  in  severity  from  time  to  time. 
The  sense  of  irritation  compels  the  patient  continually  to  attempt  to 
clear  the  throat;  the  cough  is  rough,  harsh;  the  hoarseness  varies  in 
degree  to  complete  aphonia;  and  the  expectoration  is  usually  scanty, 
occasionally  rather  abundant,  mucous,  mocopurulent,  and  rarely 
blood-streaked. 

Diagnosis. — The  diagnosis  is  usually  quite  obvious  from  the  symptoms, 
but  recourse  should  be  had  to  laryngoscopic  examination  to  ascertain 
the  exact  conditions,  and  to  exclude  tuberculosis,  syphilis,  tumors,  etc. 

Prognosis.— The  prognosis  as  to  complete  recovery  is  poor,  but 
marked  amelioration  of  the  symptoms  is  possible.  Relapses  are  com- 
mon, especially  since  the  etiological  factors  are  not  readily  controlled. 

Treatment. — Of  prime  importance  is  removal  of  the  etiological 
factor — overuse  of  the  voice,  alcohol,  tobacco,  as  the  case  may  be. 
Change  of  climate — a  sea  voyage,  residence  in  a  pine  forest,  etc. — 
is  often  of  the  greatest  benefit.  Disease  of  the  nose  and  throat 
must  be  corrected.     Cold  compresses  externally  are  often  of  service. 


522  DISEASES  OF  THE  LARYNX 

Approved  internal  remedies  comprise  the  following,  which  may  be 
applied  on  a  swab  or  by  means  of  an  atomizer:  Tannic  acid  (1  to  2 
per  cent.),  zinc  sulphate  (2  to  5  per  cent.),  potassium  chlorate  (2  to  5 
per  cent.),  silver  nitrate  (1  to  2  per  cent.),  alum  (0.5  to  1  per  cent.), 
etc.  Insufflation  of  powders,  bismuth,  etc.,  is  sometimes  of  service, 
if  done  carefully.  The  general  health  often  demands  the  administration 
of  tonics. 

LARYNGEAL   PERICHONDRITIS. 

Etiology. — Laryngeal  perichondritis  may  be  rarely  primary — when  it 
is  usually  due  to  trauma;  commonly  it  is  secondary  and  occurs  during 
the  course  of  syphilis,  tuberculosis,  typhoid  fever,  diphtheria,  scarlatina, 
erysipelas,  etc. 

Pathology. — The  cricoid  and  the  arytenoid  cartilages  are  most  fre- 
quently affected;  less  commonly  the  thyroid  and  the  epiglottis.  Rarely 
the  lesions  are  metastatic.  Commonly  there  is  at  first  more  or  less 
superficial  ulceration  of  the  mucous  membrane — whence  the  lesions 
spread  to  the  perichondrium.  Usually  the  process  goes  on  to  abscess 
formation  which  gradually  separates  the  perichondrium  from  the  under- 
lying cartilage;  soon  the  cartilage  becomes  necrotic  and  separates  into 
small  particles  which  with  the  other  contents  of  the  abscess  are  dis- 
charged— internally  (perichondritis  interna)  or  externally  (perichondritis 
externa).  The  defect  is  usually  remedied  by  cicatrization  and  conse- 
quent stenosis;  but  when  the  abscess  is  discharged  externally  a  fistula 
not  uncommonly  results. 

Symptomatology. — Occasionally,  especially  in  the  primary  affection, 
there  may  be  an  acute  invasion,  with  chill  (or  chilliness)  and  fever. 
The  characteristic  symptoms  consist  of  severe  spontaneous  pain,  tender- 
ness on  pressure  over  the  larynx,  hoarseness,  cough,  painful  dysphagia 
(especially  when  the  posterior  portion  of  the  cricoid  cartilage  is  involved), 
and  the  development  of  laryngeal  stenosis  which  may  reach  an  extreme 
and  dangerous  degree.  Laryngoscopic  examination  reveals  redness 
and  swelling  of  the  mucous  membrane,  in  some  cases  considerable 
oedema  or  a  smooth  localized  swelling  corresponding  to  the  abscess. 
One  or  both  vocal  cords  may  become  immobilized.  In  external  peri- 
chondritis the  swelling  may  be  quite  obvious  and  palpable;  fluctuation 
may  be  obtainable;  and  the  pus  may  gravitate  to  the  mediastinum. 
Chronic  laryngeal  stenosis  due  to  cicatricial  contraction  is  a  common 
event  in  the  subjects  that  recover. 

Diagnosis. — The  difficulty  of  making  a  satisfactory  laryngoscopic 
examination  often  makes  the  diagnosis  obscure;  expectoration  of  a  bit 
of  cartilage  often  makes  it  conclusive.  Tuberculosis,  syphilis  (gummas), 
and  tumors,  and  in  the  external  form,  softened  lymph  nodes,  must  be 
excluded. 

Prognosis. — Death  may  occur  from  rapidly  developing  stenosis  or 
the  rupture  of  an  abscess  into  the  larynx.     In  subjects  that  recover, 


TUMORS  OF  THE  LARYNX  523 

stenosis    of    the    larynx    and    some    impairment    of    the    voice    are 
common. 

Treatment.— In  the  acute  stage,  if  stenosis  is  not  marked,  attempts 
may  be  made  to  reduce  the  swelhng  by  the  external  use  of  an  ice  collar 
or  leeches,  and  the  internal  use  of  hot  drinks  or  hot  inhalations,  astrin- 
gents, or  scarification  of  the  mucous  membrane.  Tracheotomy  or  laryn- 
gotomy  is  often  necessary,  although  the  abscess  may  sometimes  be 
opened  internally,  with  favorable  results.  The  patient's  general  health 
must  be  maintained  by  careful  feeding  and  stimulants.  In  tuberculous 
and  syphilitic  cases  the  general  disease  should  be  treated.  In  chronic 
stenosis  dilatation  may  prove  useful,  or  the  patient  may  be  obliged  to 
wear  a  tracheal  cannula. 


TUMORS  OF  THE  LARYNX. 

Pathology. — Tumors  of  the  larynx  may  be  benign  or  malignant. 
The  benign  tumors  occur  at  all  ages,  but  are  most  common  in  adult 
life,  and  in  males  rather  than  in  females.  They  comprise:  papilloma 
(pinkish  or  grayish  wartlike,  sessile  or  pedunculated  growths,  often 
multiple);  fibroma  (spheroidal,  smooth,  firm,  dense  growth,  usually 
single);  mucous  polyp,  soft  fibroma,  myxofibroma  (soft,  translucent 
growth);  chondroma  (firm,  hard,  smooth);  lipoma  (rare,  soft,  yellow- 
ish); angioma  (reddish,  hemorrhagic);  and  cysts  (small,  transparent, 
fluctuating  growths,  usually  retention  cysts).  Papilloma  and  fibroma 
are  the  most  common,  especially  in  children.  Benign  growths  usu- 
ally spring  from  the  vocal  cords,  except  the  mucous  polyp  and  cysts 
which  are  often  found  in  the  ventricles  of  Morgagni  and  on  the  epiglottis. 
The  malignant  tumors  comprise  sarcoma  and  carcinoma.  Sarcoma 
is  rare;  occurs,  as  a  rule,  early  in  life;  and  forms  soft  or  hard,  smooth 
or  difl^use  infiltrations,  sometimes  verrucose  growths,  that  commonly 
spring  from  the  vocal  cords.  Carcinoma  is  more  common;  occurs, 
as  a  rule,  in  middle  life  or  later;  and  forms  wart -like  excrescences, 
diffuse  infiltrations,  or  soft,  nodular,  rapidly  ulcerating  growths,  that 
involve  the  vocal  cords,  the  ventricles  of  Morgagni,  or  the  epiglottis. 
Sometimes  the  carcinoma  is  secondary  to  carcinoma  of  the  tongue, 
pharynx,  or  oesophagus. 

Symptomatology.— Of  benign  tumors,  the  most  common  symptoms 
are  alterations  in  the  voice  (harsh,  croaking,  aphonia);  cough  (some- 
times croupy  in  children);  dyspnoea,  varying  in  grade,  depending  upon 
the  size  and  situation  of  the  growth,  and  sometimes  paroxysmal  when  the 
growth  is  pedunculated  and  mobile;  orthopnoea,  sometimes  progressing 
to  asphyxiation,  from  sudden  occlusion  of  the  glottis;  and  dysphagia, 
when  the  upper  surface  of  the  epiglottis  is  involved.  Pain  is  often 
inconspicuous. 

Of  malignant  tumors,  the  symptoms  are  quite  like  the  foregoing. 
In  some  cases  the  voice  is  not  affected — when  the  posterior  surface  of 


524  DISEASES   OF   THE   TRACHEA    AND   THE   BRONCHI 

the  cricoid  cartilage,  the  epiglottis,  or  the  aryteno-epiglottidean  fold 
alone  is  involved.  Hoarseness,  when  it  does  develop,  may  be  due  to 
the  growth  itself,  or  to  immobility  of  the  vocal  cords.  When  the  epi- 
glottis or  the  posterior  surface  of  the  larynx  is  involved,  dysphagia  is 
usually  marked,  and  there  may  be  increased  salivation,  a  fetid  secretion 
(sometimes  blood-streaked,  from  ulceration),  and  an  offensive  breath. 
Pain  radiating  to  the  ear  or  the  temporal  region  may  be  present.  The 
cervical  lymph  nodes  may  become  enlarged  from  metastases.  Cachexia 
develops  when  the  growth  has  become  extensive,  or  when  it  is  primary 
elsewhere. 

Diagnosis. — Tumors  of  the  larynx  are  to  be  diagnosticated  only  by 
laryngoscopic  examination.  Decision  as  to  malignancy  frequently 
depends  upon  removal  of  a  portion  of  the  growth  and  its  study  histologi- 
cally. Benign  tumors,  as  a  rule,  are  pedunculated,  multiple,  do  not 
infiltrate,  show  little  tendency  to  bleed  or  ulcerate,  and  do  not  recur 
after  removal.  Rapid  growth  and  recurrence  after  removal  are  signifi- 
cant of  malignancy.  ^lalignant  tumors  may  be  distinguished  from 
syphilis  and  tuberculosis  by  the  age  of  the  patient,  definite  tumor  forma- 
tion, its  primary  localization  to  one  side,  the  early  immobility  of  the  vocal 
cords,  early  ulceration,  tendency  to  bleeding,  pain,  glandular  involve- 
ment, the  absence  of  tubercle  bacilli  in  the  secretions,  and  the  non- 
response  to  antisyphilitic  treatment. 

Prognosis. — The  prognosis  in  benign  tumors  is  good,  both  with 
reference  to  life  and  the  preservation  of  the  voice.  In  malignant  tumors 
the  prognosis,  as  a  rule,  is  bad,  although  in  some  cases  the  growth  may 
be  removed  by  early  operative  procedures. 

Treatment. — The  treatment  of  tumors  of  the  larynx  is  surgical.  JMost 
benign  tumors  may  be  removed  by  intralaryngeal  methods  under  local 
anesthesia.  In  children  this  is  difficult,  and  thyrotomy,  subhyoid 
pharyngotomy,  or  laryngotomy  may  be  necessary.  In  malignant 
tumors  partial  or  complete  laryngectomy  offers  the  only  hope  of  success. 
When  metastasis  has  occurred  laryngectomy  is  usually  useless;  the 
patient  may  be  made  comfortable  by  tracheotomy  and»  the  subsequent 
use  of  a  tracheal  cannula. 


DISEASES  OF  THE  TRACHEA  AND  THE  BRONCHI. 


ACUTE  BRONCHITIS. 

(Anite  Bronchidl  Catarrli ;  Acute  Tracheitis:  Acute  Tracheobronchitis.) 

Etiology. — Acute  bronchitis  may  occur  at  any  age,  but  it  is  prob- 
ably most  common  during  adolescence  and  adult  life,  although  it  is 
more  serious  and  fatal  in  the  very  young  and  the  very  old.  It  is 
more  common   in  males  than  in  females,  on   account  of   their  mode 


ACUTE  BRONCHITIS  525 

of  life  and  occupations.  It  prevails  especially  during  changeable  (moist 
and  cold)  weather — the  late  fall,  the  winter,  and  the  early  spring. 
Sedentary  life,  working  in  close,  ill-ventilated  rooms,  debility  from  any 
cause  predispose  to  the  disease;  an  out-of-door  life  is  a  preventive. 
It  may  occur  as  a  primary,  independent  affection,  or  in  association 
with  (or  secondary  to)  other  disorders.  The  exciting  causes  of  the 
primary  disease  are  the  infectious,  toxic,  mechanical,  and  thermic  irri- 
tants provocative  of  acute  catarrhal  laryngitis  (page  517);  indeed,  the 
one  often  follows  the  other,  and  both  result  from  "catching  cold." 
Divers  bacteria  appear  to  be  the  most  common  cause.  As  a  second- 
ary disease,  it  occurs  in  many  infections,  such  as  measles,  scarlatina, 
pertussis,  diphtheria,  influenza,  typhoid  fever,  malaria,  syphilis,  tuber- 
culosis, etc.;  it  is  common  in  the  subjects  of  chronic  heart  disease, 
chronic  lung  disease,  Bright's  disease,  gout,  etc.  Some  persons  seem 
unusually  susceptible  (hereditary  influences?). 

Pathology. — The  mucous  membrane  of  the  trachea  and  bronchi 
is  red,  swollen,  and  covered  with  mucus  and  mucopus;  occasionally 
there  may  be  punctiform  hemorrhages.  The  lesions  may  extend  to 
the  finer  bronchi — and  collapse,  bronchopneumonia,  emphysema,  or 
oedema  and  congestion  of  the  lungs  may  result.  The  microscopic 
lesions  consist  of  inflammatory  hyperemia  of  the  mucosa,  oedema  and 
cellular  infiltration  of  the  sul)mucosa,  and  swelling  and  desquamation 
of  the  lining  epithelial  cells. 

Symptomatology. — Depending  upon  the  extent  and  intensity  of  the 
manifestations,  three  forms  of  acute  bronchitiis  may  be  distinguished: 
(1)  A  mild  form,  in  which  the  lesions  are  confined  to  the  trachea  and 
the  main  bronchi;  (2)  a  more  severe  and  more  diffuse  form,  in  which 
the  medium-sized  and  the  smaller  bronchi  also  are  involved;  and  (3) 
a  form  in  which  the  finest  bronchi  and  bronchioles  are  involved — 
capillary  bronchitis  (identical  with  bronchopneumonia).  In  rare  cases, 
the  onset  is  abrupt,  and  attended  by  a  chill;  chilliness  is  not  uncom- 
mon. In  many  cases  an  acute  coryza  precedes  the  bronchitic  phenom- 
ena; laryngeal  symptoms  also  may  be  associated. 

In  the  mild  form  the  symptoms  consist  of  sulxsternal  distress,  pain, 
or  a  sense  of  rawness  or  op])ression,  and  cough,  at  first  hard,  harsh, 
often  yjaro.xysmal  and  painful,  especially  beneath  the  sternum  and 
along  tiie  attachment  of  the  diaphragm.  In  the  beginning  there  may 
be  no  expectoration,  or  with  considerable  effort  a  small  amount  of 
tough,  viscid,  occasionally  blood-streaked  mucus  may  be  cxjx'llcd; 
after  a  few  days,  however,  the  sputum  becomes  more  abundant,  less 
viscid,  and  mucous  or  mucopurulent,  in  character.  There  may  be 
little  or  no  general  disturbance,  though  commonly  there  is  some  languor 
and  headache,  possibly,  but  not  always,  some  elevation  of  the  tempera- 
ture. In  the  more  severe  forms,  the  general  and  tlie  local  symptoms 
are  aggravated.  Languor,  weariness,  and  headache  are  usually  more 
marked;  general  neuromuscular  pains  are  often  c|uite  severe;  and  die 
temperature  may  be  102°  F.,  or  thereabouts,  for  at  least  a  day  or  (wo. 


526  DISEASES  OF  THE  TRACHEA   AND  THE  BRONCHI 

The  cough  may  be  extremely  distressing,  but,  as  in  the  milder  form,  it 
becomes  much  ameliorated  with  the  development  of  free  expectora- 
tion. There  may  be  some  dyspnoea  and  acceleration  of  the  pulse  rate. 
Cyanosis,  not  uncommon  in  the  young  and  the  aged,  suggests  capillary 
bronchitis  (bronchopneumonia). 

Physical  Signs. — In  the  mild  form,  when  the  lesions  are  confined  to 
the  trachea  and  the  main  bronchi,  there  may  be  no  abnormal  physical 
signs,  aside  from  harshness  of  the  breath  sounds  and  some  prolongation 
of  the  expiration.  In  the  more  severe  form,  in  addition  to  the  foregoing, 
sonorous  and  sibilant  rales  may  be  heard,  especially  at  the  bases  pos- 
teriorly, in  the  early  stages,  and  fine  and  coarse  bubbling  rales  later 
when  the  bronchial  secretion  has  become  freer.  In  children  there  are 
often  evidences  of  interference  with  free  ventilation  of  the  lungs — dysp- 
noea, inspiratory  retraction  of  the  lower  end  of  the  sternum  and  the 
lower  ribs,  use  of  the  accessory  muscles  of  respiration,  etc. 

Diagnosis. — ^The  diagnosis,  as  a  rule,  is  easy.  The  bilateral  distribu- 
tion of  the  physical  signs  is  important.  One  should  not  overlook  the 
fact  that  bronchitis  may  be  the  initial  manifestation  of  certain  infectious 
diseases,  such  as  measles,  pertussis,  typhoid  fever,  malaria,  etc.  A 
history  of  exposure  to  any  of  these  infections  is  valuable.  The  sputum 
should  be  examined  to  determine  the  nature  of  the  infecting  agent. 
Persistence  of  fever  for  more  than  several  days  suggests  something 
more  than  mere  bronchitis.  Capillary  bronchitis  (bronchopneumonia) 
is  indicated  by  severe  general  symptoms,  fever,  dyspnoea,  and  cyanosis. 
Croupous  pneumonia  shojild  be  readily  differentiated  by  the  absence 
of  the  characteristic  physical  signs.  Predominance  of  fine  rales  at 
the  apices,  rather  than  at  the  bases,  suggests  tuberculosis — even  in 
chronic  bronchitic  subjects.  The  diagnosis  of  the  secondary  form  of 
bronchitis  presupposes  the  recognition  of  the  primary  cardiac,  pulmon- 
ary, renal  disease,  etc. 

Prognosis. — Except  at  the  extremes  of  life,  a  fatal  termination  is 
rare.  Mild  cases  usually  subside  within  a  week,  and  convalescence 
is  established  at  the  end  of  two  weeks.  In  severe  cases  the  course  is 
more  protracted.  One  attack  often  predisposes  to  another.  In  the 
very  young  and  the  aged,  in  emphysematous,  cardiac,  and  nephritic 
subjects,  the  disease  is  commonly  serious  and  may  lead  to  a  fatal  termina- 
tion. 

Treatment. — Although  not  always  possible,  it  is  desirable  that  the 
patient  go  to  bed  for  a  day  or  two;  at  least,  he  should  remain  at  rest 
in  a  well-ventilated  room,  and  his  diet  should  be  restricted.  The 
attack  may  sometimes  be  aborted  by  Dover's  powder  (10  grains,  0.6 
gram),  hot  lemonade  (with  or  without  whiskey),  and  a  hot  mustard  foot- 
bath at  bed  time,  followed  in  the  morning  by  calomel  or  blue  mass  and 
a  saline  laxative  in  adults,  or  castor  oil  in  children.  A  mustard  plaster, 
or  turpentine  stupe  applied  to  the  chest  serves  to  relieve  the  local  tight- 
ness and  soreness;  or  the  chest  may  be  rubbed  with  camphorated  oil  or 
camphor  liniment. 


CHRONIC  BRONCHITIS  527 

In  the  early  stages  much  relief  is  afforded  by  a  sedative  diaphoretic 
mixture,  such  as  the  following: 

I^ — Spirit  of  nitrous  ether 3  drams  12,00 

Wine  of  ipecac IJ/^  drams  6  GO 

Potassium  citrate '     .       .       3  drams  12  00 

Cinnamon  water,  sufficient  to  make    ....       3  ounces  100  00 — M. 

S. — Two  teaspoonfuls  (10  c.c.)  every  three  hours  (to  an  adult). 

If  the  pulse  is  very  rapid  or  there  is  much  fever,  minim  doses  of  tincture 
of  aconite  may  be  added  to  each  dose  (especially  serviceable  in  children). 
Additional  relief  to  the  dryness  of  the  throat  and  the  difficulty  in  breath- 
ing is  afforded  by  inhalations  of  steam  impregnated  with  sodium  chloride, 
sodium  bicarbonate,  compound  tincture  of  benzoin,  etc. ;  or  the  Dover's 
powder  may  be  repeated  at  night,  or  codeine  or  heroin  substituted,  but 
discretion  must  be  exercised  in  the  use  of  these  remedies  in  the  young 
and  the  aged. 

If,  after  several  days,  the  cough  continues  troublesome  and  the 
expectoration  has  not  become  free,  the  following  old-fashioned  mixture 
will  be  found  efficacious: 

I^ — Ammonium  chloride 1}^  drams  6]00 

Syrup  of  squill 3  drams  12|00 

Compound  mixture  of  glycyrrhiza       ....  3  ounces  100  00 — M. 

S. — Two  teaspoonfuls  (10  c.c.)  four  times  daily. 

Paroxysms  of  coughing  (referable  to  bronchial  spasm)  may  be  controlled 
by  belladonna,  stramonium,  or  lobelia;  belladonna  is  efficacious  also  if 
the  expectoration  is  copious  and  continues  for  a  long  time — in  which 
event  the  balsamic  preparations  also  are  useful — such  as  terebene,  ter- 
pene  hydrate,  tar,  etc.  In  children,  if  the  expectoration  is  abundant 
and  not  well  raised  (provoking  dyspnoea  and  cyanosis)  an  emetic  should 
be  administered — alum  (20  grains,  1.3  gram)  or  wine  of  ipecac  (1  dram, 
4  c.c,  repeated  in  ten  minutes,  if  necessary).  Signs  of  prostration  and  a 
weak  heart  call  for  the  administration  of  stimulants.  During  convales- 
cence, nutritious  diet,  fresh  air,  and  tonics,  stomachics,  quinine,  strych- 
nine, iron,  and  arsenic,  should  be  given. 


CHRONIC  BRONCHITIS. 

(Chronic  Bronchial  Catarrh;  Chronic  Catarrhal  Bronchitis;  Winter  Cough.) 

Etiology. — Chronic  bronchitis  is  rare  as  a  primary  disorder;  but  it 
may  occur  as  a  result  of  repeated  acute  attacks,  or  it  may  be  chronic 
from  the  outset  in  consequence  of  the  continued  inhalation  of  irritating 
dust,  vapors,  etc.  It  is  not  uncommon  in  the  middle  aged  and  the 
aged,  recurring  each  year  with  the  cold,  damp,  and  changeable  fall  and 
winter  weather.  Often  it  is  secondary  to  chronic  cardiac,  pulmonary, 
or  renal  disease.     It  is  also  a  manifestation  of  gout. 


528  DISEASES  OF  THE  TRACHEA   AND  THE  BRONCHI 

Pathology. — The  condition  of  the  bronchial  mucous  membrane 
varies  in  different  cases.  Often  it  is  thickened  irregularly,  hyperemic, 
and  covered  with  mucopus;  in  places  the  epithelium  may  be  entirely 
wanting — granular  patches.  The  fibrous  and  muscular  coats  are 
usually  thickened  and  the  seat  of  cellular  exudation.  In  long-con- 
tinued cases  more  or  less  atrophy  occurs,  and  leads  to  cylindrical  dilata- 
tion (bronchiectasis)  or  diverticula.  Emphysema,  fibroid  induration 
of  the  lung,  and  hypertrophy  of  the  heart  (especially  of  the  right  ven- 
tricle) are  common  concomitants. 

Symptomatology. — The  principal  symptoms  are  cough,  expectoration, 
and  dyspnoea — which  vary  much  in  different  cases,  and  permit  of  the 
differentiation  of  several  types  of  the  disease. 

Chronic  Winter  Cough. — This  is  probably  the  most  common  variety, 
and  is  characterized  by  the  recurrence  each  winter  of  cough,  which 
usually  is  not  very  troublesome,  and  expectoration,  moderate  in  amount, 
mucous  or  mucopurulent  in  character.  These  usually  lessen  or  dis- 
appear during  the  late  spring,  the  summer,  and  the  early  autumn. 

Chronic  Bronchitis  with  Emphysema.— This  is  very  common,  and 
usually  results  from  repeated  attacks  of  acute  bronchitis  or  of  recurrent 
attacks  of  winter  cough.  The  cough  is  often  troublesome;  it  is  more 
marked  in  the  morning  (accumulation  of  secretion  during  the  night), 
and  may  be  violent  or  paroxysmal;  it  commonly  lessens  or  disappears 
during  the  summer.  The  expectoration  may  be  scanty,  viscid,  and  diffi- 
cult to  raise;  or  it  may  be  abundant,  and  mucopurulent  or  seropurulent 
in  character;  occasionally  nummular.  Substernal  distress,  and  more 
or  less  dyspnoea  (especially  after  coughing  or  exertion)  are  common. 
The  general  health  is  often  maintained  for  years. 

Dry  Chronic  Catarrh  (Catarrh  Sec)  of  Laennec. — This  is  characterized 
by  a  dry,  troublesome,  paroxysmal  cough,  dyspnoea,  tightness  of  the 
chest  and  very  scanty  expectoration,  which  often  contains  grayish, 
pearl-like  particles  that  are  raised  with  difficulty.  Emphysema  is  often 
associated;  asthmatic  attacks  occur  from  time  to  time;  and  the  subjects 
are  prone  to  attacks  of  acute  bronchitis. 

Gouty  bronchitis  is  an  obstinate  form,  sometimes  associated  with 
other  manifestations  of  gout.  Dyspnoea  is  often  extreme.  Marked 
pulmonary  congestion  may  lead  to  the  expectoration  of  blood-stained 
sputum.  There  is  usually  associated  disease  of  the  heart,  liver,  and 
kidneys. 

Fetid  (or  putrid)  bronchitis,  although  usually  seen  in  association 
with  gangrene  or  abscess  of  the  lung,  bronchiectasis,  the  decomposition 
of  the  contents  of  tuberculous  cavities,  the  rupture  of  an  empyema  or 
subdiaphragmatic  abscess  into  the  lung,  etc.,  sometimes  occurs  as  an 
independent  affection.  The  cough  is  usually  paroxysmal  and  severe; 
the  sputum  is  usually  abundant  (upward  of  a  pint  in  twenty-four  hours), 
malodorous,  thin,  seropurulent  in  character,  and  on  standing  separates 
into  three  layers — the  lowermost  consisting  of  purulent  material,  detritus, 
and  irregular  masses  the  size  of  peas  (Dittrich's  plugs) ;  a  middle  layer 


CHRONIC  BRONCHITIS  529 

of  discolored  fluid;  and  an  upper  layer  of  frothy  mucus.  Fever, 
loss  of  appetite,  and  other  manifestations  of  bacterial  intoxication  are 
not  uncommon.  Should  the  disorder  be  primary,  secondary  changes, 
such  as  gangrene  or  abscess  of  the  lung,  septic  metastases  (as  in  the 
brain,  etc.),  may  occur. 

Bronchorrhcea  may  follow  long  continued  bronchitis  of  the  ordinary 
type.  The  cough  and  expectoration  often  occur  in  paroxysms,  and 
are  associated  with  extreme  dyspnoea.  The  expectoration  is  very 
abundant — as  much  as  one  or  two  quarts  in  the  twenty-four  hours; 
it  is  usually  thin,  frothy,  serous  or  mucoserous,  occasionally  some- 
what purulent  or  hemorrhagic,  rarely  thick  and  distinctly  purulent, 
in  character.  The  condition  may  lead  to  permanent  dilatation  of  the 
bronchi,  and  fetid  bronchitis.  In  the  young  especially  it  often  persists 
for  a  long  time  without  noteworthy  impairment  of  the  general  health. 

Physical  Signs. — The  physical  signs  commonly  include  those  of  em- 
physema. In  the  absence  of  emphysema  the  percussion  note  is  reso- 
nant, as  a  rule;  there  may  be  some  impairment,  especially  posteriorly, 
in  the  event  of  there  being  much  secretion,  collapse  of  small  areas  of 
the  lung,  thickening  of  the  pleura,  etc.  The  breath  sounds  are  usu- 
ally harsh  and  vesicular  in  character,  the  expiration  prolonged;  and 
there  are  rales,  sibilant  and  sonorous,  or  fine  and  coarse  bubbling,  or 
crackling,  especially  posteriorly,  depending  upon  the  conditions  within 
the  bronchi.  In  the  dry  catarrh  no  rales  are  present.  Evidences  of 
hypertrophy  and  dilatation  of  the  right  ventricle  may  also  be  detected. 

Diagnosis. — ^As  a  rule,  the  diagnosis  is  easy.  Care  must  be  exercised 
to  exclude  pulmonary  tuberculosis  (repeated  examination  of  the  sputum, 
etc.),  and  one  must  remember  that  a  chronic  bronchitic  subject  may 
become  tuberculous.  Distinction  must  be  drawn  between  the  primary 
cases  and  those  due  to  chronic  cardiac,  pulmonary,  and  renal  con- 
ditions. Aortic  aneurysm,  mediastinal  and  pulmonary  tumors,  etc., 
have  been  mistaken;  but  the  physical  signs,  if  sought  for,  are  usually 
conclusive. 

Prognosis, — Chronic  bronchitis,  as  a  rule,  is  a  very  obstinate  disease, 
tends  to  recur,  and  to  become  worse  with  advancing  years;  but  recovery 
is  not  impossible,  and  marked  amelioration  of  the  symptoms  is  readily 
attained.  The  prognosis  is  good  in  young  subjects,  and  in  older  sub- 
jects able  to  live  in  a  suitable  climate.  The  prognosis  is  bad  in 
subjects  of  chronic  heart,  pulmonary,  and  renal  disease,  and  in  the  aged. 

Treatment. — Removal  to  a  warm,  moist,  equable  climate  (Florida, 
Southern  California,  Riviera,  etc.)  constitutes  the  most  successful 
treatment — prophylactic  as  well  as  curative.  Those  unable  to  avail 
themselves  of  this  should  keep  their  room  warm,  though  well  ventilated, 
live  outdoors  as  much  as  possible  in  sunny,  pleasant  weather,  avoid 
vitiated  atmospheres;  in  a  word,  avoid  the  factors  known  to  provoke 
a  "cold."  The  diet  should  be  nutritious  and  easily  assimilable.  In 
patients  die  subject  of  chronic  cardiac,  pulmonary,  or  renal  disease,  gout, 
etc.,  the  primary  disorder  must  receive  careful  and  appropriate  treat- 
34 


530  DISEASES  OF  THE  TRACHEA   AND  THE  BRONCHI 

ment.  Thus,  some  patients  are  much  improved  by  small  doses  of 
digitalis,  strophanthus,  convallaria,  and  other  heart  tonics;  attention 
to  free  elimination  by  the  kidneys  and  free  evacuation  by  the  bowels 
materially  improve  others;  whereas,  the  obese  and  the  gouty  often 
respond  markedly  to  a  proper  dietetic  regimen.  Attention  to  the 
general  health,  and  the  use  of  cod-liver  oil,  arsenic,  iron,  quinine,  and 
strychnine  are  followed  by  good  results  in  other  cases. 

Medicinal  treatment  directed  to  the  bronchitic  condition  must  be 
varied  to  suit  the  exigencies  of  each  individual  case.  In  some  cases 
the  treatment  need  not  be  different  from  that  appropriate  in  the  later 
stages  of  acute  bronchitis.  Often  potassium  (or  ammonium  or  sodium) 
iodide  is  of  marked  benefit,  especially  when  the  cough  is  paroxysmal 
and  associated  with  emphysema;  often  it  may  serviceably  be  com- 
bined with  ammonium  chloride  (or  carbonate)  and  lobelia;  or  if  secre- 
tion is  free,  with  squill  or  senega;  but  the  use  of  the  iodide  should  not 
be  too  long  continued.  In  most  cases  the  balsamic  preparations  are 
of  much  value — oil  of  sandalwood,  of  eucalyptus,  of  turpentine,  and 
of  copaiba;  balsam  of  Peru  or  of  tolu;  terpene  hydrate,  terebene,  tar, 
creosote,  etc.  I  have  seen  much  benefit  from  30  minims  (2  c.c.)  each  of 
syrup  of  tar  and  syrup  of  wild  cherry,  four  times  a  day.  If  the  cough  is 
distressing  at  night,  resort  must  often  be  had  to  opium  or  its  deriva- 
tives, codein,  heroin.  The  troublesome  morning  cough  may  sometimes 
be  relieved  by  the  use  of  alkalies  (sodium  chloride,  sodium  bicarbonate, 
potassium  acetate,  etc.)  in  hot  water.  The  dry  distressing  cough  may 
be  benefited  by  inhalations  of  steam  impregnated  with  sodium  chloride, 
tincture  of  benzoin,  oil  of  eucalyptus,  white  pine,  etc.  In  fetid  bronchitis 
the  odor  may  be  improved  by  sprays  of  carbolic  acid  (0.05  to  0.1  per  cent.), 
thymol  (0.2  to  0.5  per  cent.),  or  by  resort  to  intratracheal  medication. 
Severe  dyspnoea  and  pain  in  the  chest  may  be  relieved  by  local  applica- 
tions to  the  chest,  such  as  plasters,  dry  or  wet  cups,  hot  or  cold  com- 
presses, etc.,  or  by  venesection.  Methodic  compression  of  the  thorax 
during  expiration,  the  use  of  the  pneumatic  cabinet,  and  posture  that 
favors  the  exit  of  secretion  are  of  service  in  some  cases. 


FIBRINOUS  BRONCHITIS. 

Etiology. — Fibrinous  bronchitis,  a  disease  attended  by  the  formation 
of  so-called  fibrinous  casts  of  the  bronchi,  may  be  primary  or  secondary. 
The  primary  is  an  independent  disorder,  rare,  and  of  obscure  etiology. 
It  occurs  about  middle  life,  twice  as  frequently  in  men  as  in  women, 
prevails  during  the  winter  and  spring,  and  tends  to  recur  from  year  to 
year.  It  may  affect  persons  previously  well  or  the  subjects  of  bronchitis 
or  tuberculosis.  The  secondary  form  has  been  observed  in  certain  infec- 
tious diseases,  such  as  diphtheria,  scarlatina,  measles,  pneumonia,  influ- 
enza, typhoid  fever,  etc.;  in  certain  chronic  cardiac  and  pulmonary 
diseases;  in  diseases  of  the  skin,  such  as  pemphigus,  herpes,  impetigo, 


FIBRINOUS  BRONCHITIS  531 

etc.;  complicating  menstruation  and  pregnancy;  etc.  Casts  of  the 
bronchi  have  also  been  seen  in  association  with  the  albuminous  expec- 
toration that  sometimes  follows  tapping  a  pleural  effusion;  and  blood 
casts  occur  with  hemoptysis.  These  secondary  forms  are  not  at  present 
under  consideration. 

Pathology. — The  characteristic  lesion  consists  of  the  formation  of 
membranous,  partly  hollow,  partly  solid,  casts  of  the  bronchi,  which, 
dividing  dichotomously,  may  reach  to  the  finest  bronchi.  The  sub- 
jacent mucous  membrane  may  appear  intact,  or  its  epithelium  may  be 
shed  and  it  may  show  the  usual  evidences  of  chronic  bronchitis.  The 
lesions  are  often  curiously  confined  to  definite  areas,  which  in  the  recur- 
ring form  are  sometimes  repeatedly  and  only  involved.  The  casts  are 
grayish  white  in  color,  occasionally  covered  with  streaks  of  blood, 
and  vary  much  in  size  from  small  irregular  pieces  to  masses  measuring 
six  to  eight  inches  in  length.  On  transverse  section  they  present  a 
concentric  appearance.  Usually  said  to  be  fibrinous,  recent  investiga- 
tions seem  to  show  that  they  are  made  up  mostly  of  mucin;  some 
observers  believe  them  to  consist  of  syntonin  or  coagulated  albumin. 
Microscopically  the  ground  substance  contains  leukocytes  (mostly 
mononuclear),  epithelium,  sometimes  erythrocytes,  Charcot-Leyden 
crystals,  and  Curschmann's  spirals.  Various  microorganisms  have 
been  cultivated  from  the  membrane,  especially  pneumococci,  strepto- 
cocci, and  staphylococci.  The  nature  of  the  process  is  ill  understood, 
but  it  is  sometimes  considered  analogous  to  mucous  colitis.  The  rare 
disorder  known  as  acute  obliterating  fibrinous  bronchiolitis  is  doubtless 
of  like  nature. 

Symptomatology. — Acute  and  chronic  forms  of  the  disease  may  be 
distinguished.  The  acute  form  is  rare,  and  usually  begins  suddenly 
with  a  chill  (or  chilliness),  fever,  cough,  expectoration,  and  dyspnoea. 
At  first  and  for  several  days,  as  a  rule,  the  attack  resembles  an  ordinary 
bronchitis;  soon,  however,  the  cough  becomes  severe  and  paroxysmal; 
the  expectoration,  which  heretofore  has  been  mucous  in  character,  is 
raised  with  considerable  difficulty;  dyspnoea  becomes  urgent,  and 
eventually  with  a  more  or  less  violent  effort  the  characteristic  cast  is 
expelled — with  great  relief  to  the  patient.  The  expectoration  again 
becomes  more  abundant  and  may  contain  small  coagula.  There  is 
sometimes  associated  hemoptysis;  rarely  a  large  hemorrhage.  The 
attack  may  last  several  days  or  several  weeks. 

The  chronic  form  may  develop  out  of  a  chronic  bronchitis  or  tubercu- 
losis, and  between  attacks  there  are  usually  the  ordinary  evidences 
of  bronchitis.  The  attacks  are  less  severe  than  in  the  acute  form, 
and  they  recur  at  longer  intervals,  often  yearly;  there  is  usually  little 
or  no  fever,  and  the  dyspna^a  is  less  urgent.  Should  the  attacks  recur 
at  short  intervals,  small  coagula  are  likely  to  be  expectorated  frequently 
and  the  general  health  of  the  patient  may  deteriorate. 

Physical  Signs. — The  physical  signs  are  those  of  bronchitis.  Over 
the  portion  of  lung  affected  there  may  be  weakened  or  absent  breath 


532  DISEASES  OF  THE  TRACHEA   AND  THE  BRONCHI 

sounds,  and  fine  bubbling  rales  may  be  provoked  by  voluntary  coughing. 
After  the  loosening  of  the  cast,  before  its  expectoration,  a  rough  clicking 
sound  (bruit  de  drapeau,  Ventilgerausch)  is  said  to  be  audible. 

Diagnosis.— The  diagnosis  depends  upon  the  detection  and  recogni- 
tion of  the  casts.  These  may  be  small  and  escape  observation.  Their 
detection  is  facilitated  by  floating  them  on  water.  Severe  paroxysms 
of  coughing  and  dyspnoea  relieved  by  expectoration  are  suggestive,  and 
should  lead  one  to  search  for  the  casts.  Care  must  be  taken  to  exclude 
the  secondary  form  of  the  disease. 

Prognosis. — ^The  prognosis  in  acute  cases  is  grave,  death  occurring 
in  from  one-third  to  one-half  the  cases  from  sufi^ocation  or  broncho- 
pneumonia. The  chronic  variety  may  last  for  many  years,  but  eventu- 
ally recovery  may  ensue.  Tuberculosis,  emphysema,  atelectasis,  pleu- 
ritis,  and  chronic  heart  disease  are  rather  common  sequels. 

Treatment. — In  the  acute  cases,  the  treatment  is  that  of  acute  bron- 
chitis; and  the  only  hope  of  cure  in  the  chronic  cases  is  the  cure  of 
the  commonly  associated  chronic  bronchitis.  Inhalations  of  atomized 
sodium  carbonate  or  bicarbonate  (2  to  5  per  cent.),  lime  water,  or  com- 
pound tincture  of  benzoin,  mitigate  the  distress  and  are  said  to  assist 
in  loosening  the  membrane.  Pilocarpin,  since  it  promotes  free  bron- 
chial secretion,  is  useful  for  the  same  purpose.  Potassium  iodide  is 
probably  of  even  more  value.  Mercurial  inunctions  also  have  been 
recommended.  In  the  event  of  marked  dyspnoea,  cyanosis,  and  delayed 
expectoration,  emetics  should  be  resorted  to. 


BRONCHIECTASIS. 

Etiology. — Bronchiectasis,  dilatation  of  the  bronchi,  may  be  due  to 
a  congenital  defect — in  which  event  it  is  likely  to  be  universal;  other- 
wise, it  results  from  weakening  of  the  bronchial  wall,  which,  in  con- 
sequence, becomes  unable  properly  to  withstand  the  distending  force 
of  the  contained  air  (much  exaggerated  during  paroxysms  of  coughing). 
Acland  has  well  classified  the  causes,  as  follows:  (1)  In  the  lumen 
of  the  bronchial  tubes,  (a)  the  impaction  of  a  foreign  body,  and  (6) 
the  inhalation  of  fibrinous  plugs,  as  in  diphtheria;  (2)  (a)  acute 
affections  of  the  walls  of  the  bronchial  tubes,  resulting  from  pneu- 
monia, bronchopneumonia,  tuberculosis,  diphtheria,  and  whooping 
cough,  and  (b)  chronic  affections  of  the  wall  of  the  bronchial  tubes, 
such  as  chronic  bronchitis  (60  per  cent,  of  the  cases),  syphilitic  peri- 
bronchial fibrosis  with  stenosis,  and  tuberculosis;  (3)  affections  of  the 
parenchyma  of  the  lung,  such  as  chronic  interstitial  pneumonia  (10 
per  cent,  of  the  cases),  and  collapse  from  caused  other  than  pressure; 
(4)  affections  external  to  the  lung,  such  as  aneurysm,  neoplasm,  and 
pleural  adhesions  and  thickening  (12.5  per  cent,  of  the  cases).  The 
disease  is  more  common  in  males  than  in  females.  About  50  per  cent, 
of  the  cages  occur  between  the  twentieth  and  the  fortieth  year;  23  per 


BRONCHIECTASIS  533 

cent,  between  the  tenth  and  the  twentieth  year;  and  13  per  cent, 
between  the  fortieth  and  the  fiftieth  year. 

Pathology.— The  bronchiectatic  cavities  may  be  cylindrical,  fusiform, 
saccular,  or  moniliform,  but  the  cylindrical  and  the  saccular  are  the 
more  common,  and  may  exist  together.  The  condition  may  be  general — 
in  which  event  it  is  unilateral,  rarely  congenital,  and  commonly  follows 
pneumonia;  or  it  may  be  partial — in  which  event  it  is  bilateral  and 
occurs  in  tuberculosis  (especially  at  the  apex),  pleurisy  (especially  at 
the  base),  and  emphysema.  In  the  general  form  the  entire  bronchial 
tree  consists  of  a  series  of  sacculi  communicating  the  one  with  the  other, 
lined  with  a  smooth,  glistening  mucous  membrane  (frequently  transition 
of  cylindrical  epithelium  into  flat),  except  in  the  dependent  portions 
where  there  may  be  some  ulceration;  the  dilatations  are  sometimes 
extreme,  forming  large  cysts  that  may  extend  to  the  pleural  surface; 
the  intervening  pulmonary  tissue  is  indurated  and  fibrotic.  In  the 
partial  form,  the  mucous  membrane  is  inflamed  and  ulcerated  and 
the  muscular  tissue  thin  and  atrophic;  cicatrization  may  give  rise  to 
stenosis  of  the  lumen.  The  contents  of  the  cavities  are  often  horribly 
fetid,  and  on  culture  reveal  divers  pyogenic  microorganisms,  the 
influenza  bacillus,  etc. 

Symptomatology. — Most  of  the  symptoms  are  those  of  the  chronic 
bronchitis,  emphysema,  tuberculosis,  etc.,  with  which  the  bronchi- 
ectasis is  associated;  in  many  of  these  cases  the  existence  of  the  bronchi- 
ectasis is  not  even  suspected.  The  characteristic  symptoms  consist 
of:  (1)  Cough,  which,  from  time  to  time,  especially  in  the  morning  or 
the  evening,  or  on  sudden  change  of  posture,  becomes  exaggerated 
into  violent  paroxysms,  and  results  in  the  expulsion  of  (2)  usually  a 
large  amount  (500  c.c.  or  more)  of  grayish,  acid,  fetid,  mucopurulent 
sputum,  which  on  standing  separates  into  three  layers — the  lowermost, 
dense,  purulent,  and  granular;  the  middle,  watery  and  sometimes 
discolored;  and  the  uppermost,  frothy,  discolored,  and  mucous.  Micro- 
scopically, it  consists  of  mucus,  pus,  detritus,  fatty  acid  and  hema- 
toidin  crystals,  elastic  fibers  (when  ulceration  has  occurred),  bacteria, 
etc.  Sometimes  it  contains  a  notable  amount  of  blood;  sometimes 
large  hemorrhages  occur.  (3)  Fetor  of  the  breath,  especially  on  coughing 
(it  may  be  missed  if  the  cavities  are  in  the  apex  and  well  drained). 
(4)  The  physical  signs  of  cavity  formation.  The  temperature  is 
variable;  it  may  be  normal  even  when  the  sputum  is  fetid;  but  in 
the  event  of  necrofiis  of  the  bronchial  wall  and  toxic  absorjitiou,  it 
corresponds  to  the  septic  type.  Dyspnoea  and  cyanosis  on  exertion  are 
common. 

An  acute  and  fatal  form  of  the  disease  is  not  uncommon  in  children 
(broncliiolectasis),  and  is  usually  associated  with  bronchopneumonia. 

Comphcations  and  Sequels. — Complications  and  sequels  are  many. 
Pneumonia,  abscess  and  gangrene  of  the  lung,  interstitial  j)neuinonitis, 
empyema,  pyopneumothorax,  etc.,  are  common;  septicemia,  pyemia, 
metastatic  abscesses  (brain,  liver,  kidney),  clubbing  of  the  finger  tips, 


534         DISEASES  OF  THE  TRACHEA   AND  THE  BRONCHI 

hypertrophic  pulmonary  osteo-arthropathy,  amyloidosis,  etc.,  are  not 
uncommon. 

Diagnosis. — In  the  absence  of  the  characteristic  symptoms  the  disease 
often  escapes  clinical  recognition.  Tuberculous  cavities,  as  a  rule,  are 
more  common  at  the  apex,  preceded  by  signs  of  solidification,  progressive 
in  character,  and  the  expectoration  contains  tubercle  bacilli;  whereas, 
bronchiectatic  cavities  are  more  common  at  the  base,  followed  by  indu- 
ration of  the  lung,  often  non-progressive,  and  the  expectoration  does 
not  contain  tubercle  bacilli;  but  tuberculosis  may  supervene  upon  non- 
tuberculous  bronchiectasis.  Fetid  sputum  with  normal  temperature  is 
almost  certainly  from  a  bronchiectatic  cavity. 

Prognosis. — Cure  is  extremely  unlikely,  if  it  occurs  at  all;  but  the 
patient  may  live  for  many  years  and  lead  a  fairly  active  life.  Death 
usually  results  from  septicemia,  emaciation,  or  one  of  the  complications 
or  sequels.     The  acute  form  is  usually  fatal  from  asphyxia. 

Treatment. — Attention  to  the  primary  disorder  and  the  general  health 
of  the  patient  are  of  prime  importance.  The  best  medicinal  treatment 
consists  of  the  inhalation  of  vaporized  creosote,  for  fifteen  minutes  every 
other  day  at  first,  later  every  day.  A  dram  or  two  of  crude  creosote 
should  be  poured  on  some  water  contained  in  a  saucer  and  slowly  vapor- 
ized over  an  alcohol  lamp.  This  often  at  first  provokes  coughing,  which 
has  the  effect  of  ridding  the  bronchial  tubes  of  retained  secretion  and 
then  permitting  the  local  action  of  the  creosote  on  the  mucous  mem- 
brane. Inhalations  of  carbolic  acid,  eucalyptus,  menthol,  etc.,  are 
of  much  less  value.  Intratracheal  injections  are  sometimes  of  service; 
Grainger  Stewart's  is  one  of  the  best:  Menthol,  10,  guaiacol,  2,  and 
olive  oil,  88,  of  which  two  to  three  drams  (8  to  12  c.  c.)  should  be  injected 
at  a  time.  There  is  much  more  likelihood  of  good  effect  if  the  injection 
follows  soon  upon  a  copious  expectoration — cleansing  of  the  bronchi. 
The  internal  use  of  balsamic  preparations,  oil  of  sandalwood,  terebene, 
terpene  hydrate,  etc.,  should  be  tried.  The  adoption  of  postures  that 
favor  drainage  of  the  cavities  is  of  value.  Surgical  drainage  has  been 
practised  in  some  cases  with  good  results. 


BRONCHIAL  ASTHMA. 

{Spasmodic  Asthma.) 

Bronchial  asthma  is  a  disorder  characterized  by  attacks  of  dyspnoea 
(chiefly  expiratory)  and  a  characteristic  expectoration;  it  commonly 
occurs  in  bronchitic  subjects,  and  ultimately  leads  to  emphysema. 

Etiology. — ^Asthma  is  not  infrequently  familial;  it  is  twice  as  common 
in  men  as  in  women;  it  may  occur  at  any  age;  and  it  sometimes  develops 
during  childhood  and  persists  throughout  life.  The  attacks  are  excited 
by  divers  stimuli — emotion,  fright,  unpleasant  odors,  irritating  dust, 
certain  articles  of  diet,  too  much  food  (overloaded  stomach),  cold  and 
damp  atmosphere,  etc.     Some  subjects  are  freer  while  in  the  country. 


BRONCHIAL  ASTHMA  535 

others  while  in  the  city.  The  disorder  has  much  in  common  with  hay- 
fever,  and  both  may  occur  at  the  one  time  or  alternate  in  the  same 
subject. 

Pathology. — The  nature  of  the  disorder  is  not  well  understood.  In 
many  cases  it  seems  to  be  chiefly,  if  not  wholly,  a  neurosis,  and  due 
to  spasm  of  the  bronchial  muscles  or  swelling  of  the  bronchial  mucous 
membrane,  in  consequence  of  disorder  innervation — pneumogastric 
or  vasomotor.  Others  attribute  the  phenomena  to  spasm  of  the  dia- 
phragm, of  all  the  inspiratory  muscles,  or  of  the  musculature  of  the 
pulmonary  arteries.  In  many  cases,  however,  and  this  is  especially 
important,  although  frequently  overlooked,  there  is  inflammation  of 
the  bronchioles  (bronchiolitis  exudativa  of  Curschmann),  attended 
by  swelling  of  the  mucosa,  the  exudation  of  a  viscid  nmcus,  and 
desquamation  of  the  surface  epithelium — which  assuredly  suffice  to 
explain  the  phenomena.  In  some  cases  there  is  associated  disease  of 
the  nose  (hypertrophic  rhinitis,  polyps,  adenoids),  of  the  larynx  and 
trachea  (catarrh,  enlarged  bronchial  lymph  nodes),  disease  of  the  geni- 
talia, etc.,  which  often  apparently  stand  in  causal  relationship  to  the 
asthma.  Most  subjects  reveal  the  lesions  of  chronic  bronchitis;  others 
are  gouty,  nephritic,  etc. 

Symptomatology. — ^The  essential  symptoms  consist  of  attacks  of 
dyspnoea  followed  by  the  expectoration  of  a  characteristic  sputum. 
Though  usually  not,  the  attacks  are  sometimes  preceded  by  premonitory 
symptoms  (a  sense  of  constriction  or  oppression  of  the  chest,  flatulence, 
etc.),  aura  asthmatica.  They  commonly  come  on  during  the  night, 
the  patient  being  awakened  from  a  sound  sleep  by  dyspnoea  and  a 
sense  of  suffocation  that  soon  become  extreme  and  often  induce  him 
to  seek  an  open  window  in  the  hope  of  relief.  The  chest  soon  becomes 
fixed  in  full  expansion,  the  accessory  muscles  of  respiration  become 
tense  and  make  violent,  though  useless,  efforts,  and  the  expiration 
becomes  much  prolonged,  labored,  and  accompanied  by  loud  wheezing. 
The  respirations,  as  a  rule,  are  not  much  increased  in  frequency;  the 
pulse  is  small  and  accelerated,  the  temperature  is  usually  normal  or 
subnormal,  the  extremities  become  cool,  the  face  livid,  the  expression 
anxious,  and  sweat  not  infrequently  breaks  out. 

Early  in  the  attack  there  is  usually  little  or  no  cough  or  expectoration. 
After  several  hours,  however,  sputum  begins  to  be  expectorated;  this 
consists  of  a  small  amount  of  viscid  mucus  containing  roundish  gela- 
tinous masses  (perles  of  Laennec)  which  represent  casts  of  the  bronchioles 
(bronchiolitis);  many  of  these  have  a  twisted  spiral  arrangement 
(Curschmann's  spirals),  and  may  or  may  not  reveal  a  central  translucent 
filament.  In  addition,  the  sputum  contains  leukocytes  (mostly  eosino- 
philic), epithelium  from  the  bronchi  and  the  alveoli,  and  Charcot- 
Leyden  octahedral  crystals.  Examination  of  the  blood  usually  reveals 
an  eosinophilia  (25  to  50  per  cent.). 

A  single  attack  may  last  from  upward  of  a  half  hour  to  several  hours, 
or  the  patient  for  days,  sometimes  for  several  weeks,  may  partially 


536         DISEASES  OF  THE  TRACHEA   AND  THE  BRONCHI 

recover  and  relapse,  especially  at  night.  At  the  end  of  several  days 
in  severe  attacks,  sooner  in  milder  attacks,  the  sputum  becomes  more 
abundant,  mucopurulent  in  character,  and  Curschmann's  spirals 
disappear.  At  this  time  the  patient's  general  distress  becomes  much 
lessened,  although  he  is  likely  to  remain  weakened,  apathetic,  and 
dyspnoeic  for  some  time;  indeed,  more  or  less  dyspnoea  is  not  uncommon. 
The  patient  may  remain  free  from  attacks  of  asthma  for  weeks,  months, 
or  years  at  a  time. 

Physical  Signs. — During  the  asthmatic  attack  the  chest  is  usually 
in  full  inspiratory  expansion  and  fixed;  inspiration  is  short  and  jerky, 
the  movements  of  the  chest  are  altogether  disproportionate  to  the  efforts 
of  the  accessory  muscles  of  respiration;  the  diaphragm  is  depressed 
and  almost  immobile;  the  percussion  note  is  normal  or  hyperresonant 
(especially  in  long-standing  cases  in  which  emphysema  develops); 
on  auscultation  the  expiration  is  prolonged,  and  there  are  sibilant  and 
sonorous  rales.  Later  the  rales  become  crackling  or  fine  or  coarse 
bubbling. 

Diagnosis. — ^The  diagnosis  is  usually  easy;  the  symptoms,  the  char- 
acteristic sputum,  and  the  physical  signs  distinguish  asthma  from  other 
disorders  attended  by  dyspnoea.  Uremic  asthma  is  differentiated  by 
the  signs  of  nephritis,  high  tension  pulse,  albuminuria,  hypertrophy 
of  the  left  ventricle  (hypertrophy  of  the  right  ventricle  occurs  in  long- 
standing asthma).  Cardiac  asthma,  hysterical  asthma,  hay  fever, 
spasm  of  the  glottis,  etc.,  sometimes  must  be  considered  the  differential 
diagnosis. 

Prognosis. — ^The  prognosis  is  fairly  good  in  early  life,  especially  if 
a  local  cause  (adenoids,  nasal  polyps,  etc.)  can  be  found  and  remedied. 
Recovery  can  scarcely  be  expected  in  middle  and  advanced  life  when 
chronic  bronchitis,  emphysema,  hypertrophy  and  dilatation  of  the 
heart,  etc.,  have  developed,  but  the  patient's  suffering  may  be  much 
ameliorated  and  he  may  live  to  a  ripe  old  age.  Although  the  individual 
attacks  appear  to  be  extremely  severe,  death  during  an  attack  is  very 
rare. 

Treatment. — Careful  attention  must  be  given  to  all  the  circumstances 
of  the  patient's  life.  Some  do  much  better  in  the  city,  despite  its  smoke, 
and  dirt,  and  soot,  than  in  the  purer  atmosphere  of  the  country;  but 
climatic  treatment  must  be  instituted  with  reference  to  the  response 
of  each  individual  patient.  The  diet  must  be  carefully  regulated: 
the  gouty  and  the  obese  must  be  abstemious;  and  in  all  cases,  par- 
ticularly in  those  disposed  to  flatulency,  it  is  wise  to  advise  the  heavy 
meal  in  the  middle  of  the  day,  and  the  partaking  of  very  little  food 
toward  evening.  The  bowels  should  be  opened  at  least  once  daily. 
Sleeping  in  a  room  the  atmosphere  of  which  is  laden  with  steam  (im- 
pregnated or  not  with  the  vapor  of  oil  of  eucalyptus,  oil  of  pine,  etc.) 
or  with  the  fumes  of  burning  nitre  may  secure  freedom  from  nocturnal 
attacks  and  a  consequent  peaceful  sleep.  All  sources  of  local  irrita- 
tion (nasal,  pharyngeal,  etc.)  must  be  remedied. 


TRACHEAL  AND  BRONCHIAL  OBSTRUCTION  537 

During  the  attack  relief  may  be  obtained  by  the  inhalation  of  amyl 
nitrite  or  chloroform,  or  the  fumes  evolved  by  burning  the  leaves 
(cigarettes)  of  belladonna,  stramonium,  lobelia,  hyoscyamus,  tobacco, 
or  by  burning  paper  impregnated  with  potassium  nitrate;  by  drinking 
hot  coffee  and  whiskey  or  spirit  of  chloroform;  or  by  the  hypodermic 
use  of  morphine  (combined  with  atropine  or  cocaine),  or  pilocarpine — 
to  be  employed  with  caution.  Tincture  of  lobelia  in  dose  sufficient  to 
produce  the  physiological  effect  is  often  efficacious,  but  it  should  not 
be  employed  when  the  heart  is  weak.  An  emetic  sometimes  assists 
in  expelling  retained  secretions.  An  imminent  attack  may  sometimes 
be  warded  off,  or  aborted,  by  the  prompt  use  of  amyl  nitrite,  nitro- 
glycerin (5I5-  grain,  0.0013  gram,  hypodermicly),  or  chloroform. 

Between  the  attacks  no  drug  is  so  useful  as  potassium  (or  sodium) 
iodide;  it  has  rendered  me  the  best  service  when  combined  with 
lobelia.  From  time  to  time  one  of  the  bromides  also  may  be  added. 
Nitroglycerin  is  quite  useful  in  some  cases,  especially  in  diose  with 
high  arterial  tension.  Adrenalin  chloride  (hypodermicly),  euphorbia 
pilulifera,  arsenic,  the  compressed  air  of  the  pneiunatic  cabinet,  oxygen, 
etc.,  appear  to  have  been  useful  in  some  cases.  When  the  heart  is 
weak  strophanthus  or  digitalis,  in  small  doses,  is  serviceable. 


TRACHEAL  AND  BRONCHIAL  OBSTRUCTION. 

Etiology. — Obstruction  of  the  trachea  or  the  bronchi  may  be  due  to : 
(1)  A  foreign  body  in  the  lumen;  (2)  stenosis  the  result  of  disease  of 
the  wall;  and  (3)  compression  from  without. 

Foreign  bodies,  depending  upon  their  size,  may  cause  partial  or  com- 
plete obstruction.  Usually  the  obstruction  is  incomplete  and  bronchial 
rather  than  tracheal.  The  foreign  body  commonly  passes  through 
the  trachea  and  is  arrested  in  a  bronchus,  the  right  usually,  since  it 
is  larger  and  more  in  a  direct  line  with  the  trachea  than  the  left. 

Stenosis  due  to  disease  of  the  tracheal  or  bronchial  wall  may  be 
caused  by  syphilis  (usually),  tuberculosis,  leprosy,  polyps,  carcinoma, 
sarcoma,  ecchondroma,  etc.  When  due  to  syphilis,  the  stenosis  may 
be  annular,  but  it  is  also  often  somewhat  longitudinal.  The  new 
growths  may  be  situated  anywhere,  but  they  are  more  common  in  the 
bronchi  near  the  bifurcation  of  the  trachea. 

Compression  of  the  trachea  or  bronchi  from  without  may  be  caused 
by  tumors  and  other  enlargements  of  the  thyroid  or  thymus;  enlarge- 
ments of  the  regional  lymph  nodes  (tuberculosis,  leukemia,  Hodgkin's 
disease,  sarcoma,  carcinoma),  aneurysm,  mediastinal  abscess,  l^ott's 
disease  or  tumors  of  the  vertebra?,  etc. 

Symptomatology. — The  symptoms  vary  with  the  site  and  degree  of 
the  obstruction.  A  foreign  body  of  sufficient  size  may  lodge  suddenly 
in  the  trachea,  and  cause  complete  obstruction  and  immediate  death 
from  asphyxia.     A  small  body  in  the  trachea,  such  as  a  pin,  may  cause 


538  DISEASES  OF  THE  TRACHEA   AND  THE  BRONCHI 

only  a  local  sense  of  discomfort  and  dyspnoea.  Bodies  of  moderate 
size  (which  sometimes  may  be  unconsciously  aspirated)  occasion  sudden 
onset  of  coughing  and  dyspnoea,  paroxysmal  exacerbations  of  the  cough- 
ing and  dyspnoea  (sometimes  attributable  to  accumulation  of  secretions 
below  the  obstruction),  inspiratory  and  expiratory  stridor,  and  the 
common  phenomena  of  defective  ventilation  of  the  lungs — inspiratory 
depression  of  the  suprasternal  fossa  and  of  the  scorbiculus  cordis, 
depression  of  the  intercostal  spaces,  pulsus  paradoxus,  etc.  The  larynx 
moves  but  little  in  contrast  to  the  marked  movement  that  obtains  in 
laryngeal  obstruction;  laryngoscopic  examination  reveals  no  disorder 
of  the  larynx;  bronchoscopic  examination  may  reveal  the  cause  of  the 
s}Tnptoms.  The  factors  causing  compression  of  the  trachea  from 
without,  being  usually  in  the  neck,  are  quite  obvious  to  the  senses. 

In  bronchial  obstruction,  the  signs  and  symptoms  are  usually  uni- 
lateral, in  contrast  to  the  bilateral  phenomena  of  tracheal  obstruction. 
The  respiratory  movements  of  the  affected  side  are  limited,  and  may 
be  completely  absent  if  the  obstruction  is  of  high  grade.  If  the  obstruc- 
tion is  of  moderate  grade,  the  breath  sounds  are  harsh  and  broncho- 
vesicular  in  character  and  the  fremitus  is  diminished;  if  of  high  grade, 
the  breath  sounds  are  much  diminished  or  absent — which  with  normal 
percussion  resonance  is  of  much  significance.  A  loud  stenotic  sound 
may  be  audible  about  the  site  of  the  obstruction.  In  most  cases  there 
is  more  or  less  dyspnoea — usually  inspiratory.  In  long-standing  cases 
some  considerable  difference  in  the  circumference  of  the  two  sides  may 
develop — due  to  inactivity  of  the  aifected  side  and  compensatory  emphy- 
sema of  the  other  side.  In  some  cases  obstruction  of  one  bronchus 
is  followed  by  obstruction  of  the  other  bronchus  or  the  trachea — as 
in  mediastinal  tumors,  etc.  A  foreign  body  may  lead  to  ulceration 
of  the  bronchial  mucosa  with  consecutive  bronchopneumonia  or  abscess 
or  gangrene  of  the  lung.  Pressure  from  without,  as  by  an  aneurysm,  may 
lead  to  retention  of  secretions  with  consecutive  bronchiectasis,  broncho- 
pneumonia, and  abscess  or  gangrene  of  the  lung,  or  to  collapse  of  the  lung. 

Diagnosis. — The  diagnosis  is  usually  easy.  The  site  of  bronchial 
obstruction  may  sometimes  be  determined  by  the  area  of  diminished 
breath  sounds,  the  point  of  maximum  intensity  of  a  stenotic  murmur, 
by  recourse  to  tracheoscopic  or  bronchoscopic  examination,  or,  in  the 
event  of  certain  impervious  foreign  bodies,  by  recourse  to  the  a'-rays. 

Prognosis. — ^The  prognosis  depends  upon  the  cause  of  the  obstruction. 
Foreign  bodies,  while  they  sometimes  occasion  sudden  death,  are  also 
sometimes  retained  for  months  or  years,  and  finally  expectorated. 

Treatment. — The  treatment  depends  upon  the  cause  of  the  obstruction. 
Foreign  bodies  may  sometimes  be  removed  by  inverting  the  patient 
and  exciting  coughing;  by  direct  removal  with  the  aid  of  the  broncho- 
scope; sometimes  by  recourse  to  tracheotomy  or  bronchotomy.  Syphilis 
and  tuberculosis  are  to  be  treated  according  to  the  basic  condition. 
Tumors  may  be  removed  sometimes,  but  with  much  difficulty  and  little 
prospect  of  permanent  good. 


HEMOPTYSIS  539 


DISEASES  OF  THE  LUNGS. 

HEMOPTYSIS. 

(Pulmonary  Hemorrhage;  Bronchopulmonary  Hemorrhage.) 

Etiology. — Hemoptysis,  the  spitting  of  blood  or  the  discharge  of 
blood  from  the  respiratory  tract,  may  result  from  disease  of  the 
larynx,  the  trachea,  the  bronchi  (including  the  bronchioles),  or  the 
lung.  The  diseases  of  which  it  is  a  manifestation  are:  (1)  Dis- 
eases of  the  respiratory  system:  (a)  Diseases  of  the  larynx — acute 
and  chronic  inflammation;  tuberculous,  syphilitic,  and  malignant 
ulceration,  etc.  Laryngeal  hemorrhage  is  unusual;  occasionally  it 
is  profuse,  as  in  altered  blood  states,  etc.  (6)  Diseases  of  the  bronchi 
and  trachea — bronchitis  (especially  the  putrid  and  fibrinous  varieties); 
bronchiectasis;  tuberculous,  syphilitic,  and  malignant  ulceration  (with 
erosion  of  a  branch  of  the  pulmonary  artery);  rupture  of  an  aneurysm 
into  the  trachea  or  a  bronchus,  in  which  event  the  hemorrhage  may 
be  large  and  lead  immediately  to  a  fatal  issue;  etc.  (c)  Diseases  of 
the  lungs,  especially  tuberculosis  (80  to  90  per  cent.)  of  the  cases,  croup- 
ous pneumonia,  the  acute  exanthemas,  congestion,  thrombosis,  and 
embolism  (infarction),  abscess,  gangrene,  tumors,  actinomycosis, 
aspergillosis,  zooparasitic  infections,  etc.  In  the  early  states  of  tuber- 
culosis the  blood  usually  comes  from  the  congested  mucosa  of  small 
bronchi  (capillary  oozing);  in  the  later  stages  i'  is  due  to  erosion  of 
an  artery  or  the  rupture  of  an  aneurysmal  dilatation  of  a  branch  of 
the  pulmonary  artery.  (2)  Diseases  of  the  cardiovascular  system:  (a) 
Advanced  valvular  disease  (especially  mitral  stenosis),  leading  to  well- 
marked  passive  congestion.  The  hemorrhage  may  be  slight  and 
recurrent,  or  quite  free,  sometimes  persisting  for  several  days,  (b) 
Aneurysm  of  the  aorta,  in  which,  at  first,  the  hemorrhage  may  be  small 
and  repeated,  and  due  to  pressure  on  the  bronchial  mucosa,  or  to  leakage 
through  the  outer  (usually  fibrous)  coat  of  the  aneurysmal  sac  (so- 
called  weeping  of  the  aneurysm);  or  the  hemorrhage  may  be  very  large 
(rupture  of  the  aneurysm)  and  lead  speedily  to  death.  (3)  Diseases 
of  the  blood — hemophilia,  purpura,  scurvy,  leukemia,  anemia,  etc., 
and  the  disorganization  of  the  blood  that  occurs  in  yellow  fever,  etc. 
(4)  Diminished  atmospheric  pressure,  as  in  mountain  sickness,  and  too 
sudden  release  from  caissons.  (5)  Arteriosclerosis  and  gout,  so-called 
arthritic  hemoptysis,  sometimes  observed  in  arteriosclerotic  and  gouty 
subjects  with  disease  of  the  smaller  vessels  of  the  lungs.  (6)  Vicarious 
hemoptysis,  sometimes  observed  in  women  at  the  time  of  menstruation 
or  during  the  persistence  of  amenorrhoea.  (7)  Traumatism — injuries 
of  the  thorax,  punctured  wounds  of  the  chest  and  lung,  and  rupture 
of  a  small  vessel  due  to  overexertion.  (8)  Neurotic  hemoptysis,  occa- 
sionally observed   in   neurotic,   hysterical   (especially  female)  subjects 


540  DISEASES  OF  THE  LUNGS 

who  otherwise  are  well.  Some  of  these  subjects  remam  perfectly  well, 
but  some  subsequently  become  definitely  tuberculous. 

Symptoms. — Rarely  hemoptysis  develops  in  persons  previously  in 
perfect  health;  thus,  it  may  be  the  initial  manifestation  of  tubercu  osis 
or  of  an  aortic  aneurysm.  Usually,  however,  symptoms  of  the  causative 
disease  precede  the  hemoptysis  (which  itself  is  only  a  symptom).  The 
blood  lost  varies  in  amount  from  the  slightest  streak  in  a  previously 
mucous  sputum  to  that  sufficient  immediately  to  cause  death.  When 
small  in  amount  the  hemoptysis  itself  may  be  the  only  noteworthy 
symptom;  when  profuse,  it  is  often  preceded  by  a  sense  of  warmth 
or  discomfort  in  the  chest,  or  of  tickling  or  of  something  arising  in  the 
throat,  and  a  saline  taste  in  the  mouth — which  are  followed  immediately 
by  the  ejection  of  the  blood,  bright  red,  fluid,  and  frothy.  The  blood 
may  be  coughed  up,  or  it  may  escape  from  the  patient's  mouth  without 
obvious  effort  on  his  part.  Large  hemorrhages  are  commonly  associated 
with  mental  perturbation,  cardiac  palpitation,  marked  prostration, 
and  often  syncope;  immediate  death  may  ensue,  but  it  is  rare.  Fatal 
hemorrhage  may  occur  into  a  tuberculous  or  other  cavity  without  the 
blood  being  discharged  externally.  In  other  cases  some  of  the  blood 
effused  into  a  cavity  or  bronchus  is  retained  some  time  and  then  dis- 
charged clotted;  casts  of  the  bronchi  and  bronchioles  may  be  observed. 
Sometimes  the  blood  is  swallowed  and  later  vomited;  or  it  may  escape 
into  the  intestine  and  discolor  the  stools. 

Physical  Signs. — The  physical  signs,  as  a  rule,  are  only  those  of  the 
primary  disease,  with  the  later  development  of  fine  and  coarse  bubbling 
rales,  due  to  the  presence  of  blood  in  the  bronchi  and  bronchioles. 

Diagnosis. — The  diagnosis,  as  a  rule,  is  quite  easy.  Hemorrhage 
from  the  nose,  mouth,  fauces,  and  pharynx  must  be  excluded  (usually 
obvious  on  local  examination).  In  hematemesis  the  symptoms  and 
signs  point  to  disease  of  the  abdominal  viscera;  sensations  of  warmth 
in  the  epigastrium,  nausea,  and  of  faintness  often  precede  the  discharge 
of  blood — which  is  vomited;  the  blood  is  usually  dark  in  color,  clotted, 
acid  in  reaction,  often  mixed  with  food,  and  is  quite  likely  to  appear 
in  the  stools. 

Prognosis. — The  prognosis  depends  upon  the  underlying  disease 
and  the  amount  of  blood  lost.  Usually,  the  hemorrhage  ceases  spon- 
taneously; but  occasionally  death  occurs — more  commonly,  however, 
after  than  during  the  bleeding. 

Treatment. — Absolute  bodily  and  mental  rest  is  essential.  The 
patient  should  be  reassured.  If,  as  in  tuberculosis,  the  diseased  side 
is  known,  or  if  it  is  discoverable  by  the  presence  of  rales  anteriorly 
(the  patient  should  not  be  disturbed  for  a  physical  examination)  he 
may  he  on  the  diseased  side  (to  lessen  the  respiratory  movements  and 
to  prevent  aspiration  of  blood  into  the  bronchi  of  the  other  lung).  Ice 
may  be  given  to  the  patient  to  suck,  and  an  ice  bag  may  be  applied 
to  the  bleeding  side,  or  to  the  precordium  (to  lessen  cardiac  excite- 
ment).    Tranquillity  may  be  favored  by  the  hypodermic  use  of  morphine 


CONGESTION  OF  THE  LUNGS  541 

combined  with  atropine — which  is  also  of  value  in  restraining  the  cough ; 
morphine,  however,  should  be  used  rather  sparingly  in  large  hemor- 
rhages, since  by  lessening  the  cough  (benumbing  sensibility),  it  may 
lead  to  inundation  of  the  bronchial  system  with  blood.  Lowering 
of  the  blood  pressure  (the  formation  of  a  clot)  should  be  favored  by 
nitroglycerin,  sometimes  by  aconite,  veratrum  viride,  or  chloroform, 
etc.;  by  purgation;  by  giving  the  minimum  amount  of  food  (cold,  not 
hot)  consistent  with  the  patient's  general  condition;  and  by  avoiding 
the  use  of  cardiac  stimulants,  such  as  alcohol,  strychnine,  digitalis, 
strophanthus,  caffeine,  etc.,  even  if  syncope  ensues.  Syncope  itself 
is  a  valuable  adjunct  in  the  formation  of  a  clot.  Sodium  chloride  on 
the  tongue  (reflex  action  on  the  vagus),  and  calcium  chloride  (30  grains, 
2  grams)  may  prove  of  service.  Small  repeated  hemorrhages  may 
sometimes  be  controlled  by  the  continued  use  of  turpentine,  or  aromatic 
sulphuric  acid.  Ergot,  adrenalin  chloride,  etc.,  are  to  be  avoided, 
since  they  raise  the  blood  pressure.  Gelatin,  gallic  acid,  lead  acetate, 
etc.,  are  of  at  least  doubtful  value.  The  hypodermic  injection  of- 
normal  serum  has  been  recommended,  especially  in  recurring 
hemoptyses. 


CONGESTION  OF  THE  LUNGS. 

{Hyperemia  of  the  Lungs;  Pulmonary  Congestion.) 

Congestion  of  the  lungs  may  be  active  or  passive. 

Active  Congestion. — ^Active  congestion  of  the  lungs  usually  occurs  as 
a  secondary,  symptomatic  affection,  but  it  is  said  occasionally  to  occur 
as  a  primary,  independent  affection.  Symptomatically  it  may  be  circum- 
scribed or  diffuse,  and  involve  one  lung  or  both  lungs.  It  is  usually  seen 
in  association  with  other  disorders  of  the  lung,  such  as  pneumonia, 
pleurisy,  bronchitis,  embolism  and  thrombosis,  tuberculosis,  etc.  At 
times  it  appears  to  be  due  to  the  inhalation  of  various  toxic  agents, 
such  as  hot  air,  irritating  vapors,  etc.,  to  sudden  changes  from  cold  to 
heat,  great  physical  exertion,  profound  emotion,  etc.  In  France  it  is 
recognized  as  a  common  independent  disease,  and  has  received  the 
name  "maladie  de  Woillez."  Most  of  these  cases,  however,  are 
doubtless  atypical  pneumonias,  of  which  one  proof  is  the  finding  of 
pneumococci  in  the  sputum  (believed  by  some  writers  to  be  attenuated 
pneumococci). 

Symptoms. — The  symptoms  consist  of  cough,  dyspnoea,  and  slight 
frothy,  blood-streaked  sputum,  in  addition  to  the  symptoms  of  the 
associated  disease.  La  maladie  de  Woillez  is  manifested  by  initial  chill, 
fever  (101°  or  more),  cough,  dyspnoea,  and  pain  in  the  side  of  several 
days'  duration.  The  physical  signs  are  those  of  the  first  stage  of  pneu- 
monia— slight  impairment  of  })ercussion  resonance,  feeble  or  broncho- 
vesicular  breath  soiuids,  increased  fremitus,  and  fine  crepitant  rales. 

Treatment. — The  treatment  is  that  of  pneumonia. 


542  DISEASES  OF  THE  LUNGS 

Passive  Congestion. — Two  forms  of  passive  congestion  of  the  lungs 
are  distinguished:     (1)  Mechanical,  and  (2)  hypostatic. 

Mechanical  congestion  results  from  obstruction  to  the  return  flow 
of  blood  to  the  left  heart.  It  is  common,  therefore,  in  chronic  mitral 
valvular  disease,  dilatation  of  the  right  ventricle,  etc.;  and  it  occurs 
sometimes  in  consequence  of  the  pressure  of  mediastinal  tumors.  The 
lungs  are  enlarged,  tough,  elastic,  heavy,  and  of  a  reddish-brown  color 
(cyanotic  induration),  which  quickly  changes  to  a  bright  red  color  on 
section  and  exposure  to  the  air  (oxidation  of  the  hemoglobin).  Micro- 
scopically there  are  dilatation  of  the  interalveolar  capillaries,  over- 
growth of  fibrous  connective  tissue,  and  in  the  walls  of  the  alveoli,  as 
well  as  free  in  the  alveoli,  many  blood-pigmented  cells  (heart-disease 
cells  of  the  sputum). 

Hypostatic  congestion  occurs  in  many  acute  febrile  diseases  (typhoid 
fever,  etc.),  in  chronic  debilitating  diseases,  anemic,  marantic,  and 
cachetic  conditions,  in  coma  (apoplexy,  and  other  disorders  of  the 
brain,  morphine  and  other  narcotic  poisonings),  in  old  age,  etc. 
It  results  from  a  feeble  circulation,  loss  of  tone  of  the  pulmonary 
vessels,  and  the  influence  of  gravity.  Usually  the  condition  is  limited 
to  the  bases  of  both  lungs  posteriorly.  The  affected  portions  of  the 
lungs  are  surcharged  with  blood,  dark  red  in  color,  oedematous,  and 
often  entirely  devoid  of  air,  whence  they  sink  in  water  (hypostatic 
pneumonia;  splenization).  Occasionally  in  organic  disease  of  the  brain 
(apoplexy,  etc.),  the  condition  may  be  unilateral;  and  it  is  sometimes 
associated  with  definite  areas  of  bronchopneumonia  (aspiration  pneu- 
monia). 

Symptoms. — ^The  symptoms  are  often  equivocal.  Usually,  however, 
there  are  cough,  frothy,  blood-streaked  expectoration  (containing  pig- 
mented, so-called  heart-disease  cells),  dyspnoea,  and  more  or  less  cya- 
nosis. Physical  examination  reveals  impaired  percussion  resonance 
posteriorly  at  the  bases,  increased  fremitus,  feeble  or  bronchovesicular 
breathing,  and  fine  and  coarse  bubbling  rales. 

Diagnosis. — ^The  diagnosis  depends  more  upon  the  presence  of  a 
causative  factor  and  the  results  of  the  physical  examination  than  upon 
the  symptoms. 

Prognosis. — The  prognosis  depends  upon  the  causative  factor;  usually 
amelioration  of  the  symptoms  may  be  brought  about. 

Treatment. — ^The  underlying  cause  of  the  condition,  usually  organic 
disease  of  the  heart,  must  be  treated.  If  the  symptoms  are  urgent, 
venesection  should  be  performed;  those  who  accept  great  hazards  some- 
times suggest  tapping  the  right  auricle — a  procedure  that  does  not 
appeal  to  me.  Diffusible  stimulants  are  often  of  much  temporary 
value.  The  hypostatic  form  of  the  disease  may  often  be  prevented 
by  having  susceptible  patients  frequently  turned  in  bed,  or  placed  in 
a  semiprone  or  upright  position  in  bed  or  in  a  chair  from  time  to  time. 


(EDEMA   OF  THE  LUNGS  543 


(EDEMA  OF  THE  LUNGS. 

(Acute  and  Chronic  Pulmonary  Oedema;  Recurrent  Pulmonary  (Edema;  Acute 
Suffocative  Pulmonary  (Edema.) 

Etiology. — Pulmonary  oedema,  the  transudation  into  the  alveoli  and 
the  interstitial  tissue  of  the  lungs,  of  a  serous,  sometimes  serosanguino- 
lent,  fluid,  occurs  under  divers  circumstances:  (1)  As  an  agonal  mani- 
festation in  many  acute  and  chronic  disorders,  especially  of  the  heart 
and  bloodvessels,  kidneys,  lungs,  blood,  nervous  system  (brain),  etc.; 
(2)  as  an  acute  transitory  manifestation  in  disease  of  the  heart,  kidneys, 
and  in  certain  infectious  diseases;  (3)  as  a  chronic  process  in  disease 
of  the  heart,  and  under  circumstances  akin  to  those  that  produce 
chronic,  or  passive,  congestion;  (4)  after  thoracentesis;  (5)  associated 
with  inflammatory  processes  in  the  lung,  especially  pneumonia,  tubercu- 
losis, thrombosis,  embolism,  etc.  (so-called  inflammatory  or  collateral 
oedema;  not  a  true  oedema — rather  an  exudation);  (6)  as  an  apparently 
primary,  acute,  often  quickly  fatal  disorder,  developing  without  obvious 
exciting  cause  (acute  suffocative  pulmonary  oedema). 

The  mechanism  of  the  oedema  varies  in  dilTerent  cases.  Often,  as 
maintained  by  Welch,  it  is  "due  to  a  disproportion  between  the  working 
power  of  the  left  ventricle  of  such  a  character  that,  the  resistance 
remaining  the  same,  the  left  heart  is  unable  to  expel  in  a  unit  of  time 
the  same  quantity  of  blood  as  the  right  heart.  Such  disproportion  may 
be  brought  about  by  paralysis  or  by  spasm  of  the  left  ventricle,"  and 
increasing  the  pressure  in  the  pulmonary  circulation  it  leads  to  transu- 
dation of  serum  through  the  pulmonary  capillaries.  Disturbances  of 
the  innervation  of  the  cardiopulmonary  plexus  by  periaortitis,  consider- 
able augmentation  of  the  vascular  tension  in  the  small  circulation, 
and  acute  or  rapid  insufficiency  of  the  right  ventricle  (Huchard),  serve 
to  explain  the  cases  associated  with  angina  pectoris,  Hodgson's  disease 
and  other  diseases  of  the  aorta.  The  toxic  vasomotor  theory  (paralysis 
of  the  pulmonary  vessels)  serves  to  explain  the  cases  occurring  in  Bright's 
disease,  in  pregnancy  (without  valvular  or  other  heart  disease);  that 
associated  with  angioneurosis;  and  that  due  to  certain  drugs,  such  as 
the  iodides,  pilocarpine,  etc.  Congestion  by  recoil  (Riesman)  explains 
those  cases  developing  after  thoracentesis,  the  oedema  in  these  cases 
resulting  from  an  afflux  of  blood  to  the  expanding  lung  and  a  leakage 
of  serum  through  the  pulmonary  vessels,  which  by  reason  of  long  com- 
pression have  become  changed  and  rendered  more  permeable.  In- 
creased fluidity  of  the  blood  is  perhaps  a  factor  in  some  cases. 

Pathology. — The  oedema  may  be  limited  to  the  bases,  or  it  may  be 
gene  al  and  involve  both  lungs.  The  oedematous  lung  is  bulky,  pale, 
boggy;  contains  less  air  than  normally  (but  does  not  sink  in  water); 
and  on  section  a  clear,  frothy,  serous  or  serosanguinolent  fluid,  of  low 
specific  gravity  gnd  containing  a  trace  of  albumin,  exudes,  especially 
on  pressure, 


544  DISEASES  OF  THE  LUNGS 

Symptoms. — In  addition  to  the  symptoms  of  the  primary  disease, 
dyspnoea,  cough,  and  expectoration  are  the  noteworthy  manifestations. 
The  expectoration  is  especially  characteristic,  being  usually  abundant, 
thin,  serous  (occasionally  serosanguinolent),  and  frothy.  The  dyspnoea 
sometimes  becomes  much  aggravated  and  amounts  to  orthopnoea,  the 
accessory  muscles  of  respiration  being  called  into  activity.  As  a  rule, 
there  is  more  or  less  cyanosis;  the  pulse  becomes  small,  rapid,  and  of 
poor  tension,  and  the  extremities  become  cold.  There  is  no  fever,  unless 
bronchopneumonia  or  other  infectious  complication  ensues. 

Acute  suffocative  pulmonary  oedema  apparently  is  an  independent 
disorder  that  develops  suddenly,  often  without  obvious  exciting  cause, 
and  frequently  leads  quickly  to  a  fatal  termination,  although  recurring 
attacks  are  by  no  means  imcommon.  It  occurs,  as  a  rule,  in  arterio- 
sclerotic, cardiac,  and  nephritic  subjects,  and  is  characterized  by  the 
sudden  development,  often  at  night,  of  attacks  of  extreme  dyspnoea 
(orthopnoea),  cyanosis  (pallid  lividity),  cough,  expectoration  of  a  thin, 
frothy,  serous,  albuminous  (occasionally  blood-streaked)  fluid,  and 
marked  prostration  (with  sweating,  etc.).  The  fluid  often  drools  from 
the  patient's  mouth  without  effort  on  his  part;  I  have  seen  twelve 
ounces  of  such  fluid  expelled  within  a  few  hours.  The  attack  may 
result  in  death  within  ten  or  fifteen  minutes,  the  patient  being  virtually 
drowned  in  his  own  fluids;  or  it  may  subside  rather  soon  (within  a  half 
hour  or  thereabout),  or  it  may  last  from  three  to  twelve  or  more  hours. 
The  condition  of  the  heart  varies  during  the  attacks;  in  one  patient 
that  I  observed  the  right  heart  seemed  to  be  considerably  dilated  during 
the  attack. 

Physical  Signs. — Physical  signs  consist  of  general  impairment  of  the 
percussion  resonance,  or  scattered  foci  of  dulness  and  intervening  areas 
of  vesiculotympanitic  sound  (relaxation  of  the  lung  tissue),  feeble, 
harsh,  or  obscured  vesicular  breathing,  and  numerous  fine  and  coarse 
bubbling  rales  (localized  or  distributed  generally  throughout  both  lungs). 

Diagnosis. — The  diagnosis  is  easy;  the  symptoms  and  physical  signs 
can  scarcely  be  mistaken  for  anything  else.  An  associated  broncho- 
pneumonia should  not  be  overlooked. 

Prognosis. — The  prognosis  is  grave,  especially  in  view  of  the  asso- 
ciated phenomena,  of  which  the  oedema  is  often  a  terminal  manifestation. 

Treatment. — The  treatment,  as  a  rule,  is  that  of  the  disease  of  which 
the  oedema  is  one  manifestation.  A  hypodermic  injection  of  morphine 
{j  grain,  0.015  gram)  and  atropine  {^h^  grain,  0.0006  gram)  will 
usually  almost  immediately  relieve  the  severe  symptoms;  I  have  seen 
it  render  the  greatest  service  (apparently  save  life)  in  the  acute  suffo- 
cative type  of  the  disease.  The  injection  may  be  repeated,  if  the  cir- 
cumstances demand  it;  repeated  injections  of  atropine  are  often  of 
value  for  a  day  or  two.  In  addition,  diffusible  stimulants  are  indi- 
cated—camphor, strychnine,  ether,  whiskey,  etc.,  hypodermicly;  stro- 
phanthus,  coffee,  brandy,  whiskey,  champagne,  etc.,  by  the  mouth. 
Venesection  is  sometimes  a  life-saving  procedure,  and  should  be  resorted 


PULMONARY  EMBOLISM  AND   THROMBOSIS  545 

to  when  the  patient's  condition  is  grave  (extreme  cyanosis,  etc.). 
Counterirritation  (dry  or  wet  cups,  mustard  poultices,  etc.)  may  prove 
of  service.  Drastic  purgatives  are  often  given  in  the  hope  of  relieving 
the  system  of  fluid,  but  their  action  is  too  severe  to  recommend  their 
use  while  the  patient  is  seriously  ill.  Nor  does  the  use  of  emetics  to 
assist  in  the  expulsion  of  the  fluid  commend  itself  to  me.  Since  the 
disorder  is  often  a  terminal  manifestation,  treatment  in  these  cases  may 
not  prove  of  avail. 


PULMONARY  EMBOLISM  AND  THROMBOSIS. 

(Pulmonary  Infcn-ction;  Hemorrhagic  Infarction  of  the  Lung;  Pulmonary  Apoplexy.) 

Etiology. — Primary  thrombosis  of  the  pulmonary  artery  or  its  branches 
is  an  unusual  event,  but  it  may  result  from  slowing  of  the  circulation, 
impoverishment  of  the  blood,  and  disease  of  the  arterial  wall,  such  as 
may  occur  in  pneumonia  (and  other  infections),  arteriosclerosis,  com- 
pression of  the  vesse  by  a  tumor,  etc.  Pulmonary  embolism  results 
from  thrombotic  processes  in  the  right  side  of  the  heart  or  in  the  systemic 
veins,  especially  the  femoral  veins,  the  veins  of  the  uterus  (after  par- 
turition), the  sinuses  of  the  brain,  the  veins  of  the  abdomen,  liver,  etc. 
It  is  common  in  the  sequence  of  mitral  valve  disease,  especially  stenosis, 
in  which  passive  congestion  of  the  lungs  and  dilatation  of  the  right 
side  of  the  heart  have  supervened,  the  thrombi  developing  in  the  auricle 
or  amidst  the  columnse  carnese.  The  foundation  of  the  embolus  may 
also  be  a  newgrowth  that  has  invaded  a  vein,  a  phlebolith,  fat  set  free 
by  a  fracture  of  a  long  bone,  rupture  of  the  liver,  rupture  of  the  sub- 
cutaneous adipose  tissue,  air  bubbles,  etc.  The  embolus,  as  well  as  the 
thrombus,  may  be  infectious  or  non-infectious. 

Pathology. — The  embolus  or  thrombus  may  involve  the  main  branch 
of  the  pulmonary  artery,  one  or  several  of  the  medium-sized  branches, 
or  the  smallest  branches.  The  blocking  of  the  vessel  is  usually,  but 
not  always,  followed  by  infarction;  sometimes  not,  because  death  occurs 
almost  immediately;  in  other  cases,  because  the  obstruction  is  not 
complete,  or  the  collateral  circulation  is  sufficient,  or  the  bronchial 
arteries  maintain  the  circulation.  Stasis  of  the  pulmonary  circulation 
seems  to  be  an  important  if  not  essential  element  in  the  process  of 
infarction.  The  infarct  may  be  single,  though  they  are  usually  multiple; 
they  are  more  common  in  the  lower  lobe  on  the  right  side;  they  vary 
in  size  from  a  marl:)le  to  an  orange;  they  consist  of  pyramidal  or  wedge- 
shaped  masses,  with  the  base  toward  the  periphery,  dark  red  in  color, 
firm,  and  devoid  of  air.  Microscopicly  they  are  found  to  consist  of 
blood  filling  the  air  vesicles  and  infiltrating  the  lung  tissue.  The 
thrombus  or  embolus  often  escapes  detection.  The  overlying  pleura 
is  often  covered  with  a  fibrinous  exudation,  through  which  small  foci 
of  hemorrhage  may  be  observed.  Small  infarcts  may  be  absorbed, 
or  the  blood  may  be  removed  by  reestablishment  of  the  circulation; 
2>n 


546  DISEASES  OF  THE  LUNGS 

large  infarcts  leave  behind  a  puckered  scar.  Should  the  embolus  be 
infective,  pneumonia,  abscess  or  gangrene  of  the  lung,  pleuritis  or 
pyopneumothorax,  etc.,  may  result. 

Symptoms. — Complete  obstruction  of  a  main  branch  of  the  pulmonary 
artery  is  often  followed  by  immediate  death;  in  other  cases,  after  a 
few  moments  of  a  feeling  of  extreme  constriction  within  the  chest, 
dyspnoea,  and  terror,  the  patient  loses  consciousness,  the  pupils  dilate, 
the  face  becomes  livid,  the  pulse  rapid  and  irregular,  perspiration 
breaks  out,  and  death  occurs  within  an  hour.  In  less  severe  cases, 
that  is,  in  cases  in  which  the  obstruction  is  not  complete  or  the  obstructed 
vessel  is  small,  the  chief  symptoms  consist  of  sudden  pain  and  a  sense 
of  constriction  within  the  chest,  dyspnoea  (labored,  sometimes  Cheyne- 
Stokes  breathing),  hemoptysis,  and  more  or  less  collapse.  Bloody, 
dark-red,  non-aerated  expectoration  is  quite  significant  of  infarction. 
A  typical  "stitch  in  the  side"  sometimes  ensues,  and  is  referable  to  a 
concomitant  pleurisy;  it  is  usually  associated  with  local  tenderness 
and  a  friction  rub.  Fever  does  not  occur,  unless  the  embolus  is  infective; 
in  this  event,  to  the  general  manifestations  of  septicopyemia  are  added 
the  local  signs  of  pulmonary  abscess  or  gangrene.  Occasionally  small 
infarcts  develop  without  noteworthy  symptoms. 

Physical  Signs. — There  are  no  characteristic  physical  signs.  Small 
peripheral  and  central  infarcts  usually  occasion  no  physical  signs  what- 
ever; but  larger  infarcts  that  reach  the  pleura  may  occasion  dulness 
on  percussion,  harsh  bronchial  or  bronchovesicular  breath  sounds, 
and  crepitant  or  crackling  rales.  Should  there  be  a  local  pleuritis, 
the  breath  sounds  may  be  feeble  or  inaudible,  and  frictions  may 
develop. 

Diagnosis. — The  diagnosis  may  be  exceedingly  easy,  as  in  a  chronic 
heart  subject  in  whom  the  symptoms  develop  tj^ically;  in  other  cases, 
it  may  be  quite  difficult — in  case  of  sudden  death.  In  these  cases, 
the  diagnosis  is  facilitated  by  the  presence  of  a  causative  factor,  and 
the  absence  of  definite  causes  for  thrombosis  or  embolism  of  the  coronary 
artery,  cerebral  hemorrhage,  rupture  of  an  aneurysm,  and  other  causes 
of  sudden  death. 

Prognosis. — The  prognosis,  as  a  rule,  is  mifavorable.  If  death  does 
not  occur  soon,  the  infarction,  nevertheless,  points  to  weakness  of  the 
right  ventricle,  a  primary  thrombus  somewhere  in  the  body,  or  other 
serious  disorder.  Occasionally  the  infarct  is  absorbed  and  the  patient 
recovers  temporarily,  at  least.     Recurrences  are  rather  common. 

Treatment. — Prophylaxis  is  of  the  utmost  importance.  Patients  in 
whom  venous  thrombi  exist,  or  who  are  ill  with  diseases  known  to  favor 
the  development  of  such  thrombi,  should  be  carefully  nursed,  protected 
from  sudden  movements  that  might  dislodge  the  thrombus,  and  well 
fed.  At  the  time  of  the  development  of  the  embolism,  morphine  and 
atropine  are  usually  necessary  to  relieve  pain;  if  the  patient  does  not 
die  soon,  recourse  should  be  had  to  stimulants — camphor,  strychnine, 
ammonia,  oxygen,  etc.     Later  the  primary  disorder  requires  attention. 


ATELECTASIS  AND  COLLAPSE  OF  THE  LUNG  547 

ATELECTASIS  AND  COLLAPSE  OF  THE  LUNG. 

(Apnenmatosis ;  Compression  of  the  Lung.) 

Atelectasis  and  collapse  of  the  lung  are  much-related  conditions: 
atelectasis  properly  is  a  condition  found  in  infants  in  which  the  lungs 
or  portions  of  the  lungs  have  not  expanded;  collapse  occurs  in  older 
persons  and  is  a  reversion  to  this  condition  after  expansion  has  occurred. 
Both  terms,  however,  are  commonly  used  interchangeably.  Congenital 
and  acquired  forms  of  the  condition  are  usually  distinguished. 

Etiology. — Congenital  atelectasis  results  from  inefficient  action  of 
the  respiratory  muscles  (associated  usually  with  general  feebleness 
of  the  infant);  defective  innervation  resulting  from  a  congenital  defect 
or  from  pressure  on  the  foetal  head  by  the  forceps  or  a  contracted  pelvis ; 
obstruction  of  a  bronchus  by  mucus  or  meconium,  or  by  pressure 
from  without,  as  by  enlarged  lymph  nodes;  or  by  pressure  on  the 
lung  by  enlarged  abdominal  organs,  tympanites,  ascites,  etc. 

Acquired  atelectasis,  or  collapse,  of  the  lung  results  from:  (1) 
Obstruction  of  a  bronchus  by  mucopus,  foreign  bodies,  newgrowths, 
or  c^her  products  of  inflammation.  It  is  found  most  commonly  in  asso- 
ciation with  bronchopneumonia.  When  the  obstruction  is  complete, 
air  can  neither  enter  nor  leave  the  involved  portion  of  the  lung,  and 
absorption  of  the  air  by  the  blood  takes  place.  (2)  Compression  of  a 
bronchus  by  a  pleural  effusion,  hydrothorax,  pneumothorax,  pyothorax, 
pericardial  effusion,  extreme  cardiac  hypertrophy,  aneurysm  of  the 
arch  of  the  aorta,  newgrowths  of  the  thorax  and  mediastinum,  kypho- 
scoliosis, and  pressure  from  below  the  diaphragm  by  enlarged  viscera, 
tympanites,  ascites,  etc.  (3)  Feeble  respiratory  efforts,  such  as  occur 
in  debilitated  and  asthenic  conditions  generally — cachectic  and  maran- 
tic states,  typhoid  fever,  coma,  prolonged  dorsal  decubitus,  paralysis 
of  the  pneumogastric  nerves,  rachitis,  pleural  adhesions,  kyphoscoliosis, 
etc. 

Pathology. — Atelectasis  most  commonly  involves  the  lower  portions 
of  the  lungs;  it  may  occur  in  scattered  foci  (obstruction  within  the 
bronchi,)  or  it  may  implicate  an  entire  lobe  (compression  from  without). 
The  collapsed  portion  of  the  lung  is  reduced  in  size,  purplish  red  in 
color,  firm,  airless,  and  sinks  in  water;  sometimes  there  is  serous  infil- 
tration (splenization,  carnification).  In  the  congenital  variety  the 
atelectatic  portions  of  the  lung  may  gradually  expand,  or  they  may 
remain  unexpanded  and  become  the  seat  of  fibrous  thickening — hyj)()- 
plasia  or  aplasia  of  the  lung.  The  condition  is  often  associated  with 
congenital  anomalies  of  the  circulation  (patulous  ductus  Botalli,  fora- 
men ovale,  etc.). 

Symptoms. — Congenital  atelectasis  is  manifested  by  feeble  and  super- 
ficial respiration,  dyspnoea,  cyanosis,  cold  extremities,  feeble  iieart 
action,  drowsiness,  sometimes  muscular  twitchings  and  convulsions 
(carbon   dioxide  poisoning).     The  physical  signs  consist  of  deficient 


548  DISEASES  OF  THE  LUNGS 

expansion  of  the  chest,  retraction  of  the  intercostal  spaces,  and  defective 
inspiratory  murmur  over  the  atelectatic  portions  of  the  lung. 

The  symptoms  of  acquired  atelectasis  are  often  obscured  by  those 
of  the  primary  disorder,  commonly  bronchopneumonia,  and  the  collapse 
often  is  not  diagnosticated.  In  other  cases,  dyspnoea,  cyanosis,  feeble 
heart  action,  cold  extremities,  etc.,  develop,  but  it  is  difficult  to  say 
whether  these  are  not  due  as  much  to  the  primary  disorder  as  to  a 
supposed  collapse  of  the  lung.  In  cases  associated  with  kypho- 
scoliosis, cyanosis,  dyspnoea,  and  palpitation  of  the  heart  are  usually 
marked,  and  in  consequence  of  the  obstruction  in  the  pulmonary  circu- 
lation considerable  hypertrophy  and  dilatation  of  the  right  ventricle 
ensue;  ultimately  lack  of  compensation  supervenes. 

Physical  Signs. — ^^^len  associated  with  bronchopneumonia  there 
are  often  no  noteworthy  physical  signs  in  addition  to  those  occasioned 
by  the  bronchopneumonia;  sometimes  to  the  evidences  of  localized 
foci  of  solidification  are  added  those  of  intervening  (or  surrounding) 
foci  of  inflation.  AMien  the  collapsed  area  is  large  (compression  of 
a  bronchus  from  without),  there  is  restricted  movement  at  the  base  of 
the  chest  (or  over  the  collapsed  area),  with  increased  expansion 
elsewhere,  impaired  percussion  resonance,  diminished  fremitus,  and 
feeble  breath  sounds;  occasionally,  when  the  air  has  access  to  the  main 
bronchus,  there  may  be  increased  fremitus  and  bronchovesicular  breath- 
ing. Crackling  rales  are  not  uncommon;  frequently  they  disappear 
after  repeated  deep  inspirations. 

Diagnosis. — The  disorder  is  often  overlooked  when  the  foci  are  small; 
when  large,  the  physical  signs  serve  for  their  recognition.  Changes 
in  the  dulness,  breath  sounds,  and  rales  after  several  deep  breaths 
or  a  change  of  posture  (for  several  hours)  serve  to  exclude  many 
other  disorders,  such  as  pneumonia,  pleuritis,  thrombosis  and  em- 
bolism, etc. 

Prognosis. — The  prognosis  depends  upon  the  associated  conditions. 
Sudden  death  may  occur  in  kyphoscoliosis,  and  in  bronchopneumonia 
in  which  change  of  posture,  etc.,  does  not  lead  to  inflation  of  the  collapsed 
areas. 

Treatment. — The  treatment  in  general  is  that  of  the  primary  dis- 
order. In  addition,  measures  that  tend  to  prevent  the  development 
of  the  atelectasis  should  be  employed.  Thus,  patients  should  be  pre- 
vented from  lying  in  the  one  position  for  a  long  time,  and  deep  inspira- 
tions should  be  insisted  upon  from  time  to  time.  Cold  affusions  are 
of  service  in  preventing  the  disorder,  and  of  value  when  it  has  developed. 
Diffusible  cardiac  stimulants  (camphor,  ether,  strychnine,  ammonium 
preparations,  etc.)  are  valuable,  and  so  also  sometimes  are  oxygen, 
compressed  air,  etc.  In  congenital  atelectasis,  forcible  inflation  has 
been  productive  of  good  results. 


BRONCHOPNEUMONIA  549 

BRONCHOPNEUMONIA. 

(Lobular  Pneunionin ;  Capilldr//  Bronchitis.) 

Bronchopneumon'a  is  a  bacterial  infection  of  the  lungs  characterized 
by  inflammation  of  the  terminal  bronchioles  and  the  related  alveoli 
that  collectively  make  up  a  lobule.  It  is  not  distinguishable  from  cap- 
illary bronchitis. 

Etiology. — Bronchopneumonia  is  most  common  in  children  under 
five  years  of  age  (75  per  cent,  of  the  cases)  and  in  the  aged;  but  adults 
are  by  no  means  exempt.  It  may  occur  at  any  season  of  the  year, 
but  it  is  especially  prevalent  during  the  w^inter  and  spring.  Poor  hygienic 
surroundings,  malnutrition,  etc.,  act  as  predisposing  factors.  The 
exciting  causes  comprise  the  pneumococcus,  Friedlander's  pneumo- 
bacillus,  streptococci,  staphylococci,  the  influenza  bacillus,  the  typhoid 
bacillus,  the  tubercle  bacillus,  etc.  The  majority  of  cases  are  mixed 
infections. 

Primary  and  secondary  cases  may  be  distinguished.  The  primary 
cases  are  relatively  uncommon;  they  occur  particularly  in  previously 
healthy  children  under  two  years  of  age,  and  are  usually  due  to  the 
pneumococcus.  The  secondary  cases  are  of  several  types:  (1)  Those 
complicating  or  following  the  infectious  diseases,  especially  measles, 
pertussis,  diphtheria,  scarlatina,  influenza,  typhoid  fever,  etc.,  as  well 
as  other  diseases  attended  by  bronchitis.  This  group  is  especially 
common  in  children.  In  some  cases  of  tuberculosis  of  the  lungs  of 
the  ordinary  chronic  ulcerative  type,  bronchopneumonia  (sometimes 
terminal)  may  develop,  and  is  due  frequently  to  the  pneumococcus, 
although  the  lesions  may  be  due  to  mixed  infection.  (2)  Those  com- 
plicating chronic  debilitating  disorders,  such  as  nephritis,  diabetes, 
chronic  cardiac  disease,  prolonged  confinement  to  bed  (as  in  fracture 
of  the  femur),  etc.  This  type  is  especially  common  in  adults,  partic- 
ularly the  aged,  and  is  often  responsible  for  the  final  fatal  issue,  consti- 
tuting a  so-called  terminal  infection.  (3)  Aspiration  pneumonia,  which 
occurs  when  the  sensibility  of  the  larynx  has  become  benumbed,  as  in 
stuporous  and  comatose  states,  such  as  uremic  or  diabetic  coma,  apo- 
plexy, ether  and  chloroform  anesthesia,  or  operations  on  the  larynx  or 
trachea,  etc. — in  which  circumstances  bacteria-laden  particles  of  food, 
or  saliva,  etc.,  are  drawn  into  the  bronchi  and  ultimately  set  up  inflam- 
mation. The  pneumonia  that  may  follow  non-fatal  drowning,  the 
inhalation  of  irritating  vapors,  gases,  etc.,  is  perhaps  of  the  .same 
nature.  (4)  Perhaps  in  some  cases  the  infection  is  carried  to  the  lungs 
by  the  blood  stream  or  the  lymph  stream. 

Pathology. — The  lesions  consist  of  scattered  foci  of  solidification, 
varying  in  size  from  that  of  a  pinhead  to  a  cherry  or  larger;  the  foci 
are  bilateral  and  usually  most  marked  in  the  lower  lobes.  On  section 
they  consist  of  irregular,  dark,  reddish-brown  (later,  grayish  or  yel- 
lowish), firm,  airless  areas,  in  the  centre  of   which   a  bronchiole   can 


550  DISEASES  OF  THE  LUNGS 

often  be  detected;  it  is  usually  filled  with  mucopus,  and  its  epithelium 
is  swollen  and  reddened.  Surrounding  vesicles  are  often  atelectatic; 
perhaps  in  some  cases  the  atelectasis  precedes  the  inflammatory  phe- 
nomena. Microscopically,  the  bronchioles  show  the  ordinary  vascular 
and  exudative  lesions  of  inflammation,  especially  cellular  infiltration, 
and  proliferation  and  desquamation  of  the  epithelium,  which,  with 
the  mucopus,  obstructs  the  bronchioles;  the  related  alveoli  are  more 
or  less  filled  with  leukocytes,  some  erythrocytic  cellular  exudation,  pro- 
liferated and  desc{uamated  alveolar  epithelium,  and  some  fibrin  forma- 
tion— which  is  most  marked  in  the  pneumococcic  cases  (although 
always  less  than  in  so-called  lobar  pneumonia),  and  less  in  pyococcic 
and  influenzal  cases,  etc.;  the  alveolar  walls  are  swollen  and  infi - 
trated  and  show  the  ordinary  lesions  of  inflammation.  These  dissemi- 
nated foci  of  peribronchial  solidification  and  atelectasis,  and  embrac- 
ing areas  of  more  or  less  well  aerated  lung,  constitute  the  common 
type;  in  some  cases  bronchitis  and  bronchiolitis  with  comparatively 
little  (although  always  some)  alveolar  involvement  are  the  conspicuous 
lesions;  whereas  in  other  cases  the  lesions  spread  from  the  primary 
foci  directly  from  one  alveolus  to  adjacent  alveoli  or  through  the  lym- 
phatics until  more  or  less  of  the  lobe  is  involved  (pseudolobar  form) ;  but 
intervening  areas  of  more  or  less  congested  pulmonary  tissue  separate 
the  solidified  lobules.  The  bronchopneimionic  lesions  may  resolve 
(autolysis,  fatty  degeneration,  etc.)  and  become  absorbed,  perhaps  in 
part  expectorated;  or  if  death  does  not  ensue  from  exhaustion  and 
toxemia,  pulmonary  abscess,  gangrene,  or  fibrosis  may  ensue. 

Symptoms. — In  primary  bronchopneumonia  the  onset  may  be  sudden, 
following  slight  exposure  (as  in  ordinary  lobar  pneumonia);  there  may 
be  a  chill  (or  chilliness,  or  perhaps  a  convulsion  in  young  children), 
rapid  rise  of  temperature,  cough,  and  dyspnoea.  In  some  cases  the 
pulmonary  symptoms  are  overshadowed  by  the  general,  or  perhaps 
by  unusual  cerebral  manifestations  (stupor,  coma,  delirium,  etc.). 
Secondary  bronchopneumonia,  following,  for  instance,  one  of  the  acute 
infections  of  children  with  bronchitis,  is  usually  of  insidious  onset; 
it  is  characterized  by  exaggeration  of  the  already  existing  fever,  increased 
cough  and  dyspnoea,  and  cyanosis,  any  or  all  of  which  are  indicative 
of  bronchopneumonia  in  a  susceptible  bronchitic  subject;  rarely  the 
onset  is  sudden.  The  fully  developed  disease  is  characterized  by 
irregular  fever  (103°  to  105°),  rapid,  feeble  pulse  (140  to  160  per  minute 
in  children),  hard,  ineffectual,  and  distressing  cough,  dyspnoea  (60 
to  80  or  more  respirations  per  minute  in  children),  activity  of  the  acces- 
sory muscles  of  respiration,  inspiratory  retraction  of  the  lower  part  of 
the  chest,  cyanosis,  marked  prostration,  stupor  (and  other  so-called 
meningitic  manifestations),  leukocytosis,  etc. 

Physical  Signs. — The  physical  signs  in  the  early  stages  and  in  some 
cases  throughout  the  course  of  the  disease,  consist  of  harsh  broncho- 
vesicular  (puerile)  breath  sounds  and  fine  crackling  and  sibilant  rales 
throughout   both  lungs;   that  is,  signs  of   solidification  are  altogether 


BRONCHOPNEUMONIA  551 

wanting  (the  capillary  bronchitis  of  some  writers).  In  other  cases 
there  are  in  addition  scattered  foci  of  impaired  resonance,  sometimes 
of  more  or  less  well-marked  dulness,  and  increased  tactile  and  local 
fremitus,  especially  at  the  bases  posteriorly;  in  the  event  of  widespread 
involvement  of  a  lobe  more  or  less  outspoken  bronchial  (tubular) 
breath  sounds  may  be  heard. 

Similar  symptoms  and  physical  signs  develop  in  the  event  of  aspiration 
or  deglutition  pneumonia.  The  bronchopneumonia  that  develops  in 
adults  in  debilitated  and  cachectic  states  is  often  extremely  insidious 
in  onset;  symptoms  often  are  markedly  in  abeyance;  there  may  be 
only  a  little  dyspnoea,  or  perhaps  cyanosis,  and  the  disease  may  be 
overlooked  unless  the  chest  be  examined. 

Diagnosis. — The  diagnosis  of  the  common  secondary  broncho- 
pneumonia of  children  should  be  based  upon  the  primary  disorder 
and  the  advent  of  increased  fever,  cough,  dyspnoea,  and  cyanosis;  the 
physical  signs  of  solidification  often  may  be  entirely  absent.  Acute 
bronchitis  may  be  differentiated  by  the  low  fever,  less  dyspnoea,  and 
less  cyanosis ;  there  is  no  clinical  and  little  anatomical  difference  between 
capillj^^y  bronchitis  and  bronchopneumonia.  Lobar  pneumonia  may 
be  distinguished  by  its  comparative  rarity  in  infants,  and  its  charac- 
teristic mode  of  onset,  physical  signs,  and  course.  Efforts  should 
always  be  made  to  determine  the  etiological  factor  in  each  case  by 
examining  the  sputum. 

Prognosis. — The  course  of  bronchopneumonia  may  rarely  be  acute, 
lasting  about  a  week  or  ten  days;  usually  it  lasts  from  three  to  six  or 
eight  weeks  or  more.  Death  may  ensue  from  divers  complications, 
toxemia,  or  asthenia;  recovery  ensues  by  lysis.  The  prognosis  should 
always  be  guarded,  especially  in  the  very  young  and  the  aged;  it  is 
especially  bad  in  the  cases  following  measles  and  pertussis  in  debilitated 
and  rickety  children,  in  aspiration  pneumonias,  and  generally  when 
there  is  marked  cyanosis,  dyspnoea,  toxemia,  and  prostration. 

Treatment. — The  treatment,  in  general,  is  that  of  the  primary  dis- 
order, or  of  acute  bronchitis,  or  of  croupous  pneumonia.  The  most 
important  measure,  especially  in  young  children,  consists  of  an  abundant 
supply  of  fresh,  cool  air,  which,  ordinarily,  is  best  obtained  by  open  win- 
dows or  by  roof  gardens  at  hospitals,  etc.  Fresh,  cool  air  stimulates  the 
vasomotor  system  and  the  heart,  relieves  the  cyanosis,  and  lessens  the 
toxemia  and  its  cerebral  effects — and  is  much  superior  to  canned  oxygen 
in  a  warm,  ill-ventilated  room.  The  patient  should  be  well  protected  by 
a  sufficiency  of,  but  not  too  many,  bedclothes  (remembering  the  fever); 
the  feet  should  always  be  kept  warm  and  the  head  cool.  The  patient 
should  not  be  distressed  by  poultices,  blisters,  and  other  counter- 
irritants.  If  the  physician  must  contend  against  local  prejudices, 
let  him  apply  a  loose-fitting  cotton  jacket  (which  may  take  the  place 
of  other  clothing).  The  diet  should  be  fluid.  An  abundance  of  cold 
water  should  be  given  to  drink.  The  bowels  should  be  opened  thor- 
oughly— castor  oil  or  magnesia  in  children;  calomel  or  blue  mass  and 


552  DISEASES  OF  THE  LUXGS 

a  saline  cathartic  in  adults.  The  use  of  water  externally  and  internally 
as  recommended  in  croupous  pneumonia,  is  ser^'iceable;  in  children 
a  warm  bath  is  often  better;  in  adults,  as  well  as  in  children,  the 
desired  result  of  hydrotherapy  is  reaction  and  stimulation,  and  not 
reduction  of  temperature.  Diffusible  stimulants,  such  as  whiskey  and 
brandy,  strychnine,  ammonia,  and  camphor,  comprise  the  really  effica-. 
cious  remedies;  coal-tar  products  and  all  depressing  drugs  should  be 
absolutely  avoided.  Restlessness,  pain,  excessive  cough,  etc.,  suggest 
the  use  of  bromides,  Dover's  powder,  paregoric,  etc.,  all  of  which  should 
be  used  with  caution  in  the  young  and  the  aged.  The  other  therapeutic 
indications  are  similar  to  those  mentioned  under  bronchitis  and  croupous 
pneumonia. 

CHRONIC  INTERSTITIAL  PNEUMONITIS. 

(Chronic  Fibroid  Pneumonia;  Fibroid  Induration  of  the  Lung;  Sclerosis  of  the  Lung, 

Fibroid  Phthisis.) 

Etiology. — Chronic  interstitial  pneumonitis  may  occur  as  a  primary 
or  a  secondary  process.  The  primary  process  is  due  to  syphilis  or  to 
the  inhalation  of  irritating  dust  (pneumokoniosis).  The  secondary 
process  may  follow  croupous  pneumonia,  bronchopneumonia,  tuber- 
culosis, collapse  of  the  lung  (due  to  an  aneurysm,  a  tumor,  etc.),  chronic 
pleuritis,  etc.  A  local  fibrosis  is  common  in  association  with  healed 
foci  of  tuberculosis,  especially  at  the  apex,  gummas,  pleural  thickenings, 
gangrene,  tumors,  hydatid  cysts,  etc. 

Pathology. — ^The  lesion  may  be  localized  or  diffuse,  miilateral  or 
bilateral.  They  consist  of  proliferation  of  the  fibrous  connective  tissue, 
which  begins  in  the  interlobar  or  interlobular  septa  or  about  the  bron- 
chioles, depending  upon  the  variety  of  the  disease.  In  the  form  that 
follows  croupous  pneumonia  the  exudation,  instead  of  midergoing 
autolvsis,  becomes  organized;  fibroblasts  invade  it  and  ultimately  lead 
to  a  fibrillar  thickening  of  the  alveolar  walls  and  obliteration  of  many 
of  the  alveoli.  The  affected  portion  of  the  lung  is  contracted,  smooth, 
firm,  dense,  homogeneous,  semitranslucent,  grayish  white  in  color, 
and  almost  if  not  quite  airless.  Often  an  entire  lobe  is  involved,  in  which 
event  it  may  be  much  reduced  in  size  and  lie  against  the  spine  as  an 
irregular,  dense  mass.  In  the  form  that  follows  bronchopneumonia, 
the  fibrosis  begins  about  the  bronchi;  the  alveolar  walls  become  much 
thickened,  and  small  foci,  lobular  masses,  smooth,  firm,  grayish  in  color, 
are  found  scattered  throughout  a  lobe  or  an  entire  lung.  On  section 
these  areas  usually  reveal  a  central  bronchiole.  From  contraction  of 
the  newly  formed  fibrous  tissue  bronchiectasis  not  infrequently  results. 
The  pleurogenous  form  may  follow  prolonged  compression  of  a  lung 
by  a  pleural  exudate;  in  other  cases  bands  of  fibrous  connective  tissue 
extend  from  the  pleura  (sometimes  only  the  interlobar  pleura)  a  variable 
distance  into  the  lung,  and  by  cicatrization  lead  to  compression  and 
atrophy  of  the  lung  tissue,  and  to  bronchiectasis.     At  times  the  lung 


CHRONIC  INTERSTITIAL  PNEUMONITIS  553 

consists  virtually  of  a  series  of  bronchiectatic  cavities,  in  the  walls  of 
which  aneurysmal  dilatations  of  the  pulmonary  artery  are  not  uncommon. 
Bronchitis  (fibrous  peribronchitis)  is  a  part  of  the  general  process  of 
indurative  pneumonitis.  Tuberculosis  may  ensue.  The  uninvolved 
portion  of  the  lung,  or  the  opposite  lung,  is  commonly  the  seat  of  com- 
pensatory inflation.  The  heart  is  often  displaced,  retracted  toward  the 
diseased  side;  the  right  ventricle  is  usually  hypertrophied. 

Symptoms. — ^The  symptoms  are  often  merged  with  those  of  the  primary 
disorder — -croupous  pneumonia,  bronchopneumonia,  pleuritis,  etc.  The 
patient  does  not  fully  recover — slight  cough,  mucopurulent  expectoration, 
dyspnoea,  and  perhaps  a  little  fever  persist  for  some  time.  Gradually 
the  symptoms  become  only  those  of  chronic  bronchitis;  later,  usually 
those  of  bronchiectasis,  which  with  the  physical  signs  of  retraction  of 
the  chest  are  quite  characteristic  of  the  disease. 

Physical  Signs, — ^The  chest  is  depressed  over  the  affected  lung  or  part 
of  the  lung;  the  interspaces  are  obliterated;  the  ribs  may  overlap;  the 
shoulder  is  depressed;  the  nipple  and  the  scapula  are  nearer  the  median 
line;  scoliosis  even  may  develop.  The  inspiratory  expansion  of  the  chest 
is  restricted;  that  of  the  unaffected  lung  may  be  increased.  The  tactile 
and  the  vocal  fremitus  are  increased.  On  percussion  there  is  dulness 
or  a  vesiculotympanitic  sound  (bronchiectatic  cavity).  On  auscultation 
there  is  harsh  bronchovesicular  breathing,  or  the  breath  sounds  are 
feeble  (thickened  pleura,  etc.);  and  crackling,  sibilant,  sonorous,  and 
bubbling  rales  and  sometimes  pleural  frictions  may  be  heard.  Retrac- 
tion of  the  left  lung  by  uncovering  the  heart  causes  an  increase  in  the 
area  of  cardiac  dulness  (some  of  the  increase  is  due  to  hypertrophy  and 
dilatation  of  the  right  ventricle),  increased  visible  and  palpable  pulsa- 
tion of  the  heart  and  adjacent  vessels  (pulmonary  artery  and  the 
aorta),  palpable  closure  of  the  pulmonary  valve,  increase  of  the 
tympany  of  Traube's  semilunar  space;  etc.  Retraction  of  the  right 
lung  causes  displacement  of  the  heart  to  the  right,  elevation  of  the 
liver,  etc. 

Diagnosis. — Usually  for  some  time  the  diagnosis  is  that  of  the  primary 
disorder,  or  of  bronchitis.  With  the  development  of  retraction  of  the 
chest  the  diagnosis  becomes  quite  obvious.  Tuberculosis  should  be 
excluded. 

Prognosis. — Although  the  disease  is  incurable,  the  patient  may  live 
many  years  and  enjoy  tolerably  good  health.  Exacerbations  of  the 
bronchitis  are  not  uncommon.  Death  usually  results  from  progressive 
toxemia  (bronchiectasis),  failure  of  the  right  heart,  or  some  intercurrent 
infection  (bronchopneumonia,  etc.). 

Treatment. — The  treatment  is  that  of  chronic  bronchitis  and  bronchi- 
ectasis. A  nutritious  diet  and  the  best  hygienic  and  climatic  conditions 
are  of  prime  importance. 


554  DISEASES  OF  THE  LUNGS 

PNEUMOKONIOSIS. 

(Anthracosis;  Chalicosis;  Siderosis.) 

Etiology. — Pneumokoniosis  is  a  term  applied  to  the  fibroid  and  other 
changes  in  the  lungs  that  result  from  the  inhalation  of  various  kinds  of 
dust.  The  condition  is  essentially  an  occupation  disease,  and  is  seen 
especially  in  those  constantly  exposed  to  dust-laden  atmosphere.  Dif- 
ferent varieties  of  the  disease  are  distinguished,  depending  upon  the 
nature  of  the  dust  inhaled:  (1)  Anthracosis,  that  due  to  the  inhalation 
of  carbonaceous  pigment,  coal  dust,  soot,  charcoal,  etc.  (coal-miner's 
disease,  or  phthisis) ;  (2)  chalicosis,  that  due  to  the  inhalation  of  silicious 
dust,  such  as  sandstone,  quartz,  etc.  (stone-cutter's  phthisis,  millstone 
maker's  phthisis,  grinder's  and  potter's  rot  or  asthma);  (3)  siderosis, 
that  due  to  the  inhalation  of  mineral  dust,  especially  iron  oxide,  brass, 
bronze,  etc.;  (4)  that  due  to  the  inhalation  of  particles  of  wool,  flax, 
cotton,  etc. ;  and  (5)  that  due  to  the  inhalation  of  grain  dust,  cereals,  etc. 
(miller's  phthisis).  Associated  bacterial  infection  is  doubtless  of  some 
significance. 

Pathology. — Small  amounts  of  dust  being  inhaled  are  absorbed  by 
phagocytes  (leukocytes  and  other  cells),  which  then  are  carried  upward 
by  the  ciliated  epithelium  and  expectorated.  When  larger  amounts  are 
inhaled,  some  penetrates  to  the  mucosa  of  the  small  bronchi,  where  it  is 
attacked  (engulfed)  by  the  normal  scavengers  of  the  respiratory  tract, 
the  mucous,  and  the  alveolar  cells.  When  the  amount  of  the  dust  is 
excessive  some  of  it  reaches  the  alveoli,  and  some  of  it  penetrates  the 
mucosa  and  reaches  the  lymph  stream.  In  this  event  it  may  be  carried 
to  the  lymph  nodes  surrounding  the  bronchi  and  bloodvessels,  to  the 
interlobular  septa  beneath  the  pleura,  and  to  the  substernal,  bronchial, 
and  tracheal  lymph  nodes.  Rarely  the  dust  particles  gain  the  general 
circulation,  and  may  be  found  in  the  liver,  spleen,  kidney,  mesenteric 
and  retroperitoneal  lymph  nodes,  etc. — cases  in  which  the  pigmented 
bronchial  nodes  have  formed  an  intimate  connection  with  the  pulmonary 
veins  and  permit  the  passage  of  dust-laden  cells  into  the  veins.  In  the 
large  majority  of  cases  there  is  no  reaction  to  the  deposit  of  these  foreign 
bodies  in  the  lung,  and  the  lungs  show  no  noteworthy  deviation  from  the 
normal,  aside  from  variations  in  color  depending  upon  the  special  pig- 
ment deposited  (black,  coal  dust;  whitish  or  grayish,  stone  dust;  yellowish, 
reddish,  or  black,  iron  dust).  In  some  cases,  however,  reaction  does 
take  place:  this  consists  of  the  proliferation  of  fibrous  connective  tissue 
beginning  in  the  peribronchial  lymph  nodes,  to  which  it  may  remain 
localized — in  which  event  the  fibroid  nodules  appear  as  firm,  hard, 
circumscribed  masses,  varying  in  size  from  a  millet  seed  to  a  cherry, 
scattered  throughout  both  lungs,  and  on  section  revealing  in  the  centre  a 
bronchiole.  In  other  cases  the  process  is  more  diffuse,  and  involves 
almost,  if  not  quite,  an  entire  lobe.  In  these  cases  there  is  also  thick- 
ening of  the  alveolar  walls  and  of  the  interlobular  and  perivascular 


EMPHYSEMA  555 

tissue,  so  that  the  affected  portion  of  the  lung  is  contracted,  dense,  firm, 
and  ahnost  airless;  in  some  areas  the  bronchi  and  alveoli  may  be  com- 
pletely obliterated.  An  important  element  in  the  process  is  the  asso- 
ciated bronchitis  (which  causes  most  of  the  symptoms)  and  emphysema; 
bronchiectatic  cavities  are  common;  in  other  cases  necrosis  of  affected 
areas  takes  place  and  leads  to  the  formation  of  cavities  with  irregular 
and  roughened  walls,  traversed  by  fibrous  bands,  communicating  or 
not  with  a  bronchus,  and  containing  thick,  dark,  sometimes  blood- 
stained fluid.    Tuberculosis  is  a  common  sequel. 

Symptoms. — The  symptoms  are  those  of  chronic  bronchitis  and 
emphysema^cough,  dyspnoea  (especially  on  exertion),  and  expectora- 
tion, which,  however,  do  not  come  on  until  the  subject  has  worked  in 
the  dust  for  a  number  of  years.  The  expectoration  is  usually  profuse, 
mucopurulent,  and  blackish  in  anthracosis;  in  chalicosis  one  may  detect 
microscopically  angular  crystalloid  particles  of  silica;  and  in  siderosis, 
yellowish  or  reddish  particles  of  iron  oxide.  In  the  course  of  time  the 
general  health  begins  to  fail,  and  the  patient  may  become  much  emaciated. 

Physical  Signs. — ^The  physical  signs  are  those  of  chronic  bronchitis 
and  emphysema;  later,  those  of  chronic  induration  of  the  lung,  and  cavity 
formation. 

Diagnosis. — ^The  diagnosis  is  usually  easy,  if  the  patient's  occupation 
is  taken  into  account.  Cavities  should  not  be  misinterpreted  as  tubercu- 
lous necessarily;  tubercle  bacilli  may  be  absent  throughout  the  entire 
course  of  the  disease. 

Prognosis. — ^The  prognosis  as  regards  life  expectancy  is  rather  good. 
The  patient  may  survive  many  years.  Death  often  results  from  secondary 
tuberculous  or  other  infection  (bronchopneumonia,  etc.).  The  develop- 
ment of  bronchiectasis  and  excavation  renders  the  prognosis  unfavorable. 

Treatment. — ^The  treatment  is  that  of  chronic  bronchitis  and  emphy- 
sema. The  patient  should  give  up  his  occupation  if  possible;  if  this  be 
impossible,  he  should  spend  considerable  time  in  the  open  air. 


EMPHYSEMA. 

Emphysema  is  a  chronic  disease  of  the  lungs  characterized  by  perma- 
nent overdistention  of  the  air  vesicles  and  atrophy  of  the  vesicular 
walls. 

Etiology. — ^True  (large-lunged,  pseudohypertrophic)  emphysema  is 
peculiarly  a  disease  of  adult  life,  although  well-marked  examples  are 
occasionally  seen  in  children.  It  is  most  common  in  the  male  sex.  In 
some  cases  it  seems  to  be  predisposed  to  by  heredity  (hereditary  weak- 
ness of  the  pulmonary  elastica  and  consequent  deficiency  of  contractile 
power).  It  is  especially  common  in  those  whose  occupation  requires 
prolonged  increase  of  intrapulmonary  pressure  with  a  closed  glottis 
and  muscular  effort,  such  as  players  on  cornets  and  other  wind  instru- 
ments, glassblowers,  and  those  that  lift  or  move  heavy  bodies  (pianos, 


556  DISEASES  OF  THE  LUNGS 

etc.).  Advancing  age  is  a  predisposing  factor,  but  this  usually  results 
in  so-called  senile  (small  lunged)  emphysema.  The  disease  is  especially 
common  as  a  secondary  process  in  diseases  attended  with  violent  cough- 
ing spells  and  difficulty  in  expiration,  such  as  pertussis,  chronic  bronchitis, 
asthma,  etc.  In  these  there  is  always  obstruction  to  the  exit  of  air 
through  the  bronchioles  and  consequent  increased  intra-alveolar  pres- 
sure, which  becomes  markedly  augmented  during  the  violent  expirating 
efforts  of  coughing. 

Pathology. — Both  lungs  are  obviously  enlarged,  filling  an  enlarged 
thorax,  depressing  the  diaphragm,  and  overlapping  the  heart;  they  are 
pale  and  anemic  (aside  from  the  common  anthracosis),  and  characteris- 
tically light  and  downy  to  the  touch;  that  is,  despite  the  obvious  increase 
in  size,  there  is  a  lack  of  pulmonary  tissue.  Larger  or  smaller  bullae 
(coalescence  of  several  alveoli)  may  be  seen  at  different  parts  of  the 
lungs,  but  especially  at  the  free  margins,  anteriorly  and  basally  (which 
become  rounded),  and  the  apices  (less  well  supported  than  elsewhere), 
and  that  portion  in  the  vertebral  fossse.  The  conspicuous  lesions  con- 
sist of  dilatation  of  the  alveoli  and  infundibula;  atrophy  of  the  inter- 
alveolar  walls,  including  the  elastica;  consecutive  thrombosis  and  oblit- 
eration of  the  interalveolar  capillaries  and  also  the  lymphatics;  fatty 
and  other  degenerative  processes  of  the  epithelial  lining  of  the  alveoli; 
and  the  eventual  establishment  of  abnormal  communications  between 
adjacent  dilated  alveoli.  The  bronchi  and  bronchioles  show  the  common 
lesions  of  chronic  inflammation — being  thickened,  indurated,  dilated, 
and  distorted.  There  is  more  or  less  thickening  and  sclerosis  of  the 
pulmonary  artery,  which  together  with  restriction  of  the  arterial  tree 
from  capillary  thrombosis,  leads  to  hypertrophy  of  the  right  ventricle; 
the  increased  tension  in  the  pulmonary  artery  is  somewhat  relieved 
by  normal  communications  between  the  pulmonary  artery  and  the 
pulmonary  and  bronchial  veins — but  this  leads  to  increased  cyanosis, 
since  the  blood  thus  diverted  does  not  become  well  aerated. 

There  is  still  doubt  regarding  the  real  nature  of  the  process.  Although 
some  observers  still  hold  that  it  results  from  inspiratory  distention  or  from 
primary  degenerative  changes  of  the  alveolar  walls,  the  prevailing  view  is 
that  it  is  due  to  expiratory  difficulties  and  consequent  increase  in  intra- 
alveolar  pressure — which  becomes  especially  significant  etiologically  when 
acting  upon  lungs  reduced  in  resisting  power  by  hereditary  influences, 
chronic  inflammation  (bronchitis),  senility,  etc.  At  the  time  of  greatest 
intra-alveolar  pressure  (at  the  acme  of  coughing,  straining,  etc.)  the 
lungs  are  inflated  to  the  maximum,  the  glottis  is  closed,  and  the  thorax 
fixed,  so  that  air  is  forced  into  parts  of  the  lungs  normally  slightly 
expanded,  that  is,  the  apices  and  the  anterior  margins,  which  being  also 
ill  supported,  feel  the  strain  most  and  reveal  the  most  marked  lesions. 
In  consequence  of  repeated  insults,  the  pulmonary  tissue  gradually  loses 
its  elasticity,  and  the  lungs  gradually  become  permanently  almost,  if  not 
quite,  maximally  distended ;  and  the  chest,  permanently  in  the  condition 
of  inspiratory  expansion,  assumes  the  characteristic  barrel-shape.     Some 


EMPHYSEMA  557 

observers  have  postulated  primary  ossifying  changes  in  the  costal  car- 
tilages. 

Symptoms. — The  significant  symptoms  of  emphysema  are  progres- 
sive dyspnoea  and  cyanosis.  At  first  these  are  noticeable  only  on  severe 
exertion,  but  as  the  disease  advances  they  develop  on  the  slightest  exer- 
tion and  then  become  permanent.  The  dyspnoea  is  chiefly  expiratory, 
and  is  increased  by  mental  excitement  and  bodily  exertion.  The  respi- 
rations are  increased  in  frequency  (20  to  30),  and  ultimately  orthopnoea 
supervenes.  Cyanosis  is  an  early  and  prominent  symptom,  apparent 
first  in  the  lips,  nose,  ears,  and  extremities,  but  becoming  more  marked 
as  the  disease  advances ;  it  is  often  of  a  strikingly  high  grade,  without 
notable  discomfort  to  the  patient.  It  is  due  in  part  to  the  disease  of  the 
lungs,  in  part  also  to  failing  cardiac  compensation  (dilatation  ensuing 
upon  the  hypertrophy  due  to  the  pulmonary  disease).  Usually  there 
is  a  co-existing  bronchitis,  which  becomes  aggravated  in  the  winter, 
and  occasions  cough  and  mucopurulent  expectoration;  asthmatic 
attacks  are  common.  So  long  as  the  hypertrophy  of  the  right  ventricle 
continues  efficient  the  patient  is  tolerably  comfortable;  but  eventually 
dilatation  and  failure  of  compensation  ensue,  whereupon  increased 
dyspnoea  and  cyanosis,  pulmonary  oedema,  and  signs  of  general  venous 
engorgement  are  likely  to  supervene. 

Physical  Signs. — ^The  aspect  of  the  patient  is  often  quite  character- 
istic: if  the  disease  is  at  all  advanced  he  is  markedly  cyanotic  and  more 
or  less  dyspnoeic,  his  eyeballs  bulge,  his  head  is  thrown  back  and  the 
chest  forward,  and  the  accessory  muscles  of  respiration  are  active. 
The  chest  is  characteristically  barrel-shaped — shortened  and  increased 
anteroposteriorly;  the  neck  is  short  and  thick;  the  supraclavicular  fossae 
may  bulge;  the  sternum  is  prominent,  the  costal  angle  increased;  the 
shoulders  are  raised  and  rounded,  the  ribs  almost  horizontal,  and  the 
intercostal  spaces  widened  and  depressed.  The  movements  of  the 
chest  are  vertical  rather  than  expansile;  the  inspiratory  movements 
are  shortened,  the  expiratory  prolonged;  respiration  is  carried  on  largely 
by  the  diaphragm  and  the  abdominal  muscles,  although  the  excursions 
of  the  diaphragm  are  restricted  (obvious  by  the  use  of  the  a;-rays  and 
in  the  limitation  or  absence  of  Litten's  diaphragm  sign).  A  line  of 
distended  capillaries  and  venules  around  the  chest  often  marks  the 
attachment  of  the  diaphragm.  The  percussion  note  is  hyperresonant 
or  vesiculotympanitic;  in  some  places  dull  (imperfect  resonance  of  the 
thorax  due  to  tension  or  ossifying  costal  cartilages).  The  increased 
volume  of  the  lungs  is  revealed  in  percussion  resonance  to  the  seventh 
rib  or  below  in  the  mamillary  line  and  to  the  first  or  second  lumbar 
spine  posteriorly,  by  reduction  in  size  and  eventual  obliteration  of  the 
superficial  cardiac  dulness,  encroachment  of  resonance  on  the  hepatic 
and  splenic  dulness,  pulmonary  resonance  in  Traube's  semilunar  space, 
and  little  or  no  respiratory  movement  of  the  lower  limits  of  j)ulm()nary 
resonance  (in  Gerliardt's  space  and  at  the  cardiopulmonary  borders). 
The  breath  sounds  are  weakened,  sometimes  almost  inaudible,  an(l 


558  DISEASES  OF  THE  LUNGS 

the  expiration  is  much  prolonged  in  uncomphcated  emphysema;  with 
comphcating  bronchitis,  the  breath  sounds  are  usually  harsh  and  broncho- 
vesicular  in  character,  and  rales  may  be  heard.  Adventitious  sounds 
may  also  be  due  to  shifting  of  air  in  emphysematous  bullae,  pulmonary 
oedema,  muscular  contractions,  etc.  The  cardiac  apex  is  usually  not 
to  be  seen  or  felt;  a  common  palpable  pulsation  in  the  epigastrium 
results  from  downward  displacement  of  the  heart  and  hypertrophy 
of  the  right  ventricle.  The  heart  sounds  are  weak  and  indistinct,  and 
there  may  be  a  systolic  murmur  (cardiopulmonary;  relative  tricuspid 
or  mitral  insufficiency). 

Diagnosis. — ^The  disease  is  readily  recognized  from  the  history  and 
the  physical  signs,  although  minor  grades  are  often  overlooked  or  mis- 
interpreted. The  cyanosis,  dyspnoea,  and  a  possible  systolic  murmur 
should  not  be  mistaken  for  primary  cardiac  disease;  the  other  physical 
signs  are  unequivocal.  Pneumothorax  is  sometimes  confused,  on 
account  of  the  clear  vesiculotympanitic  percussion  rate. 

Senile  Emphysema — In  contradistinction  to  the  so-called  large 
lunged  emphysema,  a  small  lunged  (atrophic  or  senile)  emphysema 
is  often  encountered  in  elderly  people.  This  is  a  primary  atrophy  of 
the  pulmonary  tissues,  part  of  the  general  atrophy  of  senility.  It  is 
attended  by  some  dyspnoea,  but  not  much  cyanosis ;  there  may  or  may  not 
be  cough,  but  if  present  it  is  not  marked.  The  chest  is  small  and  flat; 
the  normal  obliquity  of  the  ribs  is  perhaps  accentuated;  the  muscula- 
ture is  atrophic;  the  normal  type  of  breathing  is  maintained;  the  percus- 
sion note  is  hyperresonant,  and  the  breath  sounds  are  weak,  unless 
there  be  associated  bronchitis. 

Compensatory  Inflation  (Vicarious  Emphysema).^ — In  local 
disease  of  the  lungs,  such  as  pneumonia,  bronchopneumonia,  more  or 
less  quiescent  tuberculosis,  chronic  fibrosis,  pleural  adhesions,  pleural 
effusion,  parts  of  the  lung  adjacent  to  the  diseased  foci,  or  a  lobe,  or 
the  opposite  lung,  takes  on  a  compensatory  process,  becomes  distended — 
so-called  compensatory  emphysema  (preferably  inflation  or  distention). 
This  is  at  first  a  purely  physiological  process — enlargement  of  the 
alveoli,  but  no  atrophy  of  the  walls ;  it  is  believed  to  be  inspiratory  rather 
than  expiratory  in  development;  it  may  be  temporary,  and,  as  in  pneu- 
monia or  pleural  effusion,  subside  with  the  subsidence  of  the  primary 
disorder,  but  if  long  continued,  true  emphysema  may  ensue. 

Acute  Vesicular  Emphysema. — ^Acute  vesicular  emphysema  (or  dis- 
tention) sometimes  ensues  when  violent  inspiratory  efforts  have  been 
made  in  conditions  of  bronchial  obstruction,  especially  in  bronchitis  of 
the  fine  tubes,  asthma,  pertussis,  aortic  aneurysm,  etc.  The  percussion 
note  is  hyperresonant  and  more  widely  distributed  than  normally,  the 
expiration  is  prolonged,  and  there  are  many  sonorous  and  sibilant 
rales.  It  is  readily  distinguished  by  its  usually  acute  onset,  associated 
phenomena,  and  common  subsidence. 

Interstitial  Emphysema. — Interstitial  (interalveolar,  interlobular, 
or  subpleural)  emphysema  is  a  condition  characterized  by  the  presence 


ABSCESS  OF  THE  LUNG  559 

of  air  in  the  interstices  of  the  lung,  where  it  forms  larger  or  smaller 
bullae.  It  may  be  due  to  trauma  (fracture  of  the  ribs,  punctured 
wounds  of  the  chest,  tracheotomy,  etc.);  rupture  of  the  air  vesicles 
from  overdistention  (severe  paroxysmal  coughing,  straining  of  parturi- 
tion or  defecation,  etc.);  it  may  follow  pneumothorax,  subcutaneous 
emphysema  of  the  neck,  ulceration  of  the  air  passages  and  pulmonary 
tissue,  etc.  The  air  enters  the  pulmonary  tissue  by  means  of  a  tear  in 
the  alveoli  or  bronchi.  In  mild  cases  symptoms  may  be  in  abeyance; 
in  severe  cases  there  may  be  very  urgent  dyspnoea  and  cyanosis,  usually 
of  sudden  onset  (diagnostic  importance  of  the  etiological  factors).  Ex- 
amination may  reveal  intrathoracic  creaking  and  crepitation  (perhaps 
synchronous  with  the  action  of  the  heart),  obscuration  of  the  heart 
dulness  and  sounds  and  of  the  breath  sounds,  and  sometimes  large 
areas  of  tympany,  etc. 

Prognosis. — True  emphysema  is  a  disease  of  long  duration,  upward 
of  twenty  years  in  many  cases.  Complete  recovery  is  scarcely  to  be  hoped 
for,  but  the  patient  may  be  much  benefited,  his  condition  made  bearable, 
and  his  life  prolonged.  Death  usually  results  from  cardiac  failure  or 
secondary  infections,  such  as  pneumonia,  bronchopneumonia,  tuber- 
culosis, hemoptysis,  etc. 

Treatment. — The  treatment  virtually  is  that  of  chronic  bronchitis. 
Efforts  should  be  made  to  improve  the  patient's  general  health;  he 
should  lead  a  hygienic  life,  avoid  the  causative  factors  (blowing  wind 
instruments,  etc.)  if  these  be  detectable,  and  avoid  also  lifting  heavy 
weights  and  other  severe  exertion,  as  well  as  cold  and  the  taking  of  cold. 
Life  in  a  warm,  equable  climate  is  of  the  greatest  service.  In  the  absence 
of  this,  respiratory  exercises,  which  increase  the  force  of  expiration, 
systematic  rhythmic  compression  of  the  thorax,  compressed  air  baths, 
and  the  breathing  of  rarefied  air  are  valuable.  Many  patients  are 
remarkably  improved  by  the  iodides,  in  addition  to  the  remedies  men- 
tioned for  chronic  bronchitis.  In  other  cases  alleviation  of  the  cardiac 
inadequacy  is  followed  by  much  benefit;  as  a  matter  of  fact  in  moderately 
or  well-advanced  cases  the  cardiac  factor  in  the  symptomatology  is 
often  overlooked;  small  doses  of  strophanthus  or  digitalis,  and  other 
measures  recommended  in  failing  cardiac  compensation,  often  lead  to 
material  relief.  In  the  event  of  unusual  cyanosis  and  dyspnoea  vene- 
section is  called  for.  Attention  should  be  paid  to  the  diet  to  obviate 
gastro-intestinal  derangements  and  to  correct  them  if  they  develop. 
General  tonics,  such  as  iron,  strychnine,  etc.,  are  useful  from  time  to 
time. 


ABSCESS  OF  THE  LUNG. 

Etiology. — Abscess  of  the  lung  most  frequently  follows  croupous 
pneumonia,  aspiration  pneumonia,  and  infectious  embolism.  Less  com- 
monly it  follows  ordinary  bronchopneumonia,  and  other  diseases  of  the 


560  DISEASES  OF  THE  LUNGS 

lung,  such  as  tuberculosis,  fetid  bronchitis,  bronchiectasis,  glanders, 
actinomycosis,  etc.  Occasionally  it  results  from  extension  of  suppura- 
tion from  adjacent  tissues  and  organs,  such  as  empyema,  mediastinal 
abscess,  suppurating  bronchial  lymph  nodes,  vertebral  abscess,  sub- 
diaphragmatic abscess,  hepatic  abscess,  etc.  Traumas,  perforating 
wounds  of  the  lung,  etc.,  also  are  likely  to  lead  to  abscess.  The  dis- 
ease is  much  more  common  in  debilitated  than  in  healthy  subjects; 
diminution  of  general  bodily  resistance  seems  to  be  of  considerable 
etiological  importance.  Staphylococci,  streptococci,  pneumococci,  pneu- 
mobacilli,  influenza  bacilli,  typhoid  bacilli,  colon  bacilli,  leptothrix,  etc., 
are  the  bacteria  commonly  encountered  in  the  abscess. 

Pathology. — There  may  be  a  single  abscess  (following  croupous 
pneumonia),  or  there  may  be  many  abscesses  (following  infectious 
embolism).  The  single  large  abscess  may  involve  an  entire  lobe,  or 
an  entire  lung.  When  multiple,  the  abscesses  are  usually  small,  varying 
in  size  from  that  of  a  pea  to  that  of  a  walnut,  wedge-shaped,  and  super- 
ficial; the  cavity  is  irregular,  its  walls  ragged,  its  contents  purulent,  and  it 
may  contain  considerable  necrotic  lung  tissue.  The  large  single  abscesses 
present  similar  appearances  on  a  more  extensive  scale.  When  the  abscess 
reaches  to  the  periphery  the  superjacent  pleura  is  commonly  covered 
with  a  fibrinous  exudation.  Perforation  of  the  abscess  into  a  bronchus 
and  the  discharge  of  its  contents  externally  is  not  uncommon.  Per- 
foration may  also  occur  into  the  pleura  (causing  empyema  or  pyopneu- 
mothorax), or  into  the  pericardium,  etc.  When  old,  the  walls  of  the 
abscess  cavity  may  be  very  thick,  and  bands  of  cicatrizing  connective 
tissue  may  extend  varying  distances  into  the  lung. 

Sjmiptoms. — ^The  symptoms  are  often  for  some  time  obscured  by  those 
of  the  primary  disorder — pneumonia,  sepsis,  etc.  The  small  multiple 
abscess  may  remain  altogether  undetected.  The  larger  abscesses, 
those  following  pneumonia,  for  instance,  are  often  suggested  by  the  non- 
occurrence of  the  crisis  and  an  aggravation  of  the  general  symptoms, 
septic  temperature,  chills,  sweats,  leukocytosis,  etc.  But  the  diagnosis 
may  not  be  certain  until  the  appearance  of  the  characteristic  sputum — 
purulent,  yellowish,  greenish,  or  brownish  (from  admixture  of  blood), 
malodorous  (though  never  as  fetid  as  in  gangrene  or  fetid  bronchitis, 
and  occasionally  having  little  or  no  odor),  and  containing  fragments  of 
necrotic  lung  tissue,  elastic  fibers,  fatty  acids,  hematoidin  crystals,  bac- 
teria, etc.  Sometimes  a  large  amount  of  purulent  sputum  is  expectorated 
at  one  time,  whereupon  the  physical  signs  of  cavity  formation  may 
become  apparent — in  which  event  the  diagnosis  is  no  longer  in  doubt. 
Often  large  amounts  of  sputum  are  raised  early  in  the  morning,  or  at 
other  times  upon  the  assumption  of  some  particular  posture  (which 
favors  drainage). 

Diagnosis. — ^The  diagnosis,  as  a  rule,  is  easy  when  the  symptoms  and 
signs  are  fully  developed — the  history,  the  fever  and  other  signs  of  sepsis, 
the  leukocytosis,  the  characteristic  sputum,  and  the  physical  signs  of 
cavity  formation, 


GANGRENE  OF   THE  LUNG  561 

Prognosis. — The  prognosis  is  always  grave.  Recovery  sometimes 
takes  place  when  the  abscess  has  followed  pneumonia  or  empyema. 
Multiple  abscesses  are  generally  part  of  a  pyemic  process  that  leads 
to  dea'h. 

Treatment. — As  a  rule,  medicinal  treatment  is  of  minor  importance, 
and  consists  of  attention  to  the  general  health  of  the  patient,  the  ad- 
ministration of  stimulants,  such  as  iron,  quinine,  strychnine,  whiskey, 
etc.,  and  the  use  of  nutritious  food.  Hope  of  success  lies  in  surgical 
measures  which  should  be  undertaken  as  soon  as  the  abscess  can  be 
definitely  localized. 


GANGRENE  OF  THE  LUNG. 

Etiology. — Gangrene,  the  putrefaction  of  necrotic  lung  tissue,  occurs 
under  a  variety  of  circumstances.  An  essential  factor  appears  to  be 
reduction  in  the  general  bodily  resistance,  whence  it  is  found  especially 
in  debilitated  subjects,  alcoholics,  diabetics,  syphilitics,  after  severe  infec- 
tious diseases  (typhoid  and  typhus  fevers,  smallpox,  scarlatina,  etc.),  in 
the  subjects  of  severe  mercurial  and  lead  poisoning,  etc.  It  follows  a 
variety  of  local  disorders  in  the  lung,  of  which  the  most  important  are 
the  different  forms  of  pneumonia,  especially,  however,  aspiration  pneu- 
monia following  the  entrance  of  foreign  bodies  in  a  bronchus.  The 
secretion  in  putrid  bronchitis,  the  contents  of  a  tuberculous  or  bron- 
chiectatic  cavity,  or  of  a  lung  abscess  or  a  necrotic  echinococcus  cyst, 
etc.,  may  induce  gangrene  in  adjacent  parts  of  the  lung.  A  similar 
result  may  follow  rupture  into  a  bronchus  or  the  lung  of  an  empyema, 
a  carcinoma  of  the  oesophagus  or  the  stomach,  a  gastric  ulcer  and 
subdiaphragmatic  abscess,  or  a  vertebral  abscess.  Infectious  embolism 
or  infection  of  a  benign  embolus,  pressure  of  an  aneurysm  of  the  aorta, 
perforating  wounds  of  the  lungs  and  other  traumas,  etc.,  also  may  lead 
to  gangrene  of  the  lung.  Staphylococci,  streptococci,  colon  bacilli, 
Bacillus  pyocyaneus,  Micrococcus  tetragenus,  and  the  leptothrix  are  the 
organisms  most  commonly  found  in  lung  gangrene. 

Pathology. — Two  forms  of  gangrene  may  be  distinguished:  (1)  The 
circumscribed,  and  (2)  the  diffuse.  The  circumscribed  form  is  more 
common  in  the  lower  lobes,  and  in  the  right  lung;  but  it  may  be  bilateral; 
the  diffuse  form  is  most  common  in  the  right  upper  lobe.  The  diffuse 
form  is  very  rare,  and  occurs  usually  after  lobar  pneumonia,  bronchitis, 
or  embolic  obstruction  of  a  large  branch  of  the  pulmonary  artery.  The 
gangrenous  area,  which  may  involve  an  entire  lobe,  may  be  indistinctly 
outlined,  firm,  and  greenish  black  in  color;  more  commonly  it  is  soft, 
pulpy,  and  extremely  fetid;  with  the  progress  of  the  process  large  cavities 
are  formed,  traversing  which  the  remains  of  bronchi  and  bloodvessels 
may  be  seen.  The  surrounding  lung  tissue  exhibits  the  changes  of  well- 
marked  inflammation.  The  circumscribed  form  occurs  most  commonly 
after  multiple  infarction  or  aspiration  pneumonia.  The  foci  of  gangrene 
36 


562  DISEASES  OF  THE  LUNGS 

are  multiple  and  reach  often  to  the  pleural  surface  of  the  lung;  they 
are  usually  rather  sharply  circumscribed,  irregular  in  shape,  greenish 
black  in  color,  and  extremely  malodorous;  as  the  process  advances, 
irregularly  shaped  cavities  with  shreddy  walls  are  formed.  Should 
these  cavities  communicate  with  a  bronchus,  as  occasionally  happens, 
their  contents  may  be  expectorated.  The  foci  of  gangrene  are  surrounded 
by  areas  of  inflammation;  later  they  may  become  sequestrated  and 
encapsulated,  and  healing  may  ensue.  Occasionally,  rupture  into  the 
pleura  occurs,  with  the  development  of  pyopneumothorax.  Metastatic 
emboli,  especially  to  the  brain,  are  not  uncommon. 

Symptoms. — ^The  characteristic  symptoms  consist  of  fetid  expectora- 
tion and  fetor  of  the  breath ;  but  these  do  not  develop  until  the  putrefying 
lung  tissue  communicates  with  a  bronchus.  The  symptoms,  therefore, 
for  some  time  are  those  of  the  primary  disease.  The  gangrene  may  be 
inaugurated  by  chills,  high  fever,  and  marked  prostration.  Soon,  how- 
ever, fetor  of  the  breath  is  observed,  especially  after  coughing,  and  the 
sputum  becomes  characteristically  fetid,  and  abundant,  and  when 
allowed  to  stand  separates  into  three  layers — an  uppermost  discolored, 
frothy  layer;  a  middle  clear,  greenish  or  brownish,  serous  or  mucous 
layer;  and  a  lowermost  layer  (sediment),  consisting  of  necrotic  lung 
tissue,  pus,  fibrin,  elastic  tissue,  fatty  acids,  tyrosin,  bacteria,  etc.  Occa- 
sionally there  is  also  blood.  As  a  rule,  the  patient  becomes  markedly 
prostrated,  emaciated,  and  septic,  and  soon  dies  of  exhaustion  or  a  severe 
hemorrhage. 

Physical  Signs. — The  physical  signs  are  often  obscured  by  those  of  the 
primary  disease.  Distinctive  signs  consist  of  evidences  of  solidification 
(circumscribed  foci  or  a  large  area)  followed  by  those  of  excavation. 

Diagnosis. — The  diagnosis  virtually  rests  upon  the  fetor  of  the  breath 
and  of  the  expectoration — which  can  scarcely  be  mistaken.  Abscess 
of  the  lung  may  be  excluded  by  an  examination  of  the  sputum.  Fetid 
bronchitis  may  be  distinguished  by  its  slower  course,  less  fetor,  and 
absence  of  lung  tissue  in  the  sputum. 

Prognosis. — The  prognosis  is  grave.  Death  usually  ensues,  but  re- 
covery may  take  place — less  likely  in  the  diffuse  than  in  the  circum- 
scribed form. 

Treatment. — ^Treatment  is  usually  limited  to  supporting  the  patient  by 
good  nutritious  food  and  the  use  of  stimulants — iron,  quinine,  whiskey, 
strychnine,  etc.  Efforts  should  be  made  to  lessen  the  fetor  by  sprays 
of  carbolic  acid,  or  by  inhalation,  of  creosote,  carbolic  acid,  guaiacol,  etc. 
If  the  gangrenous  area  can  be  accurately  localized,  recourse  may  be 
had  to  surgical  intervention  with  a  view  to  drainage,  and  with  hope  of 
good  result. 

TUMORS   OF  THE  LUNG. 

Etiology. — Tumors  of  the  lung  may  be  primary  (rare)  or  secondary 
(more  common).     Their  etiology  is  that  of  tumors  in  general.     Of  the 


TUMORS  OF  THE  LUNG  563 

primary  tumors,  carcinomas  developing  from  the  bronchial  mucosa 
(cylindrical  epithelioma)  or  from  the  alveolar  epithelium  (scjuamous, 
medullary,  or  scirrhus  carcinoma)  are  the  most  common;  sarcoma 
(lymphosarcoma,  round-cell,  spindle-cell)  and  endothelioma,  develop- 
ing from  the  bronchial  lymph  nodes  or  the  interstitial  tissue  of  the 
lung,  are  less  common;  still  rarer  are  fibromas,  chondromas,  osteomas, 
lipomas,  lymphomas  (of  Hodgkin's  disease),  etc.  Secondary  tumors 
comprise  carcinoma,  sarcoma,  endothelioma,  and  hypernephroma.  The 
primary  growths  occur  with  greatest  frequency  in  the  breast,  the  diges- 
tive tract,  the  genito-urinary  tract,  and  the  bones.  Metastasis  to  the 
lungs  occurs  usually  by  way  of  the  bloodvessels,  unless  the  primary 
growth  is  situated  near  the  root  of  the  lung,  in  the  oesophagus,  for 
instance,  when  metastasis  may  occur  by  way  of  the  lymphatics. 

Pathology. — Primary  tumors  generally  involve  one  lung  (the  right), 
and  the  upper  lobe  more  frequently  than  the  lower;  but  they  may  involve 
both  lungs.  They  may  occur  as  small,  firm,  sharply  circumscribed 
masses,  or  as  large  infiltrating  masses.  Primary  carcinoma  is  usually 
a  large,  firm,  whitish  or  grayish  mass,  often  sharply  circumscribed; 
sometimes  a  diffuse  infiltrating  mass;  sometimes  a  series  of  small  nodules, 
distributed  from  the  hilum  along  the  bronchi  and  the  vessels  by  way 
of  the  lymphatics.  Often  these  nodules  reach  the  pleura,  where  they 
form  flat  irregular  masses;  marked  thickening  of  the  pleura  may  occur. 
Carcinoma  shows  a  tendency  to  soften  and  to  give  metastasis  (80  to  90 
per  cent,  of  the  cases)  to  the  adjacent  lymph  nodes,  mediastinum,  liver, 
brain,  bones,  etc.  Secondary  carcinoma  occurs  as  small  miliary  or 
larger  whitish  or  grayish  nodules  (resembling  tubercles)  scattered 
throughout  both  lungs.  Rarely  they  involve  only  the  pleura.  Sarcoma 
presents  much  similar  appearances.  With  the  tumor  of  the  lung  there  is 
often  associated  bronchitis,  bronchiectasis  (with  hemorrhagic  transudate), 
etc. 

Symptoms. — The  primary  growth  may  cause  no  distinctive  symptoms 
until  it  is  far  advanced.  ^^Tien  there  is  extensive  involvement  of  the 
lung  there  is  usually  substernal  oppression,  cough,  dyspnoea,  some- 
times fever  and  sweats,  and  later  emaciation.  In  addition  there  are 
many  symptoms  referable  to  irritation  and  pressure  by  the  growth — 
cough  (bronchitis  or  pressure  on  the  bronchus);  pain  (involvement  of 
the  pleura);  dyspnoea  (pressure  on  the  trachea);  changes  in  the  voice 
(pressure  on  the  recurrent  laryngeal  nerve);  slow  pulse  or  rapid  pulse 
(pressure  on  the  pneumogastric  nerve);  cyanosis  and  oedema  of  the  face 
or  an  arm  (pressure  on  the  vems);  etc.  The  sputum  is  often  quite  char- 
acteristic, resembling  red-currant  jelly  or  prune  juice;  it  may  contain 
shreds  of  the  pulmonary  growth.  Ultimately  the  patient  becomes 
anemic  and  cachectic  and  dies  of  exhaustion.  Secondary  growths  in 
the  lungs  are  suggested  by  the  development,  in  one  who  has  or  has  had 
a  primary  tumor,  of  cough,  dyspnoea,  cyanosis,  and  blood-stained 
sputum;  but  since  the  primary  growth  is  not  always  apparent,  the  diag- 
nosis may  be  for  a  long  time  in  abeyance. 


564  DISEASES  OF  THE  PLEURA 

Physical  Signs. — The  physical  signs  depend  upon  the  size  and  seat 
of  the  tumor.  At  times  there  are  only  the  signs  of  bronchitis;  again, 
only  moderate  impairment  of  the  percussion  resonance.  AVhen  the 
growth  is  extensive  there  may  be  fixation  of  the  affected  side  (with 
compensatory  activity  of  the  other  side),  prominence  of  the  affected 
side  or  distinct  bulging,  and  widening  of  the  interspaces.  The  percussion 
note  may  be  normal  when  the  foci  are  small  and  scattered;  when  there 
is  a  large  localized  mass  there  is  dulness,  which  usually  is  very  irregular 
in  outline.  Fremitus  and  the  breath  sounds  may  be  diminished  (blockage 
of  the  bronchi),  or  increased,  that  is  bronchial  breathing  (unobstructed 
bronchi).  The  adjacent  viscera  (heart,  liver,  spleen,  etc)  may  be  dis- 
placed. The  signs  of  pleural  effusion  may  develop.  The  supraclavicular 
or  the  axillary  lymph  nodes  may  become  enlarged  (sometimes  the  first 
trustworthy  clue  to  the  correct  diagnosis). 

Diagnosis. — The  diagnosis  is  often  difficult,  especially  in  the  primary 
cases.  In  the  secondary  cases,  attention  to  the  history  of  the  patient  and 
a  study  of  the  symptomatology  and  physical  signs  often  suffice  for  a 
correct  diagnosis.  Care  should  be  taken  to  exclude  bronchitis,  chronic 
interstitial  pneumonia,  tuberculosis,  pleurisy  with  effusion,  etc. 

Prognosis. — The  prognosis  is  hopeless.  Death  usually  ensues  within 
a  year  or  eighteen  months. 

Treatment. — The  treatment  consists  in  humanitarian  efforts  to  pro- 
mote the  comfort  of  the  patient  and  relieve  his  distressing  symptoms. 


DISEASES  OF  THE  PLEURA. 
PLEURITIS. 

(Pleurisy.) 

Pleuritis  may  be  variously  classified;  it  may  be  primary  (rarely) 
or  secondary  (usually);  acute  or  chronic  in  onset  and  course;  circum- 
scribed or  diffuse;  fibrinous,  serofibrinous,  purulent,  or  hemorrhagic  as 
regards  the  character  of  the  exudate;  and  tuberculous,  streptococcic, 
staphylococcic,  pneumococcic,  etc.,  as  regards  the  specific  etiological 
factor.  Inasmuch  as  an  etiological  classification  is  scarcely  feasible  at 
the  bedside,  the  following  clinical  classification  will  be  found  serviceable: 
acute  and  chronic  pleuritis;  of  the  acute,  the  following  forms:  fibrinous, 
serofibrinous,  purulent,  and  hemorrhagic;  and  of  the  chronic  forms :  serous 
and  adhesive. 


FIBRINOUS   PLEURITIS. 

{Dri/,  Plastic,  or  Acute  Adhesive  Pleurisy.) 

Etiology. — Dry  or  fibrinous  pleuritis  seems  to  occur  sometimes  as  an 
independent,  or  primary,  disorder  following  exposure  to  cold  and  damp, 


FIBRINOUS  PLEURITIS  505 

especially  in  alcoholic  subjects;  in  most  cases,  however,  it  is  a  secontlary 
process.  It  is  most  common  in  frank  or  latent  pulmonary  tuberculosis, 
but  occurs  also  in  other  diseases  of  the  lungs,  such  as  bronchitis,  pneu- 
monia, bronchopneumonia,  pulmonary  abscess  and  gangrene,  etc.; 
in  infections  of  adjacent  organs,  such  as  pericarditis,  endocarflitis, 
mediastinitis,  disease,  including  traumatism,  of  the  bony  framework 
of  the  chest,  etc.;  in  distant  infections  (hemogenic  infections),  such  as 
of  the  abdominal  and  pelvic  organs,  tonsillitis,  etc.;  in  general  infec- 
tions, such  as  septicopyemia,  rheumatism,  typhoid  fever,  influenza,  etc.; 
and  it  is  a  common  occurrence  in  debilitated  and  asthenic  states  generally, 
such  as  advanced  cardiac  and  renal  disease,  etc.  The  specific  etiological 
factor  is  usually  the  tubercle  bacillus,  less  commonly  staphylococci, 
streptococci,  pneumococci,  etc. 

Pathology. — The  lesions  may  be  more  or  less  diffuse,  but  they  are 
usually  circumscribed,  especially  to  the  base  of  the  lungs  anteriorly  and 
laterally,  but  often  also  at  the  apex  (frequently  overlooked).  The 
inflamed  area  becomes  hyperemic,  swollen,  lustreless,  and  finally 
granular  in  appearance;  and  the  seat  of  a  more  or  less  abundant,  thick 
or  thin,  usually  slightly  adherent  fibrinous  exudation.  In  reality  the 
exudation  is  serofibrinous,  that  is,  there  is  always  some  fluid  exudation, 
but  this  is  often  minimal  (dry  pleurisy),  and  the  excess  of  fibrin  causes 
agglutination  of  the  opposed  pleural  surfaces.  Ultimately  the  exudation 
undergoes  organization  with  the  formation  of  permanent  adhesions  and 
pleural  thickening. 

Symptoms. — Symptoms  may  be  almost  if  not  entirely  in  abeyance, 
since  pleural  adhesions  constitute  a  very  common  necropsy  finding 
apparently  unassociated  with  notable  symptoms  during  life.  In  some 
cases,  however,  especially  following  exposure,  or  traumatism  of  the 
chest,  or  in  the  course  of  tuberculosis,  etc.,  there  is  a  sudden  pain  in  the 
side  (pleural  stitch),  perhaps  slight  cough  (which,  as  well  as  deep  inspi- 
ration, increases  the  pain),  and  slight  fever.  The  pain  may  occur  at  the 
site  of  inflammation,  or  laterally  or  anteriorly  where  the  movement  of 
the  lung  is  greatest,  or  it  may  be  referred  to  the  peripheral  distribution 
of  the  involved  intercostal  nerves  (anterior  aspect  of  the  lower  thorax  or 
the  upper  abdomen).  Physical  examination  discloses  restriction  of  the 
movements  of  the  chest  on  the  affected  side  and  the  pathognomonic 
friction  sound.  This  is  a  jerky  or  interrupted,  rubbing,  rasping,  creak- 
ing, or  new-leather  sound,  audible  most  commonly  during  inspiration, 
especially  at  the  end  of  inspiration,  but  sometimes  during  inspiration 
and  expiration  (to-and-fro  sound);  it  seems  to  be  near  the  auscultating 
ear,  superficial,  and  it  may  be  increased  in  intensity  by  j)ressure,  as  by 
the  stethoscope;  it  often  disappears  temporarily  after  the  patient  has 
taken  several  deep  inspirations  (smoothing  of  the  rough  aTid  irregular 
pleural  surface?);  and  it  is  not  always  audible  at  the  site  of  tlie  pain 
(but  rather  laterally).  Occasionally  the  frictions  may  be  pal])al)le.  The 
breath  sounds  are  usually  feeble,  from  restriction  of  the  movements  of 
the  cliest. 


566  DISEASES  OF  THE  PLEURA 

Diagnosis. — ^The  "stitch  in  the  side"  and  the  pleural  frictions  make 
the  diagnosis  unmistakable.  In  intercostal  neuralgia  there  are  points 
of  tenderness  along  the  course  of  the  intercostal  nerves,  and  an  absence 
of  fever  and  of  pleural  frictions.  In  pleurodynia  also  there  is  an  absence 
of  fever  and  of  pleural  frictions. 

Prognosis. — Inasmuch  as  dry  pleurisy  is  rarely  a  primary  disorder, 
the  prognosis  is  that  of  the  attendant  condition.  The  pleural  manifes- 
tations, as  a  rule,  subside  spontaneously;  but  it  is  important  to  bear  in 
mind  that  dry  pleurisy  may  be  merely  the  beginning  of  serofibrinous 
pleurisy. 

Treatment. — In  addition  to  attention  to  the  primary  disorder,  the 
treatment  should  consist  of  counterirritation  (iodine,  blisters,  or  a 
mixture  of  equal  parts  of  menthol,  camphor,  and  chloral),  opium  or 
morphine  if  the  pain  is  very  severe,  and  other  measures  to  be  mentioned 
presently  under  serofibrinous  pleuritis. 


SEROFIBRINOUS  PLEURITIS. 

(Pleurisy  with  Effusion.) 

Etiology. — There  is  no  sharp  line  of  demarcation  between  fibrinous 
and  serofibrinous  pleuritis;  they  represent  different  stages  of  the  one 
process — alike  etiologically  (bacteriologically)  and  pathologically.  Pleu- 
risy with  effusion,  however,  is  most  common  in  young  male  adults, 
apparently  previously  healthy;  it  is  often  believed  to  be  a  primary 
disorder,  developing  after  exposure,  an  alcoholic  debauch,  etc.  But 
these  act  likely  merely  as  predisposing  factors,  since  there  is  good 
evidence  that  at  least  75  per  cent,  of  so-called  primary  or  cryptogenetic 
pleuritides  are  tuberculous  in  origin,  the  source  of  infection  usually 
being  calcified  or  fibroid  bronchial  lymph  nodes  (more  or  less  quiescent 
tuberculosis).     In  children  most  cases  of  pleuritis  follow  pneumonia. 

Pathology. — As  a  rule,  the  disease  is  unilateral,  slightly  more  common 
on  the  right  side  than  on  the  left.  In  the  early  stages  the  lesions  are 
identical  with  those  of  fibrinous  (dry)  pleurisy.  Soon,  or  in  some  cases 
from  the  beginning,  a  more  or  less  abundant  fluid  exudate  is  poured  out — 
thin,  serous,  alkaline,  yellowish,  albuminous  (3  to  7  per  cent.),  usually 
at  least  slightly  turbid,  and  often  containing  fibrinous  flocculi;  in  some 
cases  the  fluid  has  a  greenish  tint;  or  it  may  be  purulent  or  hemorrhagic 
(purulent  and  hemorrhagic  pleuritis).  The  fluid  varies  in  amount  up 
to  3  to  5  liters;  and  it  may  be  entirely  free,  or  more  or  less  encapsu- 
lated— in  a  single  or  a  multilocular  enclosure.  Special  localization  of  the 
lesions  warrants  the  terms  pericarditic  pleuritis,  mediastinal  pleuritis, 
diaphragmatic  pleuritis,  interlobar  pleuritis,  etc.  The  presence  of  a 
large  amount  of  fluid  leads  to  distention  of  the  affected  side  of  the  chest, 
and  to  compression  and  displacement  of  adjacent  organs — the  lungs, 
the  mediastinum,  the  heart,  the  diaphragm,  the  liver,  the  spleen,  etc. 
As  a  rule,  the  fluid  is  absorbed  spontaneously  or  it  is  removed  by  thora- 


SEROFIBRINOUS  PLEURITIS  567 

Centesis;  following  which  the  opposed  surfaces  of  the  pleurae  become 
adherent  and  ultimately,  through  organization,  permanently  united, 
leading  to  obliteration  of  the  pleural  sac.  The  new  fibrous  tissue 
contracts  and  gives  rise  to  more  or  less  distortion  of  the  affected  side 
of  the  chest,  retraction  of  the  ribs,  narrowing  of  the  intercostal  spaces, 
scoliosis  (convexity  toward  the  healthy  side),  displacement  of  adjacent 
organs,  especially  the  heart  (retraction  toward  the  affected  side).  In 
the  course  of  time  these  may  be  almost  if  not  quite  completely  overcome, 
especially  if  not  marked  originally;  in  other  cases  the  pleural  adhesions 
may  become  extraordinarily  thickened  and  effectually  prevent  normal 
expansion  of  the  lung,  or  sending  prolongations  into  the  lungs  they  may 
lead  to  a  form  of  chronic  interstitial  pneumonitis.  The  other  lung  in 
these  circumstances  becomes  the  seat  of  so-called  compensatory  emphy- 
sema and  the  corresponding  side  of  the  chest  becomes  notably  enlarged. 

Symptoms. — The  onset  of  the  disease  may  be  frank  or  insidious.  In 
some  cases  the  symptoms  are  not  distinctive,  scarcely  even  suggestive,  and 
the  disorder  is  disclosed  only  by  physical  examination  (latent  pleurisy). 
In  other  cases  there  is  a  gradual  onset,  with  symptoms  referable  to  the 
chest.  In  still  other  cases  the  onset  is  more  or  less  abrupt,  and  attended 
by  pain  in  the  side,  cough,  and  fever,  as  in  acute  fibrinous  pleurisy; 
not  infrequently  there  is  a  chill,  or  chilliness,  which  may  last  some 
hours  or  recur,  and  there  are  usually  such  general  manifestations  of 
infection  and  toxemia  as  headache,  malaise,  anorexia,  etc.  The  pain 
is  often  extremely  severe,  stabbing  in  character,  and  localized  to  the 
side  or  the  peripheral  distribution  of  the  involved  intercostal  nerves, 
although  it  may  radiate  to  the  abdomen,  the  opposite  side,  etc.;  it  is 
aggravated  by  cough,  breathing,  pressure,  and  change  of  posture.  The 
cough  is  usually  hard  and  dry;  occasionally  there  is  slight  mucous  expecto- 
ration. The  breathing  is  usually  rapid  and  superficial,  less  from  dyspnoea 
per  se  than  from  pain  set  up  by  deep  inspirations.  The  fever  is  variable, 
and  rarely  exceeds  101°  to  102°;  at  the  end  of  a  week  or  ten  days,  as  a 
rule,  there  is  some  evidence  of  lytic  decrease  of  the  temperature,  but 
slight  fever  may  continue  for  several  additional  weeks,  and  exacerba- 
tions from  time  to  time  are  not  uncommon.  In  unusual  cases  there 
may  be  no  fever  (probably,  however,  some  fever,  if  sufficiently  often 
searched  for).  As  the  serous  exudate  is  poured  out,  and  the  inflamed  and 
sensitive  pleural  surfaces  are  separated  (the  fourth  to  seventh  day,  as  a 
rule),  the  pain  and  cough  lessen  and  may  disappear  altogether;  but 
should  the  amount  of  fluid  be  considerable,  200  c.c.  in  a  child,  800  c.c. 
or  more  in  an  adult,  symptoms  due  to  the  presence  of  the  fluid  as  such 
and  to  the  consequent  compression  and  displacement  of  adjacent  viscera 
develop.  These  comprise  especially  dyspnoea,  cyanosis,  and  frequency 
and  smallness  of  the  pulse,  which  may  or  may  not  be  present  when  the 
patient  is  quiet,  but  assuredly  develop  upon  exertion. 

Physical  Signs. — Pleurisy  may  be  suggested  by  an  initial  "stitch  in  the 
side"  and  fever,  but  the  diagnosis,  especially  of  eft'usion,  is  impossible 
in  the  absence  of  a  physical  examination.     In  the  early  (dry)  stage  the 


568  DISEASES  OF   THE  PLEURA 

patient  is  likely  to  lie  on  the  healthy  side  to  avoid  increasing  pain  by 
pressure  on  the  affected  side,  but  when  the  effusion  becomes  large  he  is 
likely  to  lie  on  the  diseased  side,  so  as  to  allow  free  and  unrestricted 
expansion  of  the  unaffected  side;  but  he  may  lie  on  his  back  or  sit  semi- 
erect  in  bed.  When  effusion  has  occurred  the  affected  side  is  usually 
enlarged  visibly  and  measurably  (normally  the  right  semicircumference 
is  about  2  cm.  greater  than  the  left);  the  interspaces  are  on  a  level  with 
the  ribs  or  bulging.  The  respiratory  movements  of  the  chest  and  dia- 
phragm on  the  affected  side  are  lessened  or  abolished,  the  functional 
incapacity  of  the  diaphragm  showing  well  in  the  absence  of  Litten's 
sign  and  upon  fluoroscopic  examination.  In  typical  cases  (there  are 
many  atypical  cases)  directly  over  the  fluid  there  are  dulness  on  percus- 
sion, increased  resistance,  diminished  or  absent  tactile  and  vocal  fremitus, 
and  weak  or  absent  breath  sounds;  the  higher  the  upper  limit  of  fluid 
(the  greater  the  amount,  as  a  rule)  the  more  marked  are  these  signs, 
and  they  increase  in  intensity  from  above  downward.  The  tactile  and 
vocal  fremitus  (normally  more  marked  at  the  right  apex  and  often 
throughout  the  right  lung)  may  be  normal  above  the  fluid  in  moderate- 
sized  effusions;  generally  they  are  increased  directly  above  the  fluid 
(at  the  upper  limit  of  dulness)  and  toward  the  vertebrae  on  account  of 
compression  of  the  lung;  they  may  be  well  marked  or  increased  also  in 
the  event  of  adhesions  binding  the  lung  to  the  chest  wall,  and  apparently 
in  children  from  unknown  causes  (perhaps  small  chests  and  considerable 
elastic  intrapleural  tension). 

The  upper  limit  of  the  dulness  varies  with  the  height  of  the  fluid  (which 
may  or  may  not  be  proportionate  to  the  amount),  but  it  does  not  directly 
indicate  the  level  of  the  fluid,  since  fibrinous  exudate  and  compressed 
lung  above  the  fluid  also  cause  dulness.  In  small  and  moderate  effusions 
the  upper  limit  of  the  fluid  (and  of  the  dulness)  varies,  being  influenced 
by  intrapleural  capillarity,  retraction  of  the  lung,  and  the  position  of  the 
patient  during  the  development  of  the  fluid.  Small  effusions  (less  than 
500  c.c.)  may  cause  a  small  area  of  dulness  posteriorly  near  the  angle 
of  the  scapula,  in  the  axilla,  in  Traube's  semilunar  space,  or  in  the 
cardiohepatic  (Ebstein's)  angle.  A  significant  feature  of  the  upper 
limit  of  moderate  effusions  is  their  irregular  outline;  often  this  is  low  near 
the  vertebrae,  rises  near  the  posterior  or  the  midaxillary  line,  and  falls 
again  in  front  (the  S-shaped  curve  of  Ellis  and  Garland),  due  in  part  to 
intrapleural  capillarity  and  the  lateral-prone  posture  of  the  patieiit,  espe- 
cially during  the  period  of  development  of  the  fluid.  Had  the  patient  been 
erect,  the  upper  limit  of  dulness  is  more  likely  to  be  nearly  horizontal. 
In  very  large  effusions  the  dulness  may  extend  up  to  or  above  the  third 
rib  in  front  and  the  spine  of  the  scapula  posteriorly.  In  perhaps  the 
majority  of  cases  (despite  prevailing  opinions  to  the  contrary),  the  upper 
limit  of  dulness  does  not  change  with  change  in  the  posture  of  the 
patient,  because  the  apposed  surfaces  of  the  pleura?  are  usually  adherent 
just  above  the  fluid;  in  the  less  common  cases  (few  limiting  adhesions) 
postural  change  in  the  dulness  may  occur  after  a  short  time  and  after 


SEROFIBRINOUS  PLEURITIS  560 

a  number  of  deep  inspirations.  There  is  no  respiratory  change  in  the 
upper  hmit  of  duhiess.  Above  the  duhiess  there  is  usually  a  vesiculo- 
tympanitic note  (Skodaic  resonance),  due  to  relaxation  o  the  lung; 
or  the  note  may  be  normal.  The  common  vesiculotympanitic  note 
near  the  vertebme,  in  the  depression  of  the  S-shaped  curve  of  Ellis-Gar- 
land, may  be  accentuated  and  increased  in  large  effusions  by  unusual 
compression  of  the  lung.  A  triangular  area  of  dulness  along  the  ver- 
tebrae on  the  side  opposite  the  effusion  may  be  observed  in  moderate  or 
large  effusions  (Koranyi-Grocco  triangle),  and  is  due  to  displacement 
and  compression  of  the  mediastinum  by  the  expanding  pleural  sac  and 
removal  of  the  resonant  lung  from  the  neighborhood  of  the  vertebrae. 
Williams'  tracheal  tone  and  the  so-called  cracked-pot  sound  may  some- 
times be  elicited  in  the  first  and  second  intercostal  spaces  in  the  event 
of  considerable  lung  compression.  Percussion,  as  well  as  palpation, 
also  discloses  displacement  of  the  adjacent  organs,  notably  the  heart 
and  the  liver,  less  frequently  the  spleen  and  the  stomach.  The  displace- 
ment of  the  heart  may  be  extreme,  but  torsion  does  not  occur,  and  the 
pulsation  sometimes  observed  far  to  the  right  in  left-sided  effusions 
must  not  be  interpreted  as  the  apex  beat.  The  lovv^er  border  of  the 
liver  may  reach  to  the  umbilicus  or  beyond  in  large  right-sided  effusions. 
The  lung  on  the  unaffected  side  is  commonly  hyperresonant  from 
compensatory  inflation ;  it  may  encroach  upon  the  normal  dulness  of  the 
heart,  liver,  or  spleen;  but  on  the  left  side  (in  right-sided  effusion)  heavy 
percussion  may  bring  out  a  tympanitic  note  from  the  stomach  and 
intestines,  especially  if  they  be  distended. 

The  weak  or  absent  breath  sounds  usually  heard  over  the  fluid  (or 
dull  area)  may  be  modified  by  attending  circumstances.  As  a  rule, 
in  moderate  or  large  effusions,  the  breath  sounds  decrease  in  intensity 
from  above  downward,  and  low  down  are  totally  inaudible;  but  at  the 
upper  level  of  the  dulness,  bronchovesicular  or  bronchial  breathing 
is  common  from  compression  of  the  lung  and  non-activity  of  the  alveoli; 
in  very  large  effusions  this  bronchial  breathing  may  be  audible  only 
below  the  clavicle  and  in  the  supraspinous  fossa,  or  no  breath  sounds 
may  be  audible.  In  some  cases  breath  sounds,  usually  more  or  less 
feeble  bronchial  breathing,  may  be  heard  directly  over  the  dull  area. 
This  is  due  in  some  cases  to  the  layer  of  fluid  being  thin  (less  than  2  cm.), 
to  adhesions  binding  the  lung  here  and  there  to  the  costal  pleura,  and 
to  conditions  favoring  conduction  (perhaps  related  to  intrapleural 
tension).  The  last  mentioned  seem  to  be  especially  operative  in  children 
in  whom  the  breath  sounds  in  pleural  effusion  are  often  quite  as  loud 
and  bronchial  in  character  as  they  are  in  pneumonia;  and  they  may  be 
associated  with  bronchophony.  Egophony  is  sometimes  ])resent,  usually 
over  the  upper  half  or  third  of  moderate-sized  eft'usions.  The  whisj^ered 
voice  (pectoriloquy)  is  said  to  be  transmitted  (direct  auscultation) 
through  a  serous,  but  not  through  a  ])urulent  eft'usion  (Baccelli's  sign). 
Pleural  frictions  are  commonly  audible  at  the  ujjper  limit  of  duluess; 
and  moderatelv  loud  consonatina'  rales  are  rairlv  audible  over  tlie  dull 


570  DISEASES  OE  THE  PLEURA 

area  in  the  event  of  the  breath  sounds  also  being  audible.  A  systolic 
murmur  may  develop  toward  the  base  of  the  heart,  being  due  to 
anemia,  fever,  or  pressure  on,  or  torsion  of,  the  great  vessels.  Usually 
there  is  a  slight  leukocytosis — 10,000  to  15,000. 

Diagnosis. — The  diagnosis  of  pleural  effusion  is  dependent  wholly 
upon  the  physical  signs,  of  which  the  following  are  the  most  important : 
Unilateral  increase  in  the  size  of  the  chest,  immobility  during  respiration, 
diminished  or  absent  tactile  fremitus,  dulness  on  percussion,  and  displace- 
ment of  the  adjacent  viscera  (heart,  mediastinum,  liver,  etc.).  Pneu- 
monia (sometimes  suggested  by  bronchial  breathing,  bronchophony, 
etc.)  may  be  excluded  by  the  absence  of  the  characteristic  mode  of  onset 
of  pneumonia  (initial  chill,  high  fever,  dyspnoea,  and  rusty  expectora- 
tion), and  by  the  more  marked  dulness  and  greater  resistance,  absence 
of  tactile  fremitus,  and  the  displacement  of  adjacent  viscera  that  occur 
in  pleural  effusion.  Temporary  absence  of  tactile  fremitus  and  of 
bronchial  breathing  sometimes  occur  in  pneumonia,  being  due  to  plug- 
ging of  a  large  bronchus,  but  coughing  usually  dislodges  the  obturating 
plug  of  mucus  and  fibrin,  and  tends  immediately  to  clear  the  diagnosis. 
In  the  event  of  doubt,  and  with  a  view  to  determine  the  nature  of  the 
pleurisy,  resort  may  be  had  to  exploratory  puncture  and  the  removal 
of  a  small  amount  of  fluid.  Hydrothorax  may  be  excluded  by  the  ab- 
sence of  its  special  etiological  factors  (cardiac  and  renaj  disease,  advanced 
cachectic  states,  etc.),  by  the  free  mobility  of  the  fluid  (which  is  not 
confined  by  adhesions),  and  by  examination  of  some  of  the  fluid  removed 
by  an  exploratory  needle.  Pulmonary  and  pleural  tumors,  which  may 
be  attended  with  pleural  fluid,  may  cause  diagnostic  embarrassment, 
but  they  give  rise  to  irregular  dulness,  the  general  evidences  of  tumors 
(anemia,  cachexia,  etc.),  to  obvious  local  growth  or  metastasis  (medias- 
tinum, cervical  glands,  etc.),  and  often  to  a  hemorrhagic,  sometimes  chyli- 
form  fluid,  in  which  particles  of  the  tumor  or  tumor  cells  may  be  found. 
A  pericardial  effusion  may  be  excluded  by  the  preponderance  of  physical 
signs  posteriorly  rather  than  anteriorly,  the  absence  of  the  especially 
significant  physical  signs  of  pericardial  fluid,  the  presence  of  a  displaced 
rather  than  an  obscured  heart,  and  the  less-marked  evidences  of  cardiac 
embarrassment  (dyspnoea,  cyanosis,  feeble  heart  sounds,  weak  pulse, 
etc.). 

Situation  of  the  Exudate. — ^The  foregoing  description  applies 
to  the  majority  of  cases,  in  which  the  fluid  involves  more  or  less  of  the 
pleural  sac,  and  extends  from  below  upward.  In  other  cases  the 
lesions  are  distinctly  circumscribed  and  the  fluid  sacculated.  This 
may  occur  anywhere,  but  especially  anteriorly  and  in  the  axilla;  it  gives 
rise  to  the  physical  signs  (already  mentioned)  over  a  restricted  area 
Diaphragmatic  pleurisy  gives  rise  to  pain  and  tenderness  in  the  epi- 
gastrium (especially  at  the  xyphoid),  which  may  radiate  to  the  back; 
often  it  is  very  severe  and  simulates  angina  pectoris.  There  is  often 
distressing  hiccough  and  spasm  of  the  upper  part  of  the  rectus  muscle; 
perhaps  marked  dyspnoea  and   dysphagia.      The  fluid  accumulating 


SEROFIBRINOUS  PLEURITIS  571 

between  the  diaphragm  and  the  diaphragmatic  surface  of  the  lung 
may  not  cause  noteworthy  dulness,  but  only  the  signs  of  local  compres- 
sion of  the  lung  and  displacement  of  the  adjacent  viscera.  The  fluid 
may  be  recognized  by  radiographic  examination.  Interlobar  pleurisy 
(usually  postpneumonic  and  suppurative)  may  be  detected  by  an  area 
of  dulness  corresponding  to  the  fissure  between  the  lobes,  radiographic 
examination,  and  in  most  cases  the  symptoms  of  lung  abscess  or 
empyema. 

Nature  of  the  Pleuritis. — The  nature  of  the  pleurisy  may  be 
recognized  by  a  chemical,  microscopic,  cytological,  and  bacteriological 
examination  of  the  fluid.  The  fluid,  as  a  rule,  is  pale  amber  in  color, 
slightly  cloudy,  alkaline,  has  a  specific  gravity  of  1015  to  1024,  contains 
3  to  7  per  cent,  of  albumin,  and  it  usually  clots  after  removal.  It  con- 
tains usually  a  few  erythrocytes  and  leukocytes,  and  endothelial  cells 
(mostly  fatty)  in  varying  proportion.  Cytologically  preponderance  of 
lymphocytes  is  indicative  of  the  tuberculous  nature  of  the  pleuritis; 
preponderance  of  leukocytes,  of  pyogenic  infections ;  and  preponderance 
of  endothelial  cells,  of  mere  transudation  or  malignancy.  The  tuberculous 
nature  of  the  process  may  be  further  determined  by  obvious  involvement 
of  a  lung  or  another  serous  membrane,  by  a  positive  response  of  the 
patient  to  a  tuberculin  test,  and  by  inoculating  lower  animals  with  some 
of  the  fluid;  later  this  becomes  apparent  in  about  one-third  of  the  cases 
by  the  patient  developing  tuberculosis. 

Prognosis. — In  uncomplicated  cases  the  immediate  prognosis  is  good, 
since  the  general  tendency  of  the  disease,  despite  the  common  tuber- 
culous origin,  is  toward  recovery.  The  usual  duration  is  from  three  to 
six  or  eight  weeks.  The  fever,  as  a  rule,  subsides  at  the  end  of  ten  days 
or  two  weeks,  but  recurrences  and  exacerbations  are  not  uncommon. 
With  the  decline  of  the  fever  the  fluid  tends  to  become  absorbed  (appar- 
ent in  lessening  of  the  physical  signs  of  fluid  and  the  development  of 
redux  crepitation).  This  may  occur  very  slowly,  and  it  may  not  occur 
at  all,  although  resorption  may  occur  even  after  months;  recurrence  after 
removal  is  common.  Following  absorption  or  removal  of  the  fluid, 
the  pleural  sac,  in  whole  or  in  part,  becomes  obliterated  by  fibrous 
adhesions;  these,  if  thin  and  non-indurative,  are  well  borne,  but  if  thick 
and  cicatricial  they  lead  to  induration  of  the  lung,  distortion  of  the 
chest,  and  displacement  of  the  adjacent  viscera,  which,  together  with  the 
later  possibility  of  the  development  of  pulmonary  tuberculosis,  renders 
the  ultimate  prognosis  doubtful.  Sudden  death  sometimes  occurs  from 
syncope  following  exertion,  myocardial  degeneration,  mechanical 
embarrassment  of  the  circulation  from  displacement  of  the  heart  and 
pressure  on  or  torsion  of  the  vessels,  pulmonary  embolism,  thrombosis, 
or  oedema;  or  it  may  follow  sudden  withdrawal  of  a  large  amount  of 
fluid. 

Treatment. — The  patient  should  Ije  confined  to  bed  in  a  well-venti- 
lated room  or  out-doors,  and  placed  on  a  liquid  or  semisolid,  easily 
digestible  diet.     The  bowels  should  be  thoroughly  evacuated  (calomel 


572  DISEASES  OF  THE  PLEURA 

• 
or  blue  mass  and  a  saline  cathartic),  and  they  should  be  kept  freely 

open  throughout  the  continuance  of  the  disease.  In  the  early  stage 
pain  usually  demands  relief,  and  it  should  be  relieved — by  an  ice  bag, 
dry  cups,  or  strapping  the  side  (as  in  fracture  of  the  ribs);  or  a  hypo- 
dermic injection  of  morphine  may  be  given  (it  should  not  be  withheld 
when  needed);  or  one  may  use  repeated  small  doses  of  powdered  opium 
or  extract  of  opium  in  a  pill  during  the  day,  and,  if  needed,  in  addition 
administer  a  Dover's  powder  in  the  evening.  The  use  of  opium  is 
sanctioned  by  long  usage;  it  not  only  relieves  the  pain  and  the  distress 
of  breathing,  but  it  is  also  believed  to  exercise  a  favorable,  so-called 
antiphlogistic  action  on  the  capillary  circulation  of  the  pleura  (and 
other  serous  membranes),  and  thus  to  control  the  inflammatory  phe- 
nomena. Small  doses  of  quinine  as  recommended  in  pneumonia,  seem 
to  be  a  useful  addition.  In  some  cases,  of  supposed  rheumatic  origin, 
salicyl  preparations  (salicylic  acid  and  its  salts,  salol,  salicin,  aspirin, 
etc.)  appear  to  do  good;  at  all  events,  in  sufficient  dosage  they  tend  to 
relieve  pain.  During  the  early  fever  days  of  the  disorder  the  comfort 
of  the  patient  may  be  promoted  by  simple  febrifuge  mixtures  (potassium 
citrate,  spirit  of  nitrous  ether,  solution  of  ammonium  acetate,  etc.). 

When  the  stage  of  effusion  has  been  reached  one  may  await  the 
spontaneous  absorption  of  the  fluid,  attempt  to  hasten  its  absorption 
by  medicinal  means,  or  remove  the  fluid  by  thoracentesis.  In  general 
there  is  a  tendency  toward  the  spontaneous  absorption  of  the  fluid;  but 
this  often  requires  considerable  time :  it  may  not  occur  for  months,  and 
it  may  not  occur  at  all.  Attempts  to  hasten  the  absorption  of  the  fluid 
are  sometimes  made — by  counterirritation  (iodine  and  blisters  locally, 
and  the  iodides  internally);  by  using  a  dry  diet  (very  little  fluid  at  or 
between  the  meals)  and  provoking  copious  bowel  movements  (concen- 
trated saline  cathartics  in  the  morning  before  breakfast) — so-called  Hays' 
method;  and  by  the  use  of  a  chloride-poor  diet.  More  or  less  satisfac- 
tory results  sometimes  attend  these  measures,  but,  as  a  rule,  they  are 
disappointing. 

The  most  efficacious  treatment  consists  in  withdrawal  of  the  fluid 
by  thoracentesis.  In  moderate-sized  and  large  effusions  this  may  be 
done  at  any  time  with  good  results;  but  it  is  especially  indicated  as 
soon  as  the  fluid  appears  to  be  not  increasing  in  amount.  This  may 
be  as  early  as  the  tenth  day  or  thereabout,  and  at  a  time  when  the  patient 
still  has  fever  and  few  if  any  subjective  pressure  symptoms;  but  early 
withdrawal  of  the  fluid  is  indicated  because  it  hastens  convalescence; 
because  it  relieves  the  compressed  lung  and  displaced  and  embarrassed 
heart  and  bloodvessels,  and  in  consequence  permits  of  the  early  resump- 
tion of  full  functional  activity;  and  because  it  obviates  the  danger  of 
sudden  death  which  occasionally  occurs  from  high  intrathoracic  press- 
ure. In  the  event  of  delaying  thoracentesis,  there  are  certain  positive 
indications  for  withdrawing  the  fluid  that  should  never  be  ignored; 
thus,  aspiration  is  indicated  in  all  cases  in  which  there  is  marked  dis- 
placement of  the  heart,  and  immediately  upon  the  occurrence  of  embar- 


SEROFIBRINOUS   PLEURITIS  573 

rassed  cardiac  action  (rapidity,  irregularity,  the  development  of  a  mur- 
mur), dyspnoea,  cyanosis,  or  syncope;  in  unilateral  effusion,  when  the 
dulness  extends  to  the  second  interspace,  or  if  the  dulness  does  not 
extend  so  high,  upon  the  development  of  physical  signs  of  fluid  accumu- 
lating in  the  other  side;  in  bilateral  effusions  when  both  sides  are  half 
full  (dulness  posteriorly  to  the  middle  of  the  scapula);  and  when  there 
is  no  evidence  of  absorption  of  the  fluid  after  a  week  or  ten  days  of 
normal  temperature. 

The  preferable  site  for  introducing  the  aspirating  needle  is  the 
eighth  intercostal  space  just  external  to  the  angle  of  the  scapula; 
some  physicians  prefer  the  seventh  interspace  in  the  midaxillary  line. 
The  needle  should  be  introduced  close  to  the  upper  margin  of  the  rib 
so  as  to  avoid  wounding  the  intercostal  artery.  The  fluid  should  be 
withdrawn  very  slowly;  the  amount  withdrawn  should  depend,  of 
course,  upon  the  amount  present,  but  also  on  the  reaction  of  the  patient. 
Very  slow  withdrawal  will  permit  the  withdrawal  of  considerable  fluid, 
but  it  is  rarely  necessary  or  desirable  to  remove  more  than  1000  to 
1500  c.c;  the  removal  of  a  relatively  or  actually  small  amount  is  often 
followed  by  spontaneous  absorption  of  the  remainder.  The  operation 
should  be  discontinued  when  the  pulmonary  pleura  is  found  to  impinge 
against  the  aspirating  needle  inserted  only  a  short  distance,  and  when 
the  patient  complains  of  a  short,  hacking,  paroxysmal  cough  (the 
usual  signal  for  discontinuance),  pain,  or  syncope.  A  second  aspira- 
tion, rarely  a  third,  may  be  required.  Continuous  drainage  is  prefer- 
able to  repeated  operations  in  recurrent  cases.  Barr  has  suggested  the 
introduction  into  the  pleural  sac,  during  and  after  the  withdrawal  of 
the  fluid,  of  a  volume  of  air  equal  to  one-half  or  three-fourths  of  that 
of  the  fluid  removed,  to  obviate  the  development  of  a  negative  intra- 
plueral  pressure  and  to  permit  gradual  expansion  of  the  compressed 
lung;  and  also  the  introduction  of  one  dram  (4  c.c.)  of  adrenalin  chloride 
(1  to  ICOO),  to  contract  the  bloodvessels  and  lessen  secretion.  Others 
have  suggested  the  injection  of  gases,  notably  nitrogen. 

Thoracentesis  is  occasionally  attended  by  more  or  less  serious  unto- 
ward consequences,  such  as  wounds  of  the  intercostal  artery,  the  lung, 
the  liver,  the  heart,  or  the  spleen;  pulmonary  oedema  (albuminous  ex- 
pectoration), which  is  usually  due  to  the  too  rapid  w^ithdrawal  of  the 
fluid  (it  should  be  treated  with  morphine  and  atropine  hypodermicly); 
pneumothorax,  hemothorax,  sul)cutaneous  emphysema,  syncope  (cere- 
bral anemia),  sudden  death  from  pulmonary  or  cerebral  embolism,  etc. 

The  patient's  strength  must  be  conserved  throughout  the  course  of  the 
disease,  especially  during  convalescence,  by  the  use  of  tonics,  such  as 
iron,  quinine,  strychnine,  cod-liver  oil,  the  hypophosphites,  etc.,  good 
food,  and  fresh  air.  Should  the  lung  not  be  speedily  restored  to  good 
function,  pulmonary  exercises  designed  to  inflate  the  lung,  such  as 
repeated  deep  inspirations  several  times  djiily,  or  the  blowing  of  water 
through  a  narrow  tube  from  one  large  flask  to  another,  sjiould  be  re- 
sorted to. 


574  DISEASES  OF  THE  PLEURA 

PURULENT   PLEURITIS. 

(Suppurative  Pleurisy;  Empyema.) 

Etiology. — Purulent  pleuritis  is  usually  a  secondary  process  caused  by 
the  pneumococcus,  the  streptococcus,  or  the  staphylococcus,  rarely  per- 
haps to  the  tubercle  bacillus,  the  colon  bacillus,  the  typhoid  bacillus,  etc. 
In  some  cases  the  disorder  begins  as  a  serofibrinous  pleuritis  and  is  set  up 
^by  the  usual  etiological  (bacterial)  factors  of  this  form  of  pleuritis;  some 
serofibrinous  exudations,  perhaps  originally  more  opaque  and  cell-rich 
than  is  the  rule,  become  still  more  opaque  and  cell-rich,  that  is,  sero- 
purulent,  even  distinctly  purulent  (the  last  mentioned  usually  the  result  of 
secondary  infection  set  up  perhaps  by  thoracentesis,  or  other  factors). 
In  other  cases  the  process  is  purulent  from  the  beginning  or  speedily 
becomes  purulent.  In  children  the  pneumococcus  is  the  common  cause, 
most  of  the  cases  following  pneumonia  (metapneumonic  form).  In 
adults  streptococci  and  staphylococci  are  the  more  frequent  causes, 
but  pneumococcic  forms  also  occur.  The  common  antecedent  disorders 
are:  Tuberculous  pulmonary  cavities  ruptured  into  the  pleura  (the 
empyema  in  these  cases  being  a  mixed  and  not  a  pure  tuberculous 
infection);  tuberculosis,  suppurative  and  traumatic  disease  of  adjacent 
tissues — such  as  the  mediastinum,  the  bony  framework  of  the  chest, 
the  abdominal  organs,  etc.  (lymphogenic  infection);  and  distant  local- 
ized infections  (septicopyemia),  or  general  infections  (scarlatina,  measles, 
dysentery,  typhoid  fever,  etc.),  in  which  secondary  pyogenic  infections 
are  rather  common. 

Pathology. — In  cases  with  less  pus  and  more  serum  the  changes  in  the 
pleura  are  quite  like  those  of  serofibrinous  pleuritis,  although  more 
marked;  the  pleura  is  thickened  and  covered  with  a  thick  fibrinopuru- 
lent  exudate;  and  there  is  marked  polynuclear  leukocytic  infiltration; 
the  fluid  is  more  opaque  and  contains  more  cells.  In  cases  frankly 
purulent  the  fluid  usually  separates  into  a  heavy  corpuscular  lower 
layer  exhibiting  the  ordinary  characteristics  of  pus,  and  a  lighter  upper 
serous  layer,  greenish  yellow  in  color.  In  the  pneumococcic  cases, 
especially  in  children,  the  exudate  is  likely  to  be  thick  and  creamy  and 
to  have  a  sweetish  disagreeable  odor;  in  the  streptococcic  and  staphylo- 
coccic cases  the  fluid  usually  is  thinner.  The  fluid  may  become  fetid 
(fetid  or  putrid  pleurisy),  especially  in  cases  following  stab  wounds 
of  the  chest,  abscess  or  gangrene  of  the  lung,  carcinoma  of  the  oesophagus, 
appendicitis,  etc. 

Symptoms. — In  some  cases  the  onset  and  the  course  of  the  disease  for 
some  time  are  identical  with  those  of  serofibrinous  pleuritis,  of  which 
purulent  pleuritis  may  be  only  an  advanced  stage.  In  other  cases 
following  antecedent  symptoms  of  the  primary  disorder,  the  develop- 
ment of  the  pleuritis  may  be  abrupt,  with  a  chill,  high  temperature, 
severe  pain  in  the  side,  and  general  evidences  of  toxemia.  In  many 
cases  the  suppurative  character  of  the  exudate  is  not  suspected  for 


PURULENT  PLEURITIS  575 

some  time,  unless  the  disease  develops  into  a  frank  case  of  septicopyemia. 
Long  continuance  of  fever  otherwise  unexplained,  however,  suggests 
the  suppuration,  as  do  also  progressive  pallor,  weakness,  and  loss  of 
flesh;  this  is  rendered  more  certain  by  the  occurrence  of  paroxysms  of 
chills  (or  chilliness),  fever,  sweats,  and  augmented  polynuclear  leuko- 
cytosis. 

Physical  Signs. — The  physical  signs  in  general  are  identical  with  those 
of  serofibrinous  pleuritis,  that  is,  the  physical  signs  no  not  disclose  the 
character  of  the  exudation.  However,  in  purulent  pleuritis  the  inter- 
costal spaces  are  more  likely  to  be  bulging  than  in  serofibrinous  pleuritis 
on  account  of  paresis  (seropurulent  infiltration)  of  the  intercostal 
muscles;  in  children  there  may  be  an  extraordinary  enlargement  of  the 
affected  side  of  the  chest;  whispered  pectoriloquy  is  less  well  transmitted 
through  a  purulent  than  through  a  serous  exudation  (Baccelli's  sign); 
and  a  localized  area  of  oedema  may  develop  over  the  fluid — which  is 
almost  if  not  quite  pathognomonic  of  the  purulent  character  of  a  pleural 
exudate.  In  exceptional  cases  the  purulent  exudate  (very  rarely  also  a 
serofibrinous  exudate)  transmits  a  cardiac  systolic  pulsation  to  the 
chest  wall  (pulsating  empyema)  between  the  second  and  fourth  ribs 
anteriorly,  or  the  third  and  fifth  ribs  in  the  axilla,  or  over  a  very  wide 
area.  The  cause  of  this  is  not  definitely  known,  but  important  factors 
seem  to  be  left-sided  pleural  exudation  (it  is  very  rare  in  right-sided 
effusions),  a  large  amount  of  fluid,  paresis  (relaxation,  due  to  oedema- 
tous  infiltration)  of  the  intercostal  muscles,  and  forcible  action  of  the 
heart.  Some  observers  believe  the  pulsation  to  be  transmitted  from  the 
aorta  rather  than  from  the  heart.  This  swelling  may  rupture  through 
the  costal  pleura  and  form  a  pulsating  mass  directly  beneath  the  skin 
(empyema  necessitatis),  and  it  may  rupture  externally — usually  toward 
the  lower  part  of  the  thorax  or  near  the  sternum;  or  by  gravitation 
the  empyema  may  reach  even  as  low  as  the  groin;  or  it  may  rupture 
into  the  lung  and  be  evacuated  through  a  bronchus,  the  trachea,  and 
the  mouth,  or  into  the  oesophagus,  the  stomach,  etc. 

Diagnosis. — The  physical  signs  so  essential  in  the  diagnosis  of  any 
pleural  effusion  do  not  determine  the  character  of  the  fluid;  but  long- 
continued  fever,  local  oedema  of  the  chest  wall,  and  recurring  chills, 
fever,  sweats,  and  polynuclear  leukocytosis  constitute  conclusive  evi- 
dence of  the  purulent  character  of  the  fluid.  In  any  case  of  doubt 
recourse  should  be  had  to  the  exploring  needle,  and  a  small  amount 
of  fluid  should  be  removed  and  examined  bacteriologically  and  cyto- 
logically.  In  many  cases  the  amount  of  fluid  (pus)  is  small  and  dis- 
tinctly localized — to  the  base,  between  the  lobes,  etc.,  and  being  detected 
serves  to  explain  ill-understood  fever  states  (delayed  convalescence 
from  pneumonia,  inexplicable  attacks  of  fever  after  scarlatina,  typhoid 
fever,  etc.).  It  is  scarcely  likely  that  a  pulsating  empyema  will  be 
mistaken  for  an  aneurysm. 

Prognosis. — Purulent  pleuritis  not  properly  treated  is  a  chronic 
disorder  tending  ultimately  to  death.     Sometimes  the  cases  that  per- 


576  DISEASES   OF   THE  PLEURA 

forate  spontaneously  or  through  the  lung  end  in  recovery,  the  fistulous 
tract  finally  healing;  or  the  fistula  may  persist  with  more  or  less  dis- 
comfort to  the  patient  and  perhaps  eventual  amyloidosis,  etc.  The 
prognosis  is  better  in  children  than  in  adults,  especially  under  appro- 
priate treatment.  Marked  retraction  and  deformity  of  the  chest  usually 
follow  in  the  event  of  recovery. 

Treatment. — Purulent  pleuritis  is  essentially  a  surgical  disorder,  and 
should  be  treated  on  surgical  principles;  as  an  abscess  anywhere  in  the 
body,  so  should  an  empyema  be  promptly  evacuated  upon  discovery 
and  thoroughly  drained.  Preliminary  aspiration  is  not  necessary, 
unless  with  a 'view  to  relieve  pressure  pending  more  thorough  evacua- 
tion. The  basis  of  successful  treatment  is  free  drainage,  which  sometimes 
may  be  achieved  by  simple  free  incision,  especially  in  children;  in 
other  cases  it  may  be  necessary  to  resect  one  or  more  ribs.  Irrigation 
of  the  cavity  is  sometimes  resorted  to  in  cases  of  putrid  pleuritis,  but 
otherwise  is  not  necessary.  Following  evacuation  of  the  pus,  persistent 
efforts  must  be  made  to  cause  expansion  of  the  compressed  lung — by 
calisthenic  exercises,  pulmonary  gymnastics,  blowing  water  through 
a  narrow  tube  from  one  bottle  to  another,  etc.  Mutilating  (Estlander) 
operations,  comprising  resection  of  several  ribs,  are  sometimes  necessary 
finally  to  close  the  cavity. 


HEMORRHAGIC   PLEURITIS. 

Etiology. — In  virtually  all  cases  of  serofibrinous  pleuritis  the  fluid 
exudate  contains  a  variable  number  of  erythrocytes.  Usually  these 
pass  unnoticed  unless  the  fluid  is  examined  microscopically;  sometimes, 
however,  the  erythrocytes  are  in  such  excessive  numbers  as  to  give  a 
more  or  less  well-marked  hemorrhagic  tint  to  the  fluid.  This  occurs  in 
certain  cases  of  the  so-called  primary  or  idiopathic  pleuritis  which  on 
careful  study  are  found  to  be  tuberculous,  as  well  as  the  more  frankly 
tuberculous  cases  with  the  eruption  of  miliary  tubercles  (rupture  of 
new-formed  capillaries) ;  in  primary  and  secondary  tumors  of  the  pleura ; 
in  the  pleurisy  of  asthenic  and  cachectic  states,  such  as  chronic  nephritis, 
cirrhosis  of  the  liver,  purpura,  scurvy,  leukemia,  and  other  blood  dyscra- 
sias,  etc.  (in  which  cases  it  is  not  always  a  true  inflammation). 

Pathology. — The  lesions  vary  with  the  causative  factors  (tuberculosis, 
tumors,  etc.).  In  many  cases  they  are  quite  like  those  of  the  analogous 
serofibrinous  pleuritis — with  the  addition  of  some  blood  to  the  exudate. 
In  cachectic  states  the  pleura  often  shows  hemorrhagic  foci  (usually 
petechial). 

Symptoms. — The  symptoms  are  usually  those  of  serofibrinous  pleuritis, 
from  which  hemorrhagic  pleuritis  is  not  to  be  distinguislied  except  by 
examination  of  the  fluid.  In  other  cases  the  symptoms  are  those  of  tumor 
of  the  lung  or  pleura,  to  which  the  physical  signs  of  fluid  in  the  chest 
become  superadded.     In  other  cases  (blood  dyscrasias,  asthenic  states) 


CHRONIC  PLEURITIS  577 

the  phenomena  are  analogous  to  those  of  hydrothorax,  and  are  disclosed 
usually  only  by  a  physical  examination  of  the  chest. 

Diagnosis. — The  diagnosis  is  dependent  upon  the  physical  signs  of 
fluid  in  the  pleura  and  an  examination  of  the  fluid;  its  hemorrhagic 
character  can  at  most  be  merely  suspected  before  some  of  the  fluid  is 
withdrawn.  The  condition  should  be  distinguished  from  hemothorax 
(hemorrhage  into  the  pleural  sac),  which  may  result  from  traumatism 
and  injury  to  the  chest  wall  or  the  thoracic  organs,  puncture  of  an 
intercostal  vessel  during  aspiration,  rupture  of  an  aneurysm,  ulcerative 
processes  involving  the  pleura?  and  pulmonary  vessels,  etc. ;  the  symptoms 
are  the  general  manifestations  of  more  or  less  rapid  bleeding  and  the 
physical  signs  of  the  more  or  less  rapid  accumulation  of  fluid  in  the 
pleura. 

Treatment. — The  treatment  of  hemorrhagic  pleuritis,  in  so  far  as  it 
differs  from  that  of  serofibrinous  pleuritis,  is  dependent  solely  upon  the 
associated  conditions  and  causative  factors. 


CHRONIC   PLEURITIS. 

{Chronic  Pleurisy  with  Effusion;  Chronic  Adhesive  Pleurisy.) 

Two  types  of  chronic  pleuritis  may  be  distinguished — the  one  with, 
the  other  without,  a  fluid  exudation. 

Chronic  Pleuritis  with  Effusion.— This  may  develop  insidiously, 
or  it  may  follow  acute  serofibrinous  pleuritis:  the  etiological  factors, 
the  lesions,  and  the  symptoms  may  be  quite  like  those  of  the  acute  pro- 
cess. Rarely  the  fluid  persists,  little  if  at  all  changed,  for  months,  without 
occasioning  noteworthy  symptoms;  often,  however,  there  is  dyspnoea, 
especially  on  exertion.  The  physical  signs,  the  diagnostic  criteria,  and 
the  treatment,  are  quite  like  those  of  serofibrinous  pleuritis. 

Chronic  Adhesive  Pleuritis. — Etiology. — Chronic  pleural  adhesions 
are  encountered  under  varying  circumstances:  (1)  They  may  represent 
a  primary  chronic,  originally  fibrinous  pleuritis — which  perhaps  may 
develop  abruptly,  but  more  conimonly  comes  on  insidiously;  the  organi- 
zation, of  the  fibrinous  exudation  leads  to  adhesion  of  the  apposed 
layers  of  the  pleura  and  more  or  less  widespread  obliteration  of  the 
pleura  sac.  These  are  the  adhesions  so  commonly  encountered  at 
necropsies,  often  in  subjects  who  during  life  presented  no  noteworthy 
evidences  of  their  presence;  originally  inflammatory  in  nature,  they  are 
later  analogous  to  scar  tissue  formation  elsewhere  in  the  body.  (2) 
Chronic  pleural  adhesi(^ns  are  also  the  evidences  of  postserofibrinous 
and  ])urnlent  })leuritis;  they  represent  the  process  of  healing,  of  scar 
formation.  P^'ollowing  absorption  of  the  fluid  exudation,  the  apposed 
layers  become  adherent,  and  the  sequential  process  of  organization  and 
cicatrization  lead  to  their  ])crmaiient  union.  As  a  cicatrix  elsewhere, 
the  new-formed  fibi'oiis  (issue  undergoes  niore  or  less  contraction,  and, 
especially  in  cases  of  empyema,  may  lead  to  extraordinary  retraction  and 


578  DISEASES  OF  THE  PLEURA 

deformity  of  the  chest,  displacement  of  the  intrathoracic  organs,  and 
fibrous  connective  tissue  overgrowth  in  the  lung  (chronic  interstitial 
pneumonitis,  bronchiectasis,  etc.).  The  process  is  usually  most  marked 
at  the  base,  where  the  two  layers  of  the  pleura  usually  become  inseparable 
and  indistinguishable,  and  represented  by  thick  fibrous  connective  tissue. 
(3)  Chronic  adhesive  pleuritis  may  be  definitely  tuberculous;  that  is, 
both  layers  may  be  adherent,  more  or  less,  often  considerably,  thickened 
(to  5  mm.  or  more),  and  the  seat  of  large  caseous  tubercles,  as  well  as  of 
small  miliary  and  fibroid  tubercles;  the  lesions  may  involve  one  or  both 
pleura,  perhaps  also  the  pericardium,  and  give  rise  to  veritable  tumor 
masses.  (4)  Chronic  adhesive  pleuritis  may  be  part  of  a  general  serositis 
(multiple  serositis,  polyorrhomenitis),  in  which  the  pleurae,  pericardium, 
and  peritoneum  become  involved  in  varying  combinations;  the  serous 
membrane  becomes  thickened  and  hyaline  and  much  resembles  con- 
fectioner's sugar-icing  (Zuckerguss — whence  the  Zuckerguss-leber,  -milz, 
-herz,  -lunge,  etc.,  of  the  Germans).  The  pleura  and  the  other  serous 
sacs  may  be  totally  or  partially  obliterated,  and  if  partially  only,  there 
may  or  may  not  be  also  some  fluid. 

Symptoms. — The  symptoms  vary.  In  some  cases  there  may  be  a 
dragging  pain  or  general  aching  in  the  side,  aggravated  by  overexertion 
or  inclement  weather;  sometimes  even  a  sharp  pain  occurs.  Often 
there  is  more  or  less  dyspnoea,  especially  on  exertion;  and  there  may  be 
other  symptoms  due  to  associated  conditions,  such  as  cough  and  expecto- 
ration in  chronic  bronchitis,  general  evidences  of  tuberculosis,  and 
symptoms  referable  to  other  serous  membranes. 

Physical  Signs. — The  physical  signs  vary  with  the  extent  of  the  ad- 
hesions and  the  degree  of  contraction.  In  mild  cases  there  is  more  or 
less  restriction  of  the  respiratory  movement  of  the  aftected  side  of  the 
chest  and  feeble  breath  sounds.  In  more  marked  cases,  the  affected 
side  is  definitely  contracted  and  more  or  less  immobile,  especially  at  the 
base;  the  other  side  may  be  distended  and  the  seat  of  exaggerated 
compensatory  respiratory  movements;  the  tactile  and  vocal  fremitus 
and  the  breath  sounds  are  lessened  in  intensity  and  may  be  absent;  the 
percussion  note  is  impaired  and  may  be  quite  dull;  there  is  no  respiratory 
movement  of  the  percussion  resonance  at  the  edges  of  the  lung  with  the 
phases  of  respiration;  and  Litten's  sign  is  absent.  Auscultation  some- 
times reveals  peculiar,  dry-leathery,  so-called  friction  sounds.  In 
advanced  cases  the  thorax  may  be  extraordinarily  deformed,  the  ribs 
retracted  and  approximated,  the  shoulder  lowered,  the  vertebrae  curved 
(the  concavity  toward  the  affected  side);  etc.;  the  heart  may  be 
uncovered  by  the  lung,  and  it,  as  well  as  the  liver,  spleen,  etc.,  may  be 
more  or  less  displaced. 

Diagnosis. — ^The  diagnosis  depends  upon  the  past  history  of  the  patient, 
the  immobility  and  retraction  of  the  chest,  and  the  impaired  resonance, 
feeble  ]:)reath  sounds,  and  other  physical  signs  of  a  thickened  pleura 
interposed  between  the  lung  and  the  chest  wall. 


HYDROTHORAX  579 

Prognosis. — The  prognosis  varies  with  the  severity  and  extent  of  the 
adhesions  and  the  presence  or  absence  of  complicating  conditions,  such 
as  fibrosis  of  the  hmg,  bronchiectasis,  deformity  of  the  thorax,  etc. 

Treatment. — Attention  to  the  general  health  of  the  patient  is  of  prime 
importance.  The  hygienic  conditions  must  be  the  best  attainable,  and 
the  food  must  be  of  the  best  quality  and  generous  in  amount.  If  fluid 
is  present  in  the  pleura  it  should  be  removed  by  aspiration.  Regulated 
exercise  and  pulmonary  gymnastics  are  of  marked  service  in  favoring 
expansion  of  the  lung  in  mild  or  moderately  severe  cases;  but  notable 
improvement  can  scarcely  be  expected  when  the  lung  is  encased  in  a 
thick  layer  of  cicatricial  connective  tissue  and  the  thorax  is  markedly 
deformed.  In  these  cases,  however,  if  the  patient  lives  within  his  reserve 
capacity,  he  may  survive  a  long  time  in  comparative  comfort.  Tonics 
(iron,  quinine,  strychnine),  digestants  (hydrochloric  acid,  tincture  of 
nux  vomica,  etc.),  and  alteratives  (syrup  of  iron  iodide,  cod-liver  oil, 
mercury,  phosphorus,  etc.)  are  often  useful  adjuvants. 


HYDROTHORAX. 

{Pleural  Dropsy;  Pleural  G£denia.) 

Etiology. — Hydrothorax,  a  transudation  of  non-inflammatory  serous 
fluid  into  the  pleural  sac,  is  a  secondary  process  that  occurs  in  condi- 
tions that  lead  to  oedema  generally :  disease  of  the  heart  and  of  the  lungs 
(with  consecutive  cardiac  failure)  in  consequence  of  passive  congestion; 
and  in  disease  of  the  kidneys  and  anemic  and  cachectic  conditions  (car- 
cinoma, sarcoma,  pernicious  anemia,  leukemia,  scurvy,  etc.),  in  con- 
sequence of  hydremia,  and  perhaps  disease  of  the  capillary  vessels  and 
toxemia. 

Pathology. — In  cardiac  cases,  the  process  in  the  beginning  at  least  is 
likely  to  be  unilateral,  commonly  right-sided,  because  in  addition  to  the 
general  venous  engorgement,  local  obstruction  of  the  azygos  veins  or 
the  right  pulmonary  veins  (page  457)  is  added,  the  consequence  of 
pressure  by  a  dilated  right  auricle  or  vena  cava;  and  when  it  becomes 
bilateral  it  is  still  usually  most  marked  on  the  right  side.  In  renal  and 
anemic  and  cachectic  cases  it  is  usually  bilateral.  The  fluid  varies  in 
amount  from  a  few  cubic  centimeters  to  several  liters.  It  is  usually 
clear,  pale  amber  in  color,  has  a  specific  gravity  of  1006  to  1015,  and 
contains  from  1  to  3  per  cent,  of  albumin;  microscopically,  it  contains 
a  few  endothelial  cells,  erythrocytes,  and  leukocytes.  The  pleura  often 
exhibits  no  conspicuous  changes;  but  in  long-standing  cases  a  low  grade 
inflammation  may  be  set  up  and  materially  alter  the  appearance  of  the 
pleura  and  the  character  of  the  fluid. 

Symptoms. — The  symptoms  are  those  of  the  primary  condition,  to 
which  are  added  the  effects  of  pressure  on  the  intrathoracic  organs, 
dyspnoea  (orthopncra),  cyanosis,  cough  (often  paroxysmal  and  asth- 
matic), and  marked  embarrasment  and  enfeeblement  of  the  circulation. 


580  DISEASES   OF  THE  PLEURA 

The  physical  signs  are  those  of  fluid  in  the  chest,  and  are  quite  Hke 
those  of  serofibrinous  pleuritis.  The  fluid,  however,  being  thinner 
and  not  circumscribed  by  adhesions,  readily  shifts  with  change  in  the 
posture  of  the  patient  (pathognomonic  sign  of  fluid). 

Diagnosis. — The  diagnosis  depends  upon  the  etiological  factor,  the 
physical  signs  of  fluid  in  the  pleura,  and  an  examination  of  some  of  the 
fluid  removed.  It  is  especially  important  to  remember  that  often  much 
of  the  distress  of  failing  cardiac  compensation  is  due  to  a  right-sided 
hydrothorax  that  is  often  entirely  unrecognized. 

Prognosis. — The  prognosis  is  that  of  the  primary  disorder. 

Treatment. — The  treatment  is  that  of  the  primary  disorder.  In  many 
cases  of  failing  cardiac  compensation,  the  greatest  improvement  follows 
removal  of  the  fluid  by  aspiration.  The  condition  should  always  be 
borne  in  mind  and  searched  after,  and  when  detected,  if  the  patient 
does  not  speedily  improve,  the  thoracentesis  should  be  promptly  per- 
formed; delay  may  precipitate  a  fatal  issue,  which  otherwise  might 
be  avoided. 


PNEUMOTHORAX. 

(Pyopneumothorax ;  Serofihrino'pneimiothorax ;  Hemopneumothorax.) 

Pneumothorax,  the  presence  of  air  or  gas  in  the  pleural  cavity,  is  an 
exceedingly  rare  disorder.  The  causative  factors  are  such  that  an  inflam- 
mation of  the  pleura  is  also  induced,  and  inasmuch  as  this  is  usually 
purulent,  the  condition  in  the  great  majority  of  cases  is  pyopneumo- 
thorax; rarely  the  inflammatory  phenomena  are  analogous  to  those 
of  serofibrinous  pleuritis — serofibrinopneumothorax;  and  still  more 
rarely  the  exudation  is  hemorrhagic — hemopneumothorax. 

Etiology. — Pneumothorax  (pyopneumothorax  and  its  other  modifi- 
cations) is  most  common  in  males,  in  adult  life,  and  on  the  right  side. 
It  results  from  the  access  of  air  (which  is  usually  infected)  to  the 
pleura.  This  may  occur:  (1)  In  perforating  wounds  of  the  chest,  such 
as  traumatisms  (when  it  may  be  associated  with  subcutaneous  emphy- 
sema), thoracentesis,  etc.  (2)  In  rupture  of  the  lung,  which  is  the 
most  common  cause,  especially  the  rupture  of  tuberculous  pulmonary 
cavities;  less  commonly  the  rupture  of  a  pulmonary  abscess  and  gangrene, 
bronchiectatic,  bronchopneumonic,  and  embolic  cavities,  echinococcus 
cyst,  emphysematous  bulla,  etc.;  or  the  rupture  into  the  lung  of  an 
empyema,  or  traumatic  rupture  of  the  lung  due  to  a  fractured  rib 
without  laceration  of  the  overlying  skin;  rarely  perhaps  violent  mus- 
cular effort  or  coughing  may  cause  rupture  of  a  lung  bound  down  by 
adhesions.  (3)  In  ulcerative  processes  in  the  oesophagus,  stomach, 
intestines,  etc.  (with  perhaps  a  primary  subphrenic  abscess).  (4)  Rarely 
pneumothorax  may  arise  spontaneously,  in  consequence  of  infection  with 
Bacillus  aerogenes  capsulatus  (Welch)  or  other  gas-producing  micro- 
organism. 


PNEUMOTHORAX  581 

Pathology. — The  process  is  usually  unilateral;  rarely  bilateral.  The 
containetl  air  may  or  may  not  be  malodorous;  it  varies  in  amount  up  to 
2000  c.c.  or  more;  and  it  is  commonly  associated  with  more  or  less 
seropurulent  or  distinctly  purulent  fluid  and  lesions  similar  to  those  of 
purulent  pleuritis — all  of  which,  soon  overcoming  the  negative  intra- 
pleural pressure  of  4  to  6  mm.  of  mercury,  causes  proportionate  com- 
pression and  displacement  of  the  intrathoracic  and  upper  abdominal 
organs.  In  rupture  of  a  previously  healthy  or  an  emphysematous  lung 
there  may  be  no  fluid;  and  in  traumatic  cases,  as  well  as  in  cases  due 
to  ulcerative  processes,  there  may  be  also  blood — hemopneumothorax 
(or  hemopyopneumothorax).  The  air  or  gas  may  be  circumscribed  or 
diffuse  (circumscribed  or  diffuse  pneumothorax).  The  point  of  rupture 
in  the  lung  may  be  small  or  large;  usually,  but  not  always  it  may  be 
found;  it  may  close  after  permitting  the  access  of  air  to  the  pleura. 

The  following  varieties  of  pneumothorax  may  be  distinguished:  (I) 
Open  pneumothorax,  in  which  the  air  enters  and  leaves  the  pleura 
during  the  phases  of  respiration;  (2)  closed  pneumothorax,  in  which 
the  point  of  rupture  (usually  in  the  lung)  becomes  closed,  and  shuts 
off  from  the  outside  air  that  contained  in  the  pleural  sac;  and  (3) 
valvular  pneumothorax,  which  permits  usually  the  entrance,  but  not 
the  exit  of  air  from  the  pleura;  the  entrance  of  air  usually  ceases 
when  the  intrapleural  pressure  is  sufficient  to  close  the  opening  or 
to  overcome  the  pressure  of  the  entering  air. 

Symptoms. — Rarely,  the  onset  is  insidious,  and  not  attended  by 
noteworthy  symptoms;  the  condition  may  be  found  accidentally  by 
physical  examination  during  life  or  at  the  necropsy.  In  the  great 
majority  of  cases,  however,  the  onset  is  sudden  and  characterized  by 
severe  pain  in  the  chest,  the  development  of  (or  increase  of  previously 
existing)  dyspnoea  and  cyanosis,  and  not  infrequently  collapse,  with 
rapid,  feeble  pulse,  sweating,  etc. 

Physical  Signs. — The  patient  is  likely  to  lie  on  the  affected  side,  to 
permit  free  and  unrestrained  movement  of  the  healthy  lung.  The  affected 
side  is  distended,  and  almost  if  not  quite  immobile;  the  intercostal 
spaces  bulge  and  may  transmit  a  downy  or  crepitant  sensation  on 
palpation.  The  tactile  fremitus  is  markedly  diminished  or  absent. 
The  note  obtained  by  percussion  varies,  depending  upon  the  intrapleural 
tension,  the  tension  of  the  chest  wall  (due  largely  to  the  condition  of  the 
intercostal  muscles),  and  whether  the  pneumothorax  is  of  the  open  or 
closed  variety.  As  a  rule,  the  percussion  note  is  full,  clear,  and  hyper- 
resonant  or  tympanitic;  it  is  said  to  have  an  amphoric  or  metallic  quality 
in  open  pneumothorax  (not  a  conclusive  or  trustworthy  sign  to  be  thus 
interpreted).  Of  special  importance  is  the  fact  that  the  hyperresonant 
or  tympanitic  note  extends  far  beyond  the  normal  limits  of  the  lung. 
Sometimes  the  percussion  note  is  quite  dull  (said  to  l)e  cases  of  marked 
intrapleural  tension  and  contracted  intercostal  muscles).  Often  there 
is  dulness  at  the  base  of  the  chest  (due  to  concomitant  fluid  exudation), 
which  shifts  readily  with  change   in    the   posture   of  the  patient;  hut 


582  DISEASES  OF  THE  PLEURA 

fluid  may  be  present  without  dulness,  the  tympany  obscuring  or 
replacing  the  dulness.  The  so-called  cracked-pot  sound  may  some- 
times be  elicited  over  an  open  pneumothorax.  The  breath  sounds,  as 
a  rule,  are  much  diminished  or  absent,  especially  at  the  lower  part  of 
the  chest;  or  feeble  breath  sounds  of  a  bronchial,  metallic,  or  amphoric 
quality  may  be  audible;  or  this  quality  may  be  well  brought  out  by  a 
cough.  On  auscultating  posteriorly  while  an  assistant  with  a  coin  taps 
another  coin  placed  on  the  front  of  the  chest,  one  may  hear  the 
so-called  coin  sound  (bruit  d'airain  of  Trousseau).  The  vocal  fre- 
mitus (bronchophony)  also  has  a  metallic  quality,  although  it  is 
usually  less  intense  than  normally.  Bronchial  and  other  rales  may  be 
heard,  and  usually  have  a  metallic  quality.  The  metallic  tinkle  of 
Laennec,  or  falling-drop  sound,  may  be  elicited  by  coughing,  deep 
inspiration,  or  change  of  posture;  usually  attributed  to  the  falling  of 
a  drop  of  fluid  or  fibrin  on  the  accumulated  fluid,  it  is  not  unlikely 
due  to  rales  produced  in  or  about  a  cavity  in  the  lung.  A  peculiar 
whistling  sound  is  sometimes  audible  and  is  attributable  to  entrance 
or  exit  of  air  through  the  pulmonary  opening  into  the  pleura;  this  takes 
on  a  quite  characteristic  quality  when  the  opening  is  below  the  upper 
level  of  the  fluid.  A  peculiar  splashing  sound  (Hippocratic  succussion 
splash)  may  be  heard  when  the  patient  is  shaken,  and  is  pathognomonic 
of  the  presence  of  air  and  fluid;  it  may  be  heard  only  when  the 
auscultator's  ear  is  applied  to  the  chest,  but  sometimes  at  a  distance; 
and  it  may  be  quite  apparent  to  the  patient.  In  addition  to  the  fore- 
going, the  physical  signs  of  displacement  of  the  adjacent  viscera, 
especially  the  heart,  are  present;  the  heart  sounds,  although  mufiled, 
may  have  a  metallic  quality. 

Diagnosis. — The  diagnosis,  as  a  rule,  is  easy:  the  etiological  factor, 
the  mode  of  onset,  the  enlarged  and  immobile  chest,  the  hyperresonant 
or  tympanitic  percussion  note,  the  markedly  diminished  or  absent 
vocal  fremitus  and  breath  sounds,  the  metallic  quality  to  breath  sounds 
or  rales  that  may  be  audible,  the  coin  sound,  succussion  splash,  and 
displacement  of  the  adjacent  viscera  are  unmistakable.  It  is  not  likely 
that  a  careful  observer  will  mistake  the  condition  for  emphysema.  In 
the  unusual  cases  in  which  the  percussion  note  is  dull,  effusion  alone 
may  be  suspected,  but  absence  of  the  characteristic  increased  resist- 
ance to  the  percussing  finger  and  of  the  other  signs  of  pleural  effusion 
should  exclude  error;  but  one  must  remember  that  fluid  is  usually 
associated  with  the  air.  Pulmonary  cavity  may  be  excluded  by  the 
absence  of  retraction  of  the  chest  and  of  sinking  in  of  the  intercostal 
spaces,  and  by  the  presence  of  dislocation  of  the  heart,  of  the  coin  sound, 
of  succussion  splash,  etc.  Diaphragmatic  hernia  and  subphrenic  pyo- 
pneumothorax also  must  sometimes  be  considered  in  the  differential 
diagnosis.  Rontgen-ray  examination  often  affords  material  help  in  the 
diagnosis. 

Prognosis. — The  outlook  varies  with  the  associated  conditions,  but 
it  is  always  serious.    Death  occurs  in  about  three-fourths  of  the  cases; 


CHYLOTHORAX  583 

within  a  short  time  (hours  or  days)  in  a  few  cases,  within  a  few  weeks 
in  most  of  the  cases  (tuberculous  cases).  Occasionally  arrest  of  the 
tuberculous  process  in  the  lung  follows  the  development  of  the  pneumo- 
thorax. Some  cases  become  chronic  and  last  for  months  or  years. 
Recovery  may  ensue  when  the  condition  develops  in  a  previously  healthy 
subject. 

Treatment. — In  some  traumatic,  tuberculous,  and  other  cases  the  air 
becomes  absorbed  spontaneously;  the  patient,  therefore,  should  be 
watched,  kept  quiet,  and  rendered  comfortable  by  the  use  of  bromides, 
morphine,  and  other  sedatives  and  narcotics,  if  necessary;  if  no  note- 
worthy ill  consequences  ensue  the  pneumothorax  should  not  be  mo- 
lested. Removal  of  the  air  by  aspiration  may  lead  to  reopening  of  a 
healing  point  of  rupture  in  the  lung  and  convert  a  closed  into  an  open 
pneumothorax,  and  induce  or  increase  infection  of  the  pleura.  The 
cases  of  frank  pyopneumothorax,  as  a  rule,  should  be  treated  as  are 
cases  of  purulent  pleuritis,  by  incision  and  drainage;  but  one  often  has 
to  take  into  consideration  the  general  condition  of  the  patient,  the 
likelihood  of  the  pleural  fistula  opening  and  of  the  disease  of  the  lung, 
perhaps  quiescent,  becoming  reactivated,  the  condition  of  the  other 
lung,  etc.  The  likelihood  of  benefit  from  incision  and  drainage  are 
often  almost  if  not  quite  counterbalanced  by  the  possible  ill  conse- 
quences; in  general,  however,  it  is  always  wise  to  evacuate  pus.  In 
acute  cases  with  marked  cyanosis,  orthopnoea,  and  feeble  heart  action 
the  pleura  should  be  incised  or  aspirated  without  delay,  and  morphine 
and  stimulants  administered.  Otherwise  the  treatment  is  that  of  the 
associated  conditions,  chiefly  tuberculosis. 


CHYLOTHORAX. 

Chylothorax,  the  presence  of  a  milky,  opaque,  and  opalescent  fluid 
in  the  pleura,  may  be  of  two  types:  (1)  True  chylothorax,  in  which  the 
fluid  is  chyle.  This  occurs  rarely  in  the  event  of  obstruction  or  rupture 
of  the  thoracic  duct,  and  still  more  rarely  in  obstruction  of  the  sub- 
clavian vein  (thrombosis,  or  pressure  from  without  by  tumors,  etc.). 
(2)  False  chylothorax  (pseudochylothorax),  in  which  the  fluid  is  chyli- 
form  (adipose),  the  consequence  of  fatty  degeneration  of  contained 
cells  and  of  fatty  (and  perhaps  albuminous)  particles  held  in  suspension; 
it  occurs  rarely  in  tuberculous,  endotheliomatous,  and  other  forms  of 
pleuritis.  Both  forms  of  chylothorax  may  be  associated  with  similar 
disease  of  the  peritoneum.  The  symptoms  and  -physical  signs  are  like 
those  of  hydrothorax,  serofibrinous  pleurisy,  or  tumor  of  the  pleura. 
The  diagnosis  is  usually  not  made  until  the  fluid  has  been  obtained 
by  thoracentesis.  It  is  often  difficult  to  distinguish  chylous  from  chyli- 
form  fluid:  chylous  fluid  contains  sugar,  which,  however,  has  been 
found  also  in  some  cases  of  chyliform  fluid;  chylous  fluid,  as  a  rule, 
contains  a  small  amount  of  fat  (1  per  cent,  or  less),  while  chyliform 


584  DISEASES  OF  THE  MEDIASTINUM 

fluid  may  contain  5  to  6  per  cent,  or  more,  and  its  fatty  and  albuminous 
granules  are  likely  to  be  coarser  than  those  of  chylous  fluid. 


TUMORS  Of  the  pleura. 

Tumors  of  the  pleura  may  be  primary  or  secondary.  The  secondary 
growths  usually  follow  primary  tumors  of  the  lungs,  or  mediastinum 
(extension  by  contiguity  or  lymphatic  distribution),  or  of  the  kidneys 
(hypernephroma)  or  other  organs  from  which  metastasis  may  occur  by 
way  of  the  bloodvessels.  The  primary  tumors  may  be  benign  (lipoma, 
fibroma,  chondroma)  or  malignant — the  more  common  endothelioma 
and  the  rarer  sarcoma  (round-  or  spindle-cell).  They  occur  as  flat,  cir- 
cumscribed or  difi^use,  more  or  less  soft  growths;  and  cause  moderate  or 
considerable  thickening  of  the  pleura.  Metastasis  may  occur  to  the 
lungs  and  other  adjacent  organs;  and  the  growth  may  become  visible 
beneath  the  skin.  The  symptoms  are  those  of  chronic  pleurisy,  with 
perhaps  considerable  local  pain  or  distress,  and  progressive  anemia 
and  cachexia.  The  chest  may  be  irregularly  distended  and  retracted, 
and  the  dulness  may  vary  in  intensity  here  and  there  and  be  quite 
irregular  in  outline.  The  fluid  removed  by  exploratory  puncture  is 
likely  to  be  hemorrhagic,  and  may  contain  isolated  tumor  cells  or  particles 
of  the  growth.  The  prognosis  is  bad,  the  course  of  the  disease  being, 
as  a  rule,  a  few  months  only.  The  treatment  is  purely  symptomatic — 
promotion  of  the  comfort  of  the  patient,  relief  of  pain  and  distress  by 
morphine  if  necessary,  the  removal  of  large  collections  of  fluid,  etc. 


DISEASES  OF  THE  MEDIASTINUM. 

MEDIASTINITIS. 

Mediastinitis  may  be  acute  or  chronic.  The  chronic  process  is  usually 
part  of  a  chronic  obliterative  pericarditis  (mediastinopericarditis),  asso- 
ciated or  not  with  chronic  obliterative  pleuritis;  the  symptoms  are 
discussed  in  connection  with  chronic  adhesive  pericarditis. 

Acute  mediastinitis  is  sometimes  divided,  according  to  its  location,  into 
anterior  and  posterior,  the  dividing  line  being  a  plane  laterally  through 
the  middle  of  the  trachea.  The  process  may  be  simple  or  suppurative 
(often  two  stages  of  the  one  process).  It  may  be  due  to  trauma;  to 
inflammation  of  adjacent  tissues  (pleura,  pericardium,  lungs,  oesophagus, 
ribs,  sternum,  vertebrae,  connective  tissue  of  the  neck,  etc.);  or  to  infec- 
tious, especially  septicopyemic,  processes  elsewhere  in  the  body  (hemo- 
genic  infection).  The  lesions  are  those  of  inflammation,  often  asso- 
ciated with  considerable  oedema,  which  may  proceed  to  abscess  formation. 
Either  the  connective  tissues  or  the  lymph  nodes,  or  both,  may  be 
involved,  and  the  lesions  of  one  or  the  other  may  predominate.     The 


TUMORS   OF   THE  MEDIASTINUM  585 

lympli  nodes  are  especially  involved  in  tuberculosis,  syphilis,  and  other 
infections,  such  as  pertussis. 

Symptoms. — The  symptoms  consist:  (1)  Fever,  and  perhaps  initial 
chill  or  chilliness;  (2)  evidences  of  local  inflammation,  such  as  sub- 
sternal pain  and  tenderness,  and  perhaps  oedema  about  the  sternum, 
in  the  intercostal  spaces,  and  the  episternal  notch;  and  (3)  pressure 
effects,  such  as  dyspnoea,  dysphagia,  etc.  (more  fully  mentioned  under 
mediastinal  tumors).  In  the  event  of  suppuration,  irregular  chills, 
fever,  sweats,  and  leukocytosis  may  supervene;  the  pain  may  become 
more  severe  and  throbbing  in  character,  and  the  local  effects  of  pressure 
more  aggravated.  The  abscess  may  penetrate  and  ultimately  perforate 
through  an  intercostal  space,  the  trachea,  a  bronchus,  the  pleura,  the 
oesophagus,  etc.,  or  it  may  burrow  into  the  abdomen. 

Diagnosis. — ^The  bulging  sometimes  caused  in  an  intercostal  space 
may  be  mistaken  for  an  aneurysm,  especially  if  it  pulsates  and  is  fluctu- 
ating; but  the  absence  of  expansile  pulsation,  of  diastolic  shock,  and 
of  murmurs,  and  the  presence  of  the  general  and  local  evidences  of 
suppuration  should  obviate  diagnostic  error. 

Treatment. — The  treatment  is  surgical,  and  consists  of  evacuation 
and  drainage. 


TUMORS  OF  THE  MEDIASTINUM. 

Tumors  of  the  mediastinum  may  be  primary  or  secondary.  The 
secondary  growths  (carcinomas  and  sarcomas)  develop  from  extension 
of  tumors  of  adjacent  organs  or  represent  metastases  from  more  distant 
parts.  The  primary  tumors  comprise  the  exceedingly  rare  benign 
growths  (fibroma,  lipoma,  chondroma,  etc.),  and  the  more  common 
malignant  growths,  of  which  the  most  common  is  sarcoma;  carcinoma 
is  rare  (despite  older  views  to  the  contrary;  in  days  gone  by  carcinoma 
was  not  well  differentiated  from  sarcoma);  rare  endotheliomas  have 
been  reported,  as  well  as  simple  and  dermoid  cysts.  Sarcoma  may 
develop  from  the  mediastinal  connective  tissues  or  lymph  nodes,  or  from 
the  thymus;  when  advanced  it  is  often  difficult  to  determine  the  point 
of  origin.  The  common  types  are  the  lymphosarcoma  and  the  spindle- 
cell  sarcoma;  they  form  tumors  of  variable  size  and  consistency,  that 
more  or  less  completely  fill  the  mediastinum,  and  compress  the  regional 
structures  and  organs. 

Symptoms. — As  a  rule,  the  symptoms  develop  insidiously  and  pro- 
gress gradually.  The  initial  symptoms  in  most  cases  consist  of  a  hard, 
dry  cough  or  gradually  increasing  dyspnoea,  especially  on  exertion,  and 
progressive  failure  of  the  general  health;  rarely  these  develop  rather 
suddenly  and  soon  become  marked.  There  may  be  also  a  sense  of 
fulness  or  constriction  of  the  chest;  or  even  actual  substernal  pain. 

The  symptoms  are  due  almost  entirely  to  pressure,  and  they  vary 
much  in  individual  cases.     Dyspno'a  may  result  from  compression  of 


586  DISEASES  OF  THE  MEDIASTINUM 

the  trachea,  bronchus,  lung,  or  pneumogastric  nerve.  Spasm  of  the 
glottis,  paralysis  of  the  vocal  cord,  aphonia,  and  paroxysmal  dyspnoea 
may  follow  irritation  or  paralysis  of  the  recurrent  laryngeal  nerve 
(usually  the  left,  sometimes  both).  The  cardiac  activity  may  be  accelera- 
ted or  weakened,  and  attacks  of  asthma  may  occur,  from  involvement  of 
the  pneumogastric  nerve  or  compression  of  the  heart.  Cyanosis,  oedema, 
and  venous  ectasia  of  the  head,  neck,  arm,  and  upper  chest  may  result 
from  compression  of  the  ascending  vena  cava  or  one  of  its  main  branches, 
and  superficial  anastomosis  may  form  with  tributaries  of  the  inferior 
vena  cava.  Hydrothorax  may  result  from  local  venous  obstruction. 
Dysphagia  may  follow  pressure  on  the  oesophagus.  Inequality  of  the 
pupils  and  unilateral  sweating  of  the  face  may  result  from  involvement 
of  the  sympathetic  nerves.  The  growth  occasions  an  irregular  area 
of  dulness  beneath  and  beyond  the  sternum,  or  in  the  back.  The 
breath  sounds  in  a  lobe  or  in  an  entire  lung  may  be  weakened  from 
compression  of  a  bronchus,  or  they  may  be  bronchovesicular  or  bron- 
chial in  character  from  compression  of  the  lung.  The  heart  becomes 
more  or  less  displaced.  The  growth  may  erode  and  finally  penetrate 
the  sternum  or  project  through  an  intercostal  space,  in  the  episternal 
notch,  etc.;  and  it  may  exhibit  a  pulsation  (non-expansile)  transmitted 
from  the  heart  or  the  aorta;  and  it  may  give  rise  to  metastatic  enlarge- 
ment of  the  cervical  lymph  nodes,  etc. 

Diagnosis. — ^The  disease  should  be  suspected  in  all  cases  of  ill-under- 
stood cough  and  dyspnoea,  especially  if  associated  with  progressive 
deterioration  of  health.  Radiographic  examination  may  prove  of  the 
greatest  service,  revealing  a  non-expansile  tumor  mass.  The  greatest 
diflBculty  is  experienced  in  differentiating  aneurysm  of  the  aorta  (page 
501). 

Prognosis. — Death  usually  ensues  within  six  or  eight  months  of  the 
onset  of  symptoms. 

Treatment. — The  treatment,  as  a  rule,  is  symptomatic.  Attempts 
to  remove  the  growth  have  been  made  and  with  success  in  tumors  of 
the  thymus,  and  dermoid  cysts. 


SECTION   VIII. 
DISEASES  OF  THE  DICIESTIVE  SYSTEM. 


DISEASES  OF  THE   MOUTH. 
STOMATITIS. 

Although  different  varieties  of  stomatitis  are  described,  they  are  much 
related  etiologically,  and  in  many  cases  they  represent  different  stages 
of  the  same  anatomical  process.  Thus,  a  catarrhal  stomatitis  fre- 
quently proceeds  to  the  formation  of  vesicles  and  superficial  erosion 
(aphthous  stomatitis),  and  this  in  turn  to  a  well-defined  ulceration 
(ulcerative  stomatitis).  Thrush,  to  which  (although  incorrectly)  the 
term  parasitic  or  mycotic  stomatitis  is  sometimes  restricted,  is  a 
catarrhal  stomatitis  associated  with  a  growth  of  Saccharomyces 
(Oidium)  albicans.  Gangrenous  stomatitis,  however,  although  in 
some  respects  allied  to  the  milder  forms  of  stomatitis,  is  probably  a 
more  or  less  independent  affection. 

Etiology. — Stomatitis  may  occur  at  any  age,  but  is  more  frequent  in 
poorly  nourished  and  marantic  children.  Its  development  is  much 
favored  by  insanitary  surroundings,  inattention  to  the  hygiene  of  the 
mouth,  mouth-breathing  in  patients  affected  with  adenoids,  and  general 
debility  from  any  cause.  It  is  frequently  associated  with  and  follows 
inflammation  of  adjacent  structures,  such  as  the  nose,  pharynx,  and 
especially  the  gastro-intestinal  tract.  The  exciting  causes  are  either 
infectious,  toxic,  mechanical,  or  thermic. 

Infectious  stomatitis  may  arise  as  a  primary  or  a  secondary  process. 
As  a  secondary  process  it  is  common  in  certain  of  the  infectious  diseases, 
such  as  measles,  scarlatina,  influenza,  typhoid  fever,  smallpox,  syphilis, 
etc. ;  it  occurs  also  in  the  debility  of  old  age,  as  well  as  in  the  adynamia  of 
carcinoma,  tuberculosis,  profound  anemia,  etc.  A  specific  bacterial 
cause  has  not  been  isolated,  but  it  is  probable  that  many  of  the  more 
common  bacteria  which  have  been  found  in  association  with  the  lesions, 
such  as  pneumococci,  staphylococci,  streptococci,  the  tyiihoid  bacillus, 
influenza  bacillus,  the  causative  factors  of  measles  and  of  scarlatina, 
certain  leptothrix,  etc.,  are  answerable  in  different  cases.  A  special 
variety  of  stomatitis,  thrush,  to  which,  although  incorrectly,  the  term 


588  DISEASES   OF   THE  MOUTH 

parasitic  or  mycotic  stomatis  is  sometimes  restricted,  is  associated  with 
infection  of  the  mouth  by  Saccharomyces  (Oidium)  albicans,  an  organ- 
ism which,  because  of  its  polymorphism,  has  been  described  under  a 
variety  of  names.  Infection  with  this  organism  is  usually  preceded  by 
catarrhal  stomatitis,  so  that  the  disease  is  probably  the  consequence  of 
mixed  infection.  It  occurs  most  commonly  in  infants,  but  also,  especially 
as  a  terminal  infection,  in  old  age,  tuberculosis,  diabetes,  carcinoma,  etc. 
Its  development  is  facilitated  by  mouth  breathing  and  the  restricted 
movements  of  the  tongue,  so  common  in  adynamic  patients,  which 
favor  the  lodgement  and  growth  of  the  fungus.  Infection  may  be  trans- 
mitted directly,  as  by  infected  nipples,  but  it  is  usually  acquired  by 
inhalation.  Further  evidence  of  the  infectious  nature  of  some  cases  of 
stomatitis  is  found  in  the  fact  that  a  form  of  the  disease,  usually  ulcera- 
tive in  character,  sometimes  prevails  epidemically  in  insanitary  jails, 
tenements,  asylums,  barracks,  camps,  etc.  Rarely  foot-and-mouth 
disease,  aphthse  epizooticse,  affect  the  buccal  mucous  membrane  of 
human  beings.  Some  observers  have  maintained  that  the  causative 
factor  of  ulcerative  stomatitis  in  human  beings  is  allied  to  that  causing 
foot-and-mouth  disease  in  cattle — infection  being  transmitted  with  the 
milk;  others,  such  as  Payne,  have  suggested  that  the  organism  is  allied 
to  that  of  impetigo  contagiosa. 

Toxic  stomatitis  results  from  the  ingestion  of  irritant  and  corrosive 
poisons,  such  as  strong  acids  and  alkalies;  from  the  excessive  and  pro- 
longed use  of  alcohol,  tobacco,  strong  condiments,  etc.;  and  sometimes 
from  the  medicinal  or  other  use  of  mercury,  arsenic,  lead,  the  iodides, 
the  bromides,  etc. 

Mechanical  stomatitis  sometimes  attends  the  irruption  of  the  teeth  in 
infants  and  children;  it  frequently  results  from  the  irritation  caused  by 
sharp  foreign  bodies,  broken  and  carious  teeth,  the  too  vigorous  cleansing 
of  the  teeth  and  mouth,  etc.  It  is  frequently  associated  with  the  conse- 
quences of  inattention  to  the  teeth  and  the  resulting  accumulation  of 
filth,  decomposing  food,  bacteria,  incrustations,  etc. — whence  it  is  partly 
infectious  in  nature. 

Thermic  stomatitis  results  from  the  ingestion  of  overheated  food  and 
drink,  as  well  as  from  burns  due  to  other  causes. 

Pathology. — In  mild  cases  of  stomatitis  the  lesions  are  those  of  catarrhal 
inflammation  in  general — swelling,  hyperemia,  increase  of  secretion,  and 
later  some  desquamation  of  the  superficial  epithelium.  In  some  cases  the 
inflammation  may  extend  to  the  submucous  tissues  and  give  rise  to  thick- 
ening, oedema,  and  induration.  In  more  severe  cases,  in  addition  to  the 
hyperemia,  there  are  localized  areas  of  round-cell  infiltration  which  lead 
to  the  formation  of  papules  and  later  vesicles;  these,  losing  their  epi- 
thelial covering,  produce  circumscribed  whitish  patches  with  slightly 
elevated  edges,  from  which  within  a  short  time  well-defined  erosions — 
aphthse — develop.  In  more  severe  cases  the  lesions  proceed  to  ulceration 
— superficial  necrosis  with  roimd-cell  infiltration.  In  thrush  the  mucous 
membrane  is  the  seat  of  catarrhal  inflammation,  upon  which,  in  conse- 


STOMATITIS  589 

quence  of  the  development  of  Saceharomvces  (Oidium)  alhicaii.s,  small 
whitish  spots  resembling  curdled  milk  and  about  the  size  of  a  pin's  head 
develop.  The  fungus  develops  just  beneath  the  uppermost  layers  of  the 
surface  epithelium,  having  first  penetrated  the  cement  substance  of  the 
most  superficial  cells,  which  in  consequence  of  the  growth  become  the  seat 
of  pressure  atrophy.  The  fungus  rarely  penetrates  to  the  deeper  layers, 
but  it  has  been  known  to  reach  the  lymphatics  and  even  the  bloodvessels, 
and  thus  gain  access  to  distant  parts  of  the  body,  such  as  the  brain,  etc. 
The  whitish  patches,  consisting  of  the  fungus,  desquamated  and  degen- 
erated epithelium,  and  debris,  if  removed  early  may  leave  a  somewhat 
raw  surface,  but  having  existed  for  several  days,  they  may  be  removed 
with  ease  and  leave  an  almost  if  not  quite  intact  mucous  membrane.  Of 
discrete  growth  at  first,  the  fungus  later  may  spread  to  all  parts  of  the 
oral  and  nasal  cavities,  and  even  to  the  pharynx,  larynx,  oesophagus,  and 
gastro-intestinal  tract. 

Symptoms. — Clinically,  the  following  varieties  of  stomatitis  may  be 
distinguished:  (1)  Catarrhal;  (2)  aphthous;  (3)  ulcerative;  (4)  mem- 
branous; and  (5)  thrush. 

Catarrhal  stomatitis  (simple  stomatitis,  erythematous  stomatitis, 
pultaceous  stomatitis)  is  characterized  by  local  pain  (burning  sensations), 
heat,  redness,  and  swelling,  especially  of  the  lips,  gums,  and  tongue.  The 
tongue  exhibits  indentations  caused  by  the  teeth,  and  its  swollen  papillae 
may  be  visible  through  a  thick  grayish  or  yellowish  coating.  The  swollen 
oral  mucous  membrane  often  presents  distended  mucous  follicles.  The 
oral  secretions,  at  first  lessened,  soon  become  much  increased  and  are 
often  irritating  and  acid,  occasioning,  especially  in  children,  erythem- 
atous areas  about  the  angles  of  the  mouth.  Together  with  decom- 
posing remnants  of  food,  desquamated  and  degenerating  epithelium, 
leptothrix,  and  other  bacteria,  which  collect  about  the  teeth  as  well 
as  on  the  dorsum  of  the  tongue,  they  give  to  the  breath  a  fetid  odor. 
There  are  unpleasant  sensations  of  taste,  thirst  for  cool  drinks  is  marked, 
and  suckling  and  mastication  are  painful.  General  symptoms  are  rare, 
except  perhaps  in  young  children,  in  whom  restlessness  and  slight  fever 
may  occur.  Usually  the  disease  runs  its  course  in  from  five  to  seven 
days.  Occasionally,  however,  especially  in  alcoholic  subjects  and  inor- 
dinate smokers,  the  lesions  tend  to  become  subacute  or  chronic.  In 
these  cases,  the  mucous  membrane  of  the  mouth  becomes  dark  bi-own- 
ish  red  in  color,  somewhat  thickened  and  opacjue  in  scattered  areas, 
and  sometimes  fissures  develop.  The  subjective  symptoms  are  usually 
slight. 

Aphthous  stomatitis  (follicular  stomatitis,  vesicular  stomatitis, 
herpetic  stomatitis)  is  characterized  by  the  development  of  small  super- 
ficial erosions  or  ulcerations  (2  to  4  mm.  in  diameter)  surrounded  by  a 
reddish  inflammatory  zone.  The  symptoms  are  those  of  catarrhal 
stomatitis,  which  is  usually  also  ])resent,  but  the  local  j)aiii  is  perhaps  more 
severe.  Aphtluv  may  come  out  singly  or  in  a  grouj);  usually  all  ap|)ear 
within  hventv-foui-  liours.     They  are  most  numerous  on  tlic  tip  mid  ('(jgcs 


590  DISEASES  OF  THE  MOUTH 

of  the  tongue,  and  the  inner  aspects  of  the  Hps  and  cheeks;  they  are  rare 
on  the  pharynx.  They  appear  as  small  vesicles,  which,  usually  within 
twenty-four  hours,  rupture,  leaving  an  erosion  with  a  grayish  base  and  a 
slightly  elevated  edge.  Within  twenty-four  or  thirty-six  hours  this 
becomes  quite  sharply  defined  and  surrounded  by  a  narrow  but  distinct 
inflammatory  zone.  At  this  time  they  are  quite  painful,  and  although 
suggesting,  they  differ  from,  ordinary  ulceration  in  the  absence  of  sup- 
puration. Rarely  from  confluence  a  large  ulcer  is  formed.  The  general 
symptoms  consist  of  restlessness  and  slight  fever  or  merely  an  aggrava- 
tion of  the  symptoms  of  the  primary  disorder — usually  gastro-intestinal 
catarrh.  The  disease  commonly  runs  its  course  in  less  than  a  week, 
although  occasionally  it  is  protracted  by  successive  crops  of  aphthae, 
or  by  extension  of  the  lesions  to  the  fauces  and  pharynx. 

Ulcerative  stomatitis  (fetid  stomatitis,  putrid  sore  mouth,  phleg- 
monous stomatitis,  phagadenic  stomatitis,  stomacace)  is  a  form  of  stom- 
atitis characterized  by  the  development  of  ulceration.  The  cases  vary 
much  in  severity,  from  the  mildest  to  those  with  extensive  and  wide- 
spread destruction  of  tissue,  implicating  sometimes  the  bone.  The 
mildest  cases  may  begin  as  a  catarrhal  or  herpetic  stomatitis,  proceed  to 
ulceration,  and  soon  result  in  recovery.  A  single  small,  so-called  simple 
ulcer,  is  by  no  means  uncommon  on  the  mucous  membrane  of  the  lips 
and  cheeks,  especially  in  gastro-intestinal  derangements,  and  also  it  is 
said  in  nursing  women.  More  severe  lesions  sometimes  occur  in  the 
course  of  certain  infective  diseases,  such  as  measles,  scarlatina,  typhoid 
fever,  pertussis,  etc.,  especially  in  debilitated  and  emaciated  children; 
they  are  common  in  scorbutus;  they  sometimes  appear  during  the 
course  of,  and  sometimes  as  the  initial  manifestation  of,  leukemia;  and 
they  not  infrequently  follow  the  administration  of  metallic  poisons,  such 
as  mercury,  lead,  arsenic,  phosphorus,  as  well  as  iodine,  bromine,  etc. 
Certain  severe  cases  often  appear  epidemically,  especially  in  insanitary 
jails,  tenements,  asylums,  barracks,  camps,  etc.  The  development  of  the 
affection  is  much  favored  by  poor  and  insufficient  food,  inattention  to 
the  hygiene  of  the  mouth,  the  presence  of  carious  teeth,  and  the  winter 
season.  A  specific  cause  seems  likely,  but  it  has  not  yet  been  isolated, 
although  it  has  been  said  to  be  allied  to  the  cause  of  foot-and-mouth 
disease  of  cattle  and  to  the  cause  of  impetigo  contagiosa. 

The  disease  begins  at  the  margin  of  the  gums,  usually  near  the  molar 
teeth,  but  especially  about  a  carious  tooth.  The  gums  become  red, 
swollen,  oedematous  and  painful;  they  bleed  readily,  and  frequently 
retract,  thus  exposing  the  teeth  to  the  point  of  insertion  in  the  jaw.  The 
lesions  spread  to  the  adjacent  cheek  and  sometimes  the  lip,  and  the 
mucous  membrane  becoming  necrotic  leads  to  the  formation  of  a  more 
or  less  extensive  sphacelus  and  ulceration.  In  severe  cases  mucopuru- 
lent matter  collects  beneath  the  gums  and  gives  rise  to  a  very  extensive 
sloughing,  the  exposed  teeth  loosen  and  may  drop  out,  and  inflammation 
and  necrosis  of  the  bone  may  result.  In  addition  to  the  ulceration  there 
is  catarrhal  and  aphthous  inflammation  of  the  oral  mucous  membrane, 


STOMATITIS  591 

profuse  salivation,  extremely  foul  breath,  enlargement  of  the  regional 
lymph  nodes,  gastro-intestinal  derangements,  moderate  fever  (102°  F.), 
etc.  In  some  cases  evidence  of  sepsis,  including  an  erythematous  (measly) 
rash,  leukocytosis,  sweats,  etc.,  develop,  and  the  patient  emaciates 
rapidly.  The  majority  of  cases  run  their  course  in  from  a  week  to  ten 
days,  and  terminate  in  recovery.  Certain  severe  cases,  however,  result 
fatally. 

In  mercurial  stomatitis  (ptyalism),  in  addition  to  the  inflammation 
of  the  mucous  membrane  of  the  mouth,  there  is  also  inflammation  of  the 
salivary  glands.  The  disease  begins  with  a  metallic  taste  and  soreness 
of  the  teeth  on  closing  them  vigorously.  These  are  soon  followed  by 
increased  flow  of  saliva  and  tenderness  and  sponginess  of  the  gums. 
The  tongue  becomes  swollen  and  flabby,  the  breath  foul,  the  regional 
glands  enlarged,  and  mastication  and  deglutition  difficult  and  painful. 
Should  the  mercury  not  be  stopped,  well-developed  ulceration  and  necro- 
sis, with  loosening  and  eventual  falling  of  the  teeth  and  necrosis  of  the 
bone,  may  ensue. 

Various  other  forms  of  ulcerative  stomatitis  have  been  described. 
Thus,  Riga's  disease  (Riga's  aphtha),  common  in  Southern  Italy  and 
sometimes  occurring  epidemically  in  young  (especially  marantic) 
children  about  the  time  of  irruption  of  the  first  teeth  (lower  incisors), 
consists  of  the  development  of  a  grayish  induration,  proceeding  to  ulcera- 
tion, situated  at  the  frenum  of  the  tongue.  A  similarly  situated  ulcera- 
tion sometimes  occurs  in  pertussis  from  the  forcible  projection  of  the 
tongue  against  the  lower  incisor  teeth  during  the  paroxysms  of  coughing. 
Bednar's  aphthae  (aphthae  of  the  palate)  which  sometimes  occur  in  young 
marantic,  especially  bottle-fed  babies,  consist  of  grayish  patches  of  super- 
ficial necrosis  proceeding  to  ulceration  of  both  halves  of  the  posterior  part 
of  the  hard  palate  near  the  alveolar  processes.  It  is  usually  looked  upon 
as  a  pressure  necrosis  with  subsequent  bacterial  infection,  occasioned  by 
the  nipple  or  the  nurse's  finger.  Jacobi  has  described  a  chronic  neurotic 
stomatis,  in  some  respects  akin  to  pemphigus  vegetans,  occurring  in 
neurotic  individuals  with  hereditary  predispositions,  and  characterized 
by  recurring  attacks  of  herpetic,  sometimes  pemphigoid,  eruption. 
Parrot  has  described  a  form  of  ulcerative  stomatitis  occurring  in  debili- 
tated, newly  born  children,  and  consisting  of  small  ulcers  situated  sym- 
metrically on  both  sides  of  the  hard  palate,  frequently  chronic,  and  tend- 
ing to  increase  in  size  and  involve  the  bone.  Lemaistre  has  described, 
under  the  term  la  perleche,  a  condition  consisting  of  painful  fissures  and 
elevations  at  the  angles  of  the  mouth,  occurring  epidemically,  due  to  a 
micrococcus,  and  running  its  course  in  two  or  three  weeks. 

Membranous  stomatitis  (croupous  stomatitis)  is  characterized  by 
the  formation  of  a  false  membrane.  It  is  usually  diphtheritic  in  char- 
acter and  due  to  the  Klebs-I^oeffler  bacillus;  but  it  sometimes  results 
from  the  action  of  streptococci,  staphylococci,  goiiococci,  or  Treponema 
pallidum.  The  local  and  constitutional  symptoms  are  usually  those  of 
diphtheria. 


592     .  DISEASES  OF  THE  MOUTH 

Thrush  (parasitic  stomatitis,  mycotic  stomatitis,  soor,  muguet)  fs  a 
form  of  stomatitis  due  to  Saccharomyces  (Oidium)  albicans,  and  char- 
acterized by  the  development  of  small  whitish  spots  which  tend  to 
coalesce  and  spread  more  or  less  extensively  throughout  the  oral  cavity. 

The  disease  begins  usually  on  the  dorsum  of  the  tongue,  the  saccha- 
romyces, consisting  of  branching  filaments,  developing  in  the  superficial 
layers  of  the  mucosa,  and  giving  rise  to  small  whitish  spots  that  are 
slightly  elevated.  As  the  spots  become  old,  they  tend  to  become  dis- 
colored, yellowish,  and  brownish.  The  lesions  of  catarrhal  and  of 
aphthous  stomatitis  are  usually  associated,  but  the  mouth  is  dry  and  the 
oral  secretions  usually  lessened.  The  general  symptoms  are  inconspicu- 
ous, and  scarcely  differ  from  those  of  catarrhal  or  of  aphthous  stomatitis, 
although  perhaps  gastro-intestinal  derangements,  especially  diarrhoea, 
are  more  common.  The  disease,  however,  occurring  in  the  course  of 
other  diseases,  is  frequently  overlooked  on  account  of  the  absence  of 
local  symptoms.  Under  appropriate  treatment  it  is  usually  curable 
within  two  weeks,  but  it  sometimes  runs  a  protracted  course. 

Diagnosis. — The  diagnosis  of  the  different  varieties  of  stomatitis  is 
usually  quite  obvious  from  an  inspection  of  the  mouth.  Thrush  should 
not  be  mistaken  for  milk  curds  nor  for  aphthous  or  ulcerative  stomatitis, 
from  which,  it  is  distinguished  by  the  absence  of  pain  and  erosion  or 
ulceration,  and  the  presence  of  dryness  of  the  mouth  and  the  specific 
fungus. 

Prognosis. — The  prognosis  is  good,  at  least  as  regards  the  lesions  in  the 
mouth.  The  diseases  with  which  the  stomatitis  is  frequently  associated, 
however,  often  terminate  fatally,  the  stomatitis  being  a  local  terminal 
infection. 

Treatment. — Prophylaxis  is  much  more  important  than  treatment  as 
such.  The  hygiene  of  the  mouth  must  be  carefully  attended  to,  especially 
in  young  nursing  children  and  in  the  debilitated  of  all  ages.  The  mouth 
should  be  carefully  and  repeatedly  cleansed  with  bland  antiseptic  solu- 
tions, such  as  a  saturated  solution  of  boric  acid  in  rose  water,  to  which 
5  to  10  per  cent,  of  glycerin  may  be  added.  Should  the  disease  be 
developed  strict  cleanliness  is  imperative.  The  causative  factors  in 
each  case  must  be  corrected.  In  the  milder  cases  it  suffices  to  use  boric 
acid,  borax,  sodium  bicarbonate,  or  potassium  chlorate  (2  per  cent,  solu- 
tions) to  which  5  per  cent,  of  tincture  of  myrrh  may  be  added.  Or  one 
may  use  a  mouth  wash  of  potassium  permanganate  (1  per  cent.)  or  of 
hydrogen  peroxide  (2  to  10  per  cent.);  or  the  following: 

I^ — Thymol 5  minims  GJS 

Oil  of  eucalyptus 10  minims  0  6 

Benzoic  acid 1  dram  4  0 

Distilled  water 3  ounces       100  0 

^Miller. 

Cool  drinks  are  usually  accepted  gratefully.  Should  aphtlue  develop 
they  should  be  touched  with  the  solid  stick  of  silver  nitrate  (one  applica- 
tion of  which  usually  suffices  to  effect  a  cure),  or  a  o  per  cent,  solution  of 


GANGRENE  OF  THE  CHEEK;  NOMA  593 

silver  nitrate  may  be  used.  Potassium  chlorate  is  looked  upon  as  almost 
a  specific  in  aphthous  and  ulcerative  stomatitis.  Locally  it  may  be  used 
in  powder  form,  or  in  a  2  to  5  per  cent,  solution  as  a  mouth  wash;  inter- 
nally, 1  to  3  grains  (0.06  to  0.3  gram)  carefully  to  a  child,  10  to  20  grains 
(0.65  to  1.3  gram)  to  an  adult,  may  be  given  three  times  a  day.  The 
followino'  formula  is  serviceable: 


I^ — Potassium  chlorate 2  drams  8 

Tincture  of  iron  chloride 2  drams  8 

Camphor  water 6  ounces  200 

S. — One  tablespoonful  (15  c.c.)  four  times  a  day. 


0 
0 

0— M. 


In  very  severe  cases  of  ulcerative  stomatitis,  especially  in  such  as 
develop  epidemically,  the  patient  should  be  isolated  and  the  strictest 
antiseptic  precautions  carried  out.  The  ulcerated  surfaces  should  be 
brushed  with  silver  nitrate  (2  to  5  per  cent.). 

Patients  who  are  taking  mercury  should  use  a  potassium  chlorate  or 
potassium  permangate  or  other  antiseptic  mouth  wash.  Upon  the  devel- 
opment of  stomatitis  the  mercury  must  be  withdrawn,  the  mouth  wash 
continued,  and  a  brisk  purgative  administered — ^whereupon  most  cases 
subside  within  a  few  days.  Should  ulcers  develop  they  should  be  brushed 
with  silver  nitrate,  and  potassium  chlorate  may  be  given  internally. 
Atropine  is  often  useful  in  controlling  the  excessive  salivation. 

In  thrush,  in  addition  to  the  foregoing,  especially  cleanliness  of  the 
mouth  and  nursing  nipples,  alkaline  mouth  washes,  such  as  lime  water 
or  sodium  bicarbonate,  to  lessen  the  acidity  of  the  secretions,  and  the 
withdrawal  of  starches  and  sugars  from  the  dietary,  are  requisite. 
Locally,  boric  acid,  borax,  hydrogen  peroxide,  potassium  permanganate, 
potassium  chlorate,  or  sodium  sulphite,  may  be  used,  and  after  the  thrush 
spots  have  been  removed  the  exposed  mucous  surface  may  be  brushed 
with  silver  nitrate.  In  all  varieties  of  stomatitis,  but  especially  in  thrush, 
attention  must  be  directed  to  the  diet,  which  must  be  nourishing,  and  to 
the  general  health,  which  should  be  improved  by  bitter  tonics,  iron, 
quinine,  strychnine,  cod-liver  oil,  etc. 


GANGRENE  OF  THE  CHEEK;  NOMA. 

{Gangrenous  Stomatitis;  Cancrum  Oris.) 

Noma  is  a  rapidly  spreading  gangrene  of  the  cheek,  usually  unilateral 
and  frequently  terminating  fatally. 

Etiology. — The  disease  occurs  between  the  second  and  seventh  years 
(althougii  it  may  occur  later),  and  in  girls  rather  than  boys,  more  espe- 
cially in  tliose  debilitated  by  certain  specific  infective  diseases,  particularly 
measles  (more  than  one-half  the  cases),  pertussis,  typhoid  fever,  scar- 
latina, etc.  The  disease  is  doubtless  due  to  infection.  Recently  etio- 
logical significance  has  been  attributed  to  a  strcj)t{)thrix  described  by 
Perthes  and  Seiffert. 
38 


594  DISEASES  OF  THE  TONGUE 

Symptoms. — ^The  disease  usually  begins  insidiously,  commonly  during 
convalescence  from  measles  or  other  infective  diseases,  and  manifests 
itself  as  a  discolored  area  which  soon  becomes  necrotic,  ulcerated,  and 
malodorous,  and  about  which  there  speedily  develop,  from  within 
outward,  a  brawny  induration  and  often  widespread  oedema,  involving 
the  side  of  the  face  and  the  neck.  In  mild  cases  the  ulcer  remains  inter- 
nal; but  usually,  sometimes  within  forty-eight  or  seventy-two  hours, 
perforation,  preceded  by  marked  external  discoloration,  occurs.  Some- 
times the  gangrene  extends  to  the  lips,  chin,  even  the  eyes  and  ears,  and 
may  involve  the  bone.  The  adjacent  bloodvessels  being  thrombosed, 
hemorrhage  is  rare,  but  the  gangrenous  area  is  surrounded  by  an  in- 
flammatory zone.  The  regional  lymph  nodes  are  moderately  enlarged, 
but  local  pain  is  not  marked.  The  general  symptoms  are  usually  severe : 
high  fever  (104°  F.  or  more),  rapid  pulse,  extreme  prostration,  low  mut- 
tering delirium,  etc.  Diarrhoea  is  common,  and  may  be  associated  with 
colitis.  Death  usually  ensues  at  the  end  of  about  a  week,  from  toxemia 
or  aspiration  bronchopneumonia. 

Diagnosis. — The  diagnosis  is  usually  unmistakable.  Some  confusion 
with  malignant  pustule  (anthrax)  may  arise,  but  the  previous  history 
of  the  case  is  different;  malignant  pustule  is  more  common  in  adults, 
begins  on  the  outside  of  the  cheek,  and  the  anthrax  bacillus  may  be 
detected  in  the  local  lesions  and  in  the  blood.  Diphtheria  may  be 
readily  differentiated  by  isolating  the  bacillus.  Ulcerative  stomatitis 
can  scarcely  be  confused  with  gangrene,  except  perhaps  in  the  earliest 
stages. 

Prognosis. — ^The  prognosis  is  bad,  the  mortality  rate  being  70  to  90  per 
cent.;  a  few  patients  recover  with  extensive  cicatrization  and  deformity. 

Treatment. — ^The  treatment  is  usually  unavailing.  The  disease  is  often 
far  advanced  before  discovered.  The  gangrenous  area  must  be  removed 
preferably  with  the  actual  cautery,  or  with  fuming  nitric  acid  or  the 
knife.  The  best  results  are  likely  to  be  achieved  by  the  use  of  the 
actual  cautery  before  gangrene  has  supervened.  Subsequently  strict 
antisepsis  must  be  maintained,  and  the  patient  supported  by  concen- 
trated nutritious  food  and  stimulants.  I  have  seen  diphtheria  antitoxin 
do  temporary  good  in  one  case  occurring  in  typhoid  fever,  from  which 
the  diphtheria  bacillus  was  isolated. 


DISEASES  OF  THE  TONGUE. 

Glossitis. — Glossitis,  or  inflammation  of  the  parenchyma  of  the  tongue, 
is  a  rare  affection,  although  inflammation  of  the  lingual  mucous  mem- 
brane is  commonly  a  part  of  stomatitis. 

Acute  or  parenchymatous  glossitis  results  usually  from  injuries,  or 
infections,  or  intoxications,  such  as  mercury,  the  bites  of  insects,  etc. 
The  lesions,  which  may  be  unilateral,  especially  in  the  beginning,  are 
those  common  to  inflammation  in  general;  usually  they  subside,  but 


BLACK  TONGUE  595 

they  may  go  on  to  abscess  formation.  The  symptoms  consist  of  pain 
and  extreme  swelling  of  the  tongue,  which  may  even  project  beyond  the 
teeth.  All  movements  such  as  occur  in  speaking,  chewing,  swallowing, 
even  breathing,  are  extremely  painful,  and  hence  restricted,  at  times 
almost  impossible.  Sloughing  sometimes  occurs.  There  may  be 
moderate  fever.  The  treatment  consists  in  the  local  use  of  antiseptics, 
ice,  cocaine,  etc.,  general  depurative  measures,  and  surgical  procedures, 
such  as  scarification  or  incision,  should  swelling  be  extreme  or  suppura- 
tion result. 

Chronic  glossitis,  usually  associated  with  chronic  stomatitis,  some- 
times results  from  repeated  acute  attacks,  but  especially  from  continued 
irritation  caused  by  carious  and  broken  teeth,  alcohol,  tobacco,  irritating 
food,  etc.  The  tongue  is  swollen,  reddened,  hypersensitive,  furrowed 
or  fissured,  and  unnaturally  smooth  in  circumscribed  areas,  due  to 
atrophy  of  the  papillae.  A  condition  in  which  the  fissures  and  furrows 
are  unduly  marked,  and  the  tongue  irregular  and  ragged  in  appearance 
and  painful  (on  account  of  superficial  ulcerations),  is  spoken  of  as  glossitis 
desiccans.  The  treatment  consists  of  the  avoidance  of  all  irritating  food 
and  drink,  the  use  of  antiseptic  mouth  washes,  brushing  with  silver 
nitrate  (5  per  cent.),  and  tonics. 

Eczema. — Eczema  of  the  tongue  (geographical  tongue,  ringworm 
of  the  tongue,  psoriasis  of  the  tongue,  tylosis  of  the  tongue,  wandering 
rash  of  the  tongue)  is  a  rare  affection,  of  unknown  and  doubtless  varying 
etiology,  characterized  by  superficial  hyperplasia  and  desquamation 
of  the  lingual  epithelium.  The  lesions  tend  to  heal  in  the  centre  and 
spread  at  the  margins,  giving  rise  to  irregular  circinate,  map-like  patches. 
The  disease  is  chronic,  and  occasions  only  mild  local  symptoms,  such  as 
itching.  The  treatment  consists  in  the  use  of  tonics  and  antiseptic 
mouth  washes,  the  local  application  of  silver  nitrate,  tannic  acid,  alum, 
or  potassium  chlorate. 

Leukoplakia. — Leukoplakia  of  the  tongue  (leukoplakia  oris  et  buccalis, 
leukoma,  ichthyosis  of  the  tongue,  keratosis,  smoker's  tongue)  is  a  rather 
rare  disease  of  unknown  etiology,  encountered  usually  in  inordinate 
smokers,  and  characterized  by  the  development  of  dense,  white,  some- 
what elevated  patches,  varying  in  size  and  configuration,  and  situated 
usually  on  the  tongue,  rarely  elsewhere  on  the  oral  mucous  membrane. 
Usually  smooth,  the  patches  may  become  papillomatous,  and  even 
epithelioma  may  develop.  The  condition  is  chronic.  The  treatment, 
which  is  unsatisfactory,  consists  in  the  use  of  antiseptic  mouth  washes, 
and  silver  nitrate,  chromic  acid,  or  iodine.  The  use  of  tobacco  must  be 
prohibited,  and  to  syphilitics  appropriate  treatment  should  be  given. 
Should  the  patches  become  papillomatous,  they  should  be  removed. 

Black  Tongue. — Black  tongue  (nigrities)  is  a  rare  disorder,  usually 
attributed  to  the  action  of  a  parasite,  but  by  some  observers  to  benign 
tumor  growth,  or  to  intentional  staining,  and  is  characterized  by  the 
development  of  a  blackish-brown  discoloration  of  the  dorsum  of  the 
tongue,  associated  with  elongation  of  the  papilla?.     The  treatment  con- 


596  DISEASES  OF  THE  SALIVARY  GLANDS 

sists  of  attention  to  the  general  health,  and  the  local  use  of  silver  nitrate, 
hydrogen  peroxide,  salicylic  acid,  boric  acid,  etc. 

Macroglossia. — ^Macroglossia  is  a  condition  of  enlargement  of  the 
tongue,  sometimes  found  in  akromegaly,  myxoedema,  and  cretinism, 
and  due  usually  to  a  lymphangioma,  rarely  to  muscular  hyperplasia. 
In  extreme  cases  operative  intervention  may  be  called  for. 

Acute  CEdema. — ^Acute  oedema  of  the  tongue,  usually  associated  with 
oedema  of  the  aryteno-epiglottidean  fold,  is  a  rare  manifestation  of  urti- 
caria. Though  extreme,  the  swelling  rarely  lasts  more  than  twenty- 
four  hours.  Treatment  must  be  prompt — a  drastic  purge,  scarification, 
or  leeching  of  the  tongue,  and  in  extreme  cases,  tracheotomy. 

Ranula. — Ranula  is  a  cystic  growth,  situated  on  the  under  surface  of 
the  tongue,  near  the  frenum,  and  due  to  dilatation  of  Wharton's  duct, 
or  to  enlargement  of  a  mucous  gland. 


DISEASES  OF  THE  SALIVARY  GLANDS. 

Ptyalism. — Ptyalism  (hypersecretion  of  the  salivary  glands,  salivation) 
has  already  been  mentioned  as  a  symptom  of  mercurial  stomatitis. 
It  sometimes  results  also  from  the  use  of  other  drugs,  such  as  gold, 
copper,  iodine,  tobacco,  jaborandi,  muscarin,  etc.  It  occurs  sometimes 
during  pregnancy,  rarely  during  menstruation;  it  is  occasionally  associ- 
ated with  disease  of  the  pancreas,  variola,  and  rabies;  and  it  is  not  in- 
frequent in  certain  diseases  of  the  nervous  system,  such  as  hysteria, 
insanity,  and  divers  diseases  of  the  pons  and  medulla.  The  amount 
of  saliva  is  sometimes  very  great  (four  or  five  liters),  exceeding  many  times 
the  normal  (one  to  one  and  one-half  liters).  The  treatment  is  that  of 
mercurial  stomatitis. 

Xerostomia. — Xerostomia  (hypersecretion  of  the  salivary  glands, 
dry  mouth,  aptyalism),  deficiency  or  suppression  of  the  salivary  and 
buccal  secretions,  is  a  rare  condition  of  unknown  etiology  (although 
usually  said  to  be  a  neurosis),  occurring  especially  in  neurotic  women, 
in  whom  it  follows  sudden  fright  or  shock.  The  mouth  is  unusually 
dry;  sordes  collect  on  the  teeth  and  gums;  the  tongue  may  become 
fissured;  and  the  breath  is  fetid.  The  condition  is  to  be  distinguished 
from  the  dry  mouth  of  fever  conditions,  and  that  associated  with  the 
mouth-breathing  of  adenoids.  Treatment  is  unsatisfactory,  although 
oily  applications  locally,  pilocarpin  lozenges  (y^  gi'ain,  0.004  gram) 
slowly  dissolved  in  the  mouth  several  times  daily,  and  gajvanism  locally, 
may  be  productive  of  good. 

Parotitis. — Inflammation  of  the  parotid  gland  may  develop,  (1)  as 
an  acute  specific  infective  disease — mumps  (page  260);  (2)  as  a  symp- 
tomatic aft'ection — symptomatic  parotitis,  parotid  bubo;  and  (3)  as  a 
chronic  affection. 

Acute  symptomatic  parotitis  results  from:  (1)  Infections,  such  as 
typhoid  fever,  typhus  fever,  scarlet  fever,  pneumococcic  infection,  strep- 


LUDWIG'S  ANGINA  597 

tococcic  infection  (pyemia,  erysipelas,  etc.);  (2)  disease  or  injury  of 
the  abdominal  or  pelvic  organs;  and  (3)  in  association  with  inflammation 
of  the  facial  nerve.  In  most  cases  the  disease  is  infectious,  the  infecti^■e 
agent  being  carried  through  the  blood  or  by  way  of  the  parotid  (Sten- 
son's)  duct.  The  inflammation  is  unilateral  (in  contradistinction  to 
mumps,  which  is  bilateral).  The  gland  is  swollen,  painful,  and  tender, 
especially  on  opening  the  mouth,  and  in  50  per  cent,  of  the  cases  pro- 
ceeds to  suppuration.  The  general  symptoms  are  moderate,  as  a  rule 
— malaise,  headache,  and  slight  fever.  The  treafment  consists  of 
general  depurative  measures,  and  the  local  application  of  ice,  leeching, 
lead  water  and  laudanum,  etc.  In  the  event  of  suppuration,  surgical 
measures  are  called  for. 

Chronic  parotitis  rarely  follows  mumps,  or  the  continued  use  of  mer- 
cury, potassium  iodide,  and  lead.  It  has  been  observed  in  chronic 
nephritis  and  in  syphilis.  Rare  cases  of  chronic  painless  symmetrical 
enlargement  of  both  parotid  and  lacrymal  glands  have  been  observed 
by  Mikulicz  (^Mikulicz's  disease)  and  others. 

Gaseous  Distention. — Gaseous  distention  of  the  parotid  duct  and 
gland  has  been  observed  in  glassblowers  and  musicians. 

Calculi. — Salivary  calculi  occasionally  form  in  the  parotid  duct,  and 
may  give  rise  to  distention  of  the  duct  and  enlargement  of  the  parotid 
gland. 

LUDWIG'S  ANGINA. 

Ludwig's  angina  (angina  Ludovici,  cynanche  gangrenosa)  is  a  rare 
phlegmonous  cellulitis  of  the  floor  of  the  mouth  and  of  the  neck,  com- 
monly due  to  the  streptococcus,  and  occurring  usually  as  a  complication 
of  certain  infective  diseases,  especially  scarlet  fever  and  diphtheria. 
It  occasionally  follows  local  trauma,  and  rarely  occurs  as  an  apparently 
primary  affection.  The  symptoms,  which  develop  and  progress  with 
great  rapidity,  consist  of  pain,  tenderness,  redness,  marked  swelling, 
and  induration,  arising  usually  in  the  neighborhood  of  the  submaxillary 
gland  on  one  side,  and  speedily  involving  the  floor  of  the  mouth,  the 
entire  neck,  and  even  the  upper  part  of  the  chest  wall.  The  swelling  of 
the  tissues  of  the  neck  and  an  associated  oedema  of  the  glottis  frequently 
give  rise  to  an  extreme,  alarming,  and  sometimes  fatal  dyspncKa  (asphyxi- 
ation). Extensive  sloughing  and  gangrene  are  common.  The  general 
symptoms  are  those  of  profound  sepsis  (toxemia).  Although  the  out- 
look is  extrejnely  grave,  prompt  surgical  intervention,  supportive 
measures,  and  antistreptococcic  serum  may  result  in  cure. 


598     DISEASES  OF  THE  FAUCES,   TONSILS,  AND  PHARYNX 


DISEASES  OF  THE  FAUCES,  TONSILS,  AND 
PHARYNX. 

ACUTE  TONSILLITIS. 

(.Acute  Faucitis,  Tonsillitis,  and  Pharyngitis;  Sore  Throat;  Angina.) 

Etiology. — ^Acute  tonsillitis,  usually  associated  with  faucitis  and 
pharyngitis,  may  occur  at  any  age,  but  is  most  common  in  adolescents, 
especially  rheumatic  and  scrofulous  subjects,  and  in  those  debilitated 
from  any  cause.  It  is  especially  prevalent  in  the  spring  and  the  early 
fall,  and  its  development  is  much  favored  by  insanitary  surround- 
ings. The  exciting  causes  are  infectious,  toxic,  mechanical,  or  thermic 
irritants.  Infectious  angina  may  be  primary  or  secondary.  Most 
primary  cases  bear  an  undoubted  relation  to  exposure  or  "catching 
cold."  Contrary  to  former  opinions,  this  is  now  believed  to  act  by  re- 
ducing the  resistance  of  the  tissues,  thus  permitting  the  easy  operation  of 
bacteria,  of  which  the  most  important  etiologically  are  the  streptococcus, 
the  staphylococcus,  the  pneumococcus,  the  ■  influenza  bacillus,  and  the 
pneumobacillus  (Friedlander).  Ai\  angina  is  also  an  initial  manifesta- 
tion in  certain  specific  infective  diseases,  such  as  diphtheria,  scarlet 
fever,  measles,  etc.  Secondary  infectious  anginas  are  common  in  other 
infective  diseases,  such  as  variola,  varicella,  typhoid  fever,  tuberculosis, 
syphilis,  etc.  A  form  of  infectious  angina  sometimes  prevails  epidem- 
ically, especially  in  institutions,  etc.  Toxic  anginas  result  from  the 
inhaling  of  irritant  vapors,  such  as  acids  and  alkalies;  from  the  excessive 
and  prolonged  use  of  alcohol,  tobacco,  etc. ;  and  from  the  medicinal  and 
other  use  of  mercury,  the  iodides,  etc.  Inhalation  of  hot  vapors  and 
the  ingestion  of  too  hot  food  and  drink  sometimes  provokes  acute 
angina.  An  acute  angina,  especially  acute  tonsillitis,  is  frequently 
the  initial  manifestation  of  a  systemic  infection,  the  infectious  agent 
gaining  access  to  the  general  circulation  by  way  of  the  tonsils — thus 
rheumatic  fever,  acute  endocarditis,  chorea,  influenza,  streptococcic 
infection,  tuberculosis,  syphilis,  etc.     Recurrences  are  common. 

Pathology. — The  lesions  may  involve  the  fauces,  tonsils,  and  pharynx, 
singly  or  conjointly,  and  equally  or  unequally.  In  most  cases  all  are 
more  or  less  involved.  In  mild  cases,  the  faucial  and  pharyngeal  mucous 
membrane  and  submucous  tissues  are  injected  and  swollen,  and  later 
covered  with  a  slight  amount  of  mucous  or  mucopurulent  exudate 
(catarrhal  faucitis,  tonsillitis,  or  pharyngitis;  sore  throat).  In  other  cases 
the  tonsils  present  scattered  yellowish-white  spots — distended  folHcles 
filled  with  desquamated  epithelium,  leukocytes,  granular  debris,  and 
bacteria  (follicular  tonsillitis).  Usually  the  exudate  can  be  squeezed 
from  the  follicles,  but  occasionally  several  adjacent  follicles  being  dis- 
tended, the  tonsil  appears  to  be  covered  with  a  pseudomembrane,  much 
simulating  diphtheria.     Occasionally  herpes  develop  (herpetic  tonsillitis). 


ACUTE  TONSILLITIS  599 

In  more  severe  cases  the  inflammation  involves  the  substance  of  the 
tonsil,  and  usually  one  tonsil  more  than  the  other  (parenchymatous 
tonsillitis).  The  affected  tonsil  becomes  enlarged,  sometimes  enor- 
mously swollen,  and  projects  far  beyond  the  median  line,  rendering 
phonation,  deglutition,  articulation,  and  even  respiration,  extremely 
difficult.  Usually  the  lesions  soon  proceed  to  suppuration  (suppurative 
tonsillitis,  quinsy),  and,  should  surgical  intervention  be  delayed,  the 
abscess  ruptures,  usually  through  the  free  surface  of  the  tonsil,  rarely 
through  the  soft  palate.  At  times  the  pus  may  find  its  way  into  the  tissues 
of  the  neck  or  mediastinum,  and  may  even  perforate  the  vessels  of  the 
neck.  Rarely  more  or  less  extensive  sloughing  and  subsequent  ulcera- 
tion of  the  tonsil  and  pseudomembranous  formation  occurs  (ulcerative 
tonsillitis).  The  lesions  may  extend  to  the  uvula,  soft  palate,  and  even 
the  posterior  pharyngeal  wall,  and,  when  occurring  as  a  primary  affection, 
they  are  to  be  distinguished  from  diphtheria  only  by  the  absence  of  the 
diphtheria  bacillus.  Streptococci  and  staphylococci  are  usually  present 
in  abundance. 

S3raiptoms. — Clinically  one  may  distinguish  (1)  catarrhal,  (2)  follicular, 
and  (3)  suppurative  or  phlegmonous  tonsillitis. 

Acute  catarrhal  tonsillitis,  usually  associated  with  faucitis  and  pharyn- 
gitis, is  frequently  sudden  in  onset,  with  chilliness,  sometimes  a  distinct 
chill,  and  moderate  fever.  Vomiting  may  occur  in  children.  An  initial 
sense  of  dryness  and  irritation  of  the  throat  are  soon  succeeded  by  dis- 
tinct pain,  especially  upon  swallowing,  and  a  harsh,  dry  cough.  Upon 
inspection,  the  tonsils,  fauces,  and  pharynx  are  swollen,  oedematous, 
congested,  and  covered  with  a  thin  layer  of  mucopurulent  matter,  which 
at  the  end  of  thirty-six  or  forty-eight  hours  is  usually  sufficient  to  give 
rise  to  a  small  amount  of  tenacious  sputum.  The  general  symptoms  are 
mild,  and  the  lesions  subside  within  four  or  five  days. 

Acute  follicular  (lacunar)  tonsillitis  is  a  more  severe  infection.  The 
onset  is  frequently  quite  abrupt,  with  pronounced  chill  and  high  fever — 
103.5°  F.  in  adults,  and  frequently  105°  F.  in  children.  The  faucial 
pain  and  tenderness  and  the  difficulty  in  swallowing  are  usually  marked, 
and  there  is  sometimes  tenderness  at  the  angles  of  the  jaw,  on  account 
of  moderate  swelling  of  the  regional  lymph  nodes.  On  inspection,  in 
addition  to  catarrhal  alterations  of  the  faucial  mucous  membrane,  the 
tonsillar  crypts  are  distended  with  a  characteristic  yellowish  exudate, 
which,  upon  pressure,  may  be  generally  forced  out.  The  constitutional 
.symptoms  are  often  quite  marked,  and  consist  of  high  fever,  headache, 
general  neuromuscular  pains,  depression,  loss  of  appetite,  constipation, 
etc.  A  trace  of  albumin  in  the  urine  is  not  uncommon.  The  disease 
usually  runs  its  course  in  six  or  eight  days  and  terminates  in  recovery, 
but  endocarditis,  pericarditis,  pleuritis,  erythema  nodosum,  etc.,  may 
occur  as  sequels. 

Acute  suppurative  tonsillitis  (phlegmonous  tonsillitis,  parenchymatous 
tonsillitis,  tonsillar  and  peritonsillar  abscess,  quinsy)  does  not  differ  in 
its  initial  local  and  general  symptoms  from  those  just  mentioned,  although 


600     DISEASES  OF  THE  FAUCES,   TONSILS,   AND  PHARYNX 

they  are  usually  severe.  Pain  is  pronounced,  deglutition  is  extremely 
difficult,  and  phonation  often  practically  impossible.  On  examination, 
the  tonsil  and  adjacent  tissues  are  found  extremely  swollen,  congested, 
and  oedematous.  Not  infrequently  the  tonsils  meet  in  the  median  line; 
usually  one  is  more  inflamed  than  the  other,  and  may  project  beyond 
the  median  line,  displacing  the  markedly  oedematous  uvula.  The  glands 
at  the  angles  of  the  jaw  are  usually  swollen  and  tender,  and  there  may  be 
a  notable  fulness  in  the  neck.  The  oral  secretions  are  increased,  and 
usually  dribble  from  the  mouth.  Moderate  leukocytosis  is  usually 
present.  In  mild  cases,  resolution  takes  place,  but  in  perhaps  one-half 
of  the  cases,  at  the  end  of  forty-eight  or  seventy-two  hours,  fluctuation 
may  be  detected,  and,  if  the  tonsil  be  not  incised,  a  yellowish  spot  of 
"pointing"  soon  appears  and  the  abscess  ruptures.  Usually  this  is 
attended  by  great  relief,  and  the  expectoration  of  the  pus  is  followed 
by  speedy  subsidence  of  the  inflammatory  phenomena.  Rarely,  however, 
the  rupture  occurring  during  sleep,  for  instance,  may  lead  to  suffocation; 
or  the  purulent  matter  may  burrow  into  the  tissues  of  the  neck,  and  flnd 
its  way  externally  through  the  skin,  or  even  perforate  the  great  blood- 
vessels of  the  neck;  or  oedema  of  the  glottis  may  occur.  During  the 
height  of  the  disease  the  general  symptoms  continue  well  marked,  and 
the  temperature  remains  high  (104°  F.),  the  pulse  frequent  (120  to  130 
per  minute),  and  evidences  of  toxemia  are  found  in  concentration  of 
the  urine,  slight  albuminuria,  prostration,  perhaps  delirium,  etc.  The 
lesions  usually  subside  within  ten  days. 

Diagnosis. — The  diagnosis  is  usually  unattended  by  special  difficulties. 
It  is  sometimes  difficult  to  distinguish  follicular  tonsillitis  from  diphtheria. 
In  many  cases  the  diagnosis  rests  entirely  upon  the  detection  of  the 
diphtheria  bacillus;  in  some  cases,  however,  one  may  distinguish  follicular 
tonsillitis  by  the  fact  that  the  exudate  is  yellowish,  patchy  (corresponding 
to  the  follicles),  separated  by  intervening  areas  of  congested  red  tonsillar 
tissue,  does  not  tend  to  spread  beyond  the  tonsils,  may  be  removed  with- 
out leaving  a  bleeding  surface,  and  does  not  tend  to  reform.  In  diph- 
theria, on  the  other  hand,  the  exudate  is  usually  grayish  in  color,  uniform 
and  widespread,  tends  to  extend  beyond  the  tonsils,  and  when  removed 
tends  to  reform. 

Prognosis. — ^The  prognosis  is  good.  Most  cases  result  in  recovery, 
although  recurrences  are  common,  and  hypertrophy  of  the  tonsils 
frequently  results. 

Treatment. — In  all  but  the  mildest  cases  the  patient  should  go  to  bed 
and  curtail  as  much  as  possible  all  movements  of  the  throat,  such  as 
occur,  for  instance,  in  talking,  swallowing,  etc.  The  diet  should  be 
fluid.  A  thorough  evacuation  of  the  bowels  by  a  generous  dose  of  calo- 
mel (5  grains,  0.3  gram),  allowed  to  dissolve  slowly  on  the  tongue  and 
to  mix  with  the  oral  secretions  (whereby  it  may  exert  a  local  antiseptic 
action),  and  followed  by  a  saline  is  often  of  value.  The  course  of  the 
disease  may  sometimes  be  shortened,  in  some  cases  apparently  aborted, 
by  the  early  administration  of  sodium  salicylate  or  benzoate  in  large 


CHRONIC  TONSILLITIS  601 

doses,  15  grains  (1  gram),  four  or  five  times  a  day  for  the  first  twenty- 
four  or  thirty-six  hours.  In  other  cases,  tincture  of  iron  chloride  (30 
minims,  2  c.c),  quinine  (2  grains,  0.13  gram),  with  glycerin  and  water, 
every  four  hours  for  thirty-six  hours,  seems  to  exert  a  very  beneficial 
effect.  Neither  form  of  treatment,  however,  is  of  much  value  if  begun 
when  the  disease  is  fully  developed.  In  the  case  of  children,  full  doses 
of  aconite  have  been  much  praised.  Locally,  alkaline  and  mild  anti- 
septic solutions  may  be  used — such  as  Dobell's  solution,  potassium 
permanganate  (2  per  cent.),  thymol,  alum,  etc.,  or  one  may  use  the  old- 
fashioned  ammoniated  tincture  of  guaiac,  in  water,  as  a  gargle;  or  lozenges 
of  guaiac  may  be  dissolved  slowly  in  the  mouth.  In  some  cases  good 
results  attend  the  local  application  to  the  tonsils  of  aspirin,  silver 
nitrate  (25  per  cent.),  or  tincture  of  iron  chloride,  glycerin,  and  water. 
The  comfort  of  the  patient  may  also  be  promoted  by  ice  locally  to  the 
throat  and  dissolved  in  the  mouth,  by  the  inhalation  of  medicated  steam 
(with  compound  tincture  of  benzoin),  and  by  the  administration  at  night 
of  a  Dover's  powder  (10  grains,  0.6  gram). 

In  extreme  swelling,  especially  of  one  tonsil,  such  as  portends  suppura- 
tion, early  scarification  will  relieve  the  local  pain  and  distress.  Incision 
should  be  practised  as  soon  as  fluctuation  is  apparent,  even  suspected. 
Cocaine  (2  to  5  per  cent.),  menthol  (2  per  cent,  in  albolene),  and  hot, 
rather  than  cold,  applications  are  also  of  service. 

During  convalescence,  the  patient  requires  a  nourishing  diet  and 
tonics,  such  as  iron,  quinine,  and  strychnine;  or  Basham's  mixture  and 
strychnine.  Should  the  tonsil  remain  permanently  enlarged  (chronic 
tonsillitis),  appropriate  treatment  must  be  instituted. 


CHRONIC   TONSILLITIS. 

(Enlcn-ged  Tonsils;  Hypertrophied  Tonsils;  Adenoid  Vegetations;  Chronic  Naso- 
pharyngeal Obstruction;  M outh-hreathing ;  Aprosexia.) 

Chronic  tonsillitis,  in  which  the  tonsils  frequently  become  markedly 
enlarged,  is  usually  associated  with  hyperplastic  alterations  of  the 
adenoid  tissue  of  the  pharynx  (pharyngeal  tonsil,  Luschka's  tonsil). 
The  condition  is  of  extreme  importance,  since  it  not  only  occasions 
nasopharyngeal  obstruction  and  consequent  mouth-breathing,  but  it 
exerts  considerable  deleterious  influence  on  the  physical  and  mental 
development  (aprosexia)  of  its  victims — mostly  children. 

Etiology. — Hypertrophy  of  the  tonsils  and  pharyngeal  adenoids  are 
most  common  between  the  ages,  of  five  and  fifteen  years.  They  occur  in 
both  sexes,  but  probably  aft'ect  boys  more  than  girls,  especially  children 
of  tuberculous  and  syphilitic  parents,  and  those  who  are  poorly  nourished 
and  live  amidst  unhvffienic  surroundings.  The  affection  often  dates 
from  an  acute  attack  of  tonsillitis,  simple,  diphtheritic,  or  scarlatinous. 

Pathology. — The  lesions  are  those  of  true  hypertrophy  of  the  tonsillar 
constituents — in  most  cases,  especially  of  the  lymplioid  tissue,  in  other 


602     DISEASES  OF  THE  FAUCES,   TONSILS,  AND  PHARYNX 

cases,  of  the  stroma.  In  the  first  the  tonsils  are  much  enlarged  (twice 
or  thrice  the  normal  size),  irregular  and  rough  on  the  surface,  and 
exhibit  distended  and  ruptured  follicles.  Although  both  tonsils  are 
usually  involved,  the  process  may  be  asymmetrical.  In  the  event  of 
marked  hyperplasia  of  the  stroma,  the  tonsils  are  smaller  and  much 
firmer.  The  pharyngeal  adenoids  usually  project  from  the  pharyngeal 
vault,  growing  from  the  fossa  of  Rosenmiiller — a  depression  on  the 
posterior  pharyngeal  wall  between  the  Eustachian  orifices.  They 
consist  of  adenomatous  papillomatous  growths,  and  vary  in  size  from 
2  to  3  mm.  to  2  to  3  cm.;  they  are  reddish  in  color,  very  vascular, 
and  moderately  firm.  There  is  usually  an  associated  chronic  nasal 
catarrh;  the  hard  palate  is  often  unusually  high,  and  the  alveolar  arch 
small. 

Symptoms. — Minor  forms  of  chronic  tonsillitis  (with  hypertrophy) 
may  exist  with  no  noteworthy  symptoms.  Sooner  or  later,  however, 
there  is  interference  with  nasal  respiration,  and  mouth-breathing  de- 
velops. Although  present  during  the  day,  this  is  noticed  especially 
during  the  night,  when  the  breathing  is  loud  and  snoring  and  frequently 
inte;rrupted — ^whence  night  terrors  arise.  Coughing  is  sometimes  pro- 
voked by  lying  down.  The  mouth  is  dry  and  the  breath  foul  from 
decomposition  of  the  exudate  in  the  tonsillar  crypts.  Characteristic 
physical  and  mental  changes  soon  occur.  In  general  the  child  is  of 
stunted  growth — attributed  by  some  authors  to  the  embryological  rela- 
tionship between  the  tissues  of  the  pharynx  and  the  pituitary  body. 
The  mouth  is  usually  open,  the  expression  becomes  vacant,  the  bridge 
of  the  nose  depressed,  the  malar  prominences  ill  developed,  the  lips 
thick,  the  hearing  defective  (on  account  of  obstruction  to  the  Eustachian 
orifices,  or  extension  of  disease  along  the  Eustachian  tubes),  the  voice 
nasal,  and  articulation  indistinct  and  sometimes  stammering.  The 
so-called  pigeon-chest,  or  chicken-chest,  frequently  develops,  especially 
in  rachitic  children.  In  some  children  with  recurring  asthmatic  attacks 
a  typical  barrel-shaped  or  emphysematous  chest  may  develop.  Rarely  a 
funnel-chest  (Trickterbrust)  has  been  observed.  In  advanced  cases, 
marked  changes  in  mentality  occur.  The  child  is  listless,  backward, 
forgetful,  and  seems  unable  to  control  his  attention  (aprosexia).  He 
is  sometimes  morose  and  irritable,  and  complains  of  headache.  He  is 
usually  weakly,  anemic,  and  has  a  poor  appetite,  and  is  prone  to 
recurring  attacks  of  follicular  tonsillitis,  diphtheria,  scarlet  fever,  etc. 

Diagnosis. — The  affection  is  often  disclosed  by  the  facial,  physical, 
and  mental  characteristics  of  the  child.  The  tonsillar  changes  are 
quite  apparent  upon  inspection  of  the  throat,  but  the  detection  of  the 
pharyngeal  lesions,  which  may  exist  without  noteworthy  tonsillar  changes, 
may  require  a  rhinoscopic  or  digital  examination. 

Prognosis. — Although  the  disease  scarcely  endangers  life,  it  is  of 
much  significance  in  shaping  the  physical  and  mental  characteristics, 
and  the  bad  habits  and  general  stunting  that  it  occasions  are  sometimes 
not  outgrown  in  later  life. 


ULCERATION  OF  THE  PHARYNX  603 

Treatment. — In  mild  cases  of  chronic  tonsillitis  the  local  application 
of  iodine  and  glycerin,  Liigol's  solution  of  iodine  and  potassium  iodide, 
tincture  of  iron  chloride  and  glycerin,  tannin,  silver  nitrate,  etc.,  may 
prove  useful.  In  general,  however,  the  wise  course  is  to  removfe  the 
enlarged  tonsils  with  a  tonsillotome  or  galvanocautery,  or  by  careful 
dissection.  In  all  cases  the  pharyngeal  adenoid  should  be  immediately 
removed,  with  a  curette  or  a  finger,  even  should  the  child  as  yet  not 
present  the  facial  and  mental  characteristics  of  the  disease,  which  will 
surely  develop  in  the  course  of  time.  Attention  to  the  general  health, 
by  suitable  dress,  fresh  air,  nutritious  food,  tonics,  cod-liver  oil,  syrup 
of  iron  iodide,  etc.,  is  imperative. 


PHARYNGITIS. 

Acute  pharyngitis,  occurring  independently  of  acute  tonsillitis,  is 
unusual,  but  is  sometimes  the  lesion  in  an  ordinary  "sore  throat." 
The  symptoms  and  treatment  are  those  outlined  under  acute  tonsillitis. 

Chronic  pharyngitis  in  children  is  associated  with  hypertrophy  of 
the  tonsils.  In  adults  it  is  usually  part  of  a  chronic  nasopharyngeal 
catarrh;  it  follows  repeated  acute  attacks,  and  occurs  especially  in  alco- 
holic subjects,  inordinate  smokers,  and  in  those  who  use  the  voice  much 
and  injudiciously,  such  as  clergymen  (clergymen's  sore  throat),  public 
speakers,  singers,  hucksters,  etc.  Several  varieties  have  been  distin- 
guished: (1)  Chronic,  simple,  or  hypertrophic  nasopharyngeal  catarrh; 
(2)  chronic  atrophic  pharyngitis  (pharyngitis  sicca),  usually  associated 
with  atrophy  of  the  nasal  mucous  membrane;  and  (3)  follicular  or  granu- 
lar pharyngitis.  All  three  varieties  are  sometimes  irregularly  associated. 
There  is  usually  relaxation  of  the  faucial  and  pharyngeal  mucous 
membrane,  marked  venous  enlargement,  and  a  varying  amount  of 
hyperplastic  lymphoid  tissue  about  the  raucous  follicles.  The  symp- 
toms are  a  constant  sense  of  dryness  and  irritation  in  the  throat,  inter- 
fering with  speaking  and  singing,  and  more  or  less  persistent  "hawking." 
In  the  treatment  it  is  important  to  correct  the  cause— prohibit  smoking 
and  alcohol,  and  the  too  prolonged  and  vigorous  use  of  the  voice,  etc. 
The  subjective  symptoms  may  be  relieved  by  different  mild  antiseptic 
lotions  or  lozenges,  and  by  the  local  use  of  silver  nitrate  (2  to  5  per  cent.). 
Areas  of  glandular  hypertrophy  should  be  removed  by  the  galvano- 
cautery.    The  general  health  should  be  maintained. 


ULCERATION  OF  THE  PHARYNX. 

Ulceration  of  the  pharynx  occurs  under  a  variety  of  circumstances. 
The  only  noteworthy  symptom  is  pain,  especially  upon  deglutition,  but 
it  varies  much  in  different  cases.  Follicular  iilceratioii  is  common  in 
chronic  catarrh — the  ulcer  being  small  and  superficial.     Syphilitic  ulcers 


604     DISEASES  OF  THE  FAUCES,   TONSILS,  AND  PHARYNX 

are  usually  associated  with  mucous  patches  or  evidences  of  syphilis 
elsewhere  on  the  body;  they  are  comparatively  painless,  superficial 
(unless  the  consequence  of  softening  of  a  gumma),  fairly  regular  in  out- 
line, and  respond  readily  to  antisyphilitic  treatment.  Tuberculous  ulcers 
are  common  in  the  later  stages  of  tuberculosis,  are  exquisitely  painful, 
grayish  yellow  in  color,  and  irregular  in  outline.  Rarely  the  infectious 
atrium  in  tuberculosis  may  be  about  the  tonsil  and  take  the  form  of  an 
ulcer.  In  diphtheria  and  scarlet  fever,  superficial  ulceration  is  not 
uncommon.  Ulceration  occurs  also  in  lupus,  in  typhoid  fever,  variola, 
carcinoma,  etc. 


Acute  infectious  phlegmon  of  the  pharynx,  is  a  term  used  by  Senator 
to  designate  a  rare  condition  in  which  the  pharynx  and  the  tissues  of 
the  neck  in  general  become  the  seat  of  an  intense  inflammation  that 
rapidly  progresses  to  suppuration.  The  swelling  and  inflammatory 
oedema  may  be  so  marked  as  to  interfere  with  respiration.  The 
general  symptoms  are  those  of  sepsis.  A  suppurative  or  phlegmonous 
pharyngitis  may  also  follow  trauma,  or  suppurative  tonsillitis,  or  be 
associated  with  erysipelas.     The  treatment  is  surgical  and  supportive. 

Retropharyngeal  abscess  is  a  suppurative  inflammation  of  the  post- 
pharyngeal connective  tissues.  It  is  common  in  childhood,  especially 
before  the  end  of  the  second  year,  but  it  occurs  also  in  adults.  In  children 
it  frequently  arises  as  an  apparently  primary  infection,  the  infectious 
agent  gaining  access  through  any  of  the  lymphoid  tissues  of  that  region; 
it  sometimes  follows  diphtheria  and  scarlet  fever.  In  children  and  in 
adults  it  may  follow  caries  of  the  vertebrae.  The  symptoms,  although 
referred  to  the  throat,  are  not  characteristic.  The  diagnosis  is  quite 
apparent  upon  inspection  and  digital  examination  of  the  throat,  although 
it  may  be  overlooked  on  account  of  the  bulging  of  the  postpharyngeal 
wall  being  high  up.  The  treatment  consists  of  free  evacuation  of  the 
pus,  which  should  be  done  promptly,  or  the  patient  may  suffocate. 

Elongation  of  the  uvula,  although  frequently  imaginary  and  occasion- 
ally congenital,  sometimes  results  from  repeated  attacks  of  faucial  in- 
flammation, and  may  occur  in  conditions  of  malnutrition.  By  irritating 
or  tickling  the  throat  on  lying  down,  it  may  excite  a  reflex  cough,  or  rarely 
spasm  of  the  glottis.  The  treatment  consists  in  excision,  should  the 
measures  indicated  under  chronic  tonsillitis  not  suffice. 

The  lingual  tonsils  sometimes  share  in  inflammatory  and  other  dis- 
eases of  the  throat.  Occasionally  they  are  markedly  involved,  either 
alone  or  in  association  with  disease  of  contiguous  tissues,  and  they 
occasion  pain  and  a  feeling  of  fulness  and  discomfort  at  the  base  of  the 
tongue,  and  a  reflex  cough.  Occasionally  they  become  hypertrophied 
and  interfere  with  the  actions  of  the  epiglottis.  The  treatment  is  similar 
to  that  of  tonsillitis. 


ULCERATION  OF  THE  (ESOPHAGUS  605 

DISEASES  OF  THE  CESOPHAGUS. 

Acute  CEsophagitis. — Etiology. — CEsophagitis  may  be  due  to  in- 
fective, toxic,  mechanical,  or  thermic  irritants.  Infective  oesophagitis 
occurs  in  a  mild  or  catarrhal  form  in  many  of  the  infective  diseases,  and 
at  times  as  an  extension  of  inflammation  from  the  mouth  and  throat. 
Severer  pseudomembranous  forms  sometimes  occur  in  diphtheria,  thrush, 
pneumonia,  pyemia,  etc.,  a  pustular  form  may  occur  in  smallpox. 
Toxic  oesophagitis  may  follow  the  ingestion  of  strong  acids  and  alkalies; 
a  chronic  form  is  sometimes  observed  in  those  that  use  much  alcohol  or 
tobacco.  Mechanical  oesophagitis  may  result  from  the  irritation  pro- 
duced by  foreign  bodies.  Thermic  oesophagitis  may  follow  the  taking 
of  overheated  food  or  drink. 

Pathology. — The  lesions  vary  much  in  difl^erent  cases,  and  may  be 
described  as  catarrhal,  ulcerative,  pseudomembranous,  pustular,  phleg- 
monous, and  gangrenous.  They  exhibit  no  characteristics  that  dis- 
tinguish them  from  similar  lesions  occurring  elsewhere,  except  that 
rarely  in  the  pseudomembranous  form  casts  of  the  oesophagus  may  be 
formed  and  perhaps  expelled. 

Symptoms. — ^lild  oesophagitis  may  occasion  no  symptoms.  Usually 
there  is  substernal  pain,  which  is  much  aggravated  by  swallowing;  in 
some  cases  with  marked  lesions,  however,  there  may  be  little  or  no  pain 
except  on  swallowing.  In  severe  forms  due  to  corrosive  poisons,  swallow- 
ing may  be  impossible.  In  some  cases,  especially  in  the  event  of  a 
foreign  body  being  present,  attempts  at  swallowing  occasion  spasm  and 
regurgitation  of  food.  In  severe  cases,  mucus,  sometimes  blood  and 
pus,  are  ejected,  and  the  patient  emaciates.  A  stricture  usually  follows 
the  oesophagitis  due  to  corrosive  poisons. 

Treatment. — The  treatment  is  unsatisfactory.  In  the  mild  cases 
demulcent  drinks  and  ice  water  may  be  given.  Silver  nitrate  in  solution 
and  weak  solutions  of  cocaine  may  prove  beneficial,  especially  in  allaying 
pain.  In  severe  cases,  feeding  by  the  mouth  should  be  substituted  by 
enemas. 

Chronic  (Esophagitis. — Chronic  oesophagitis  may  result  from  an  acute 
attack,  or  from  the  long-continued  action  of  alcohol,  tobacco,  and  other 
irritants.  The  mucous  membrane  becomes  thickened  and  sometimes 
markedly  rugous.  The  symptoms  are  more  or  less  substernal  pain, 
especially  on  swallowing,  and  perhaps  regurgitation  of  food  and  mucus. 
The  treatment  is  similar  to  that  of  acute  oesophagitis. 

Ulceration. — Ulceration  of  the  oesophagus  may  occur:  (1)  As  a  part 
of  acute  oesophagitis;  (2)  occasionally  in  cachectic  states;  (3)  in  typhoid 
fever,  when  it  may  be  followed  by  cicatricial  stenosis,  and  in  syphilis; 
(4)  in  malignant  disease;  (5)  in  consequence  of  pressure,  as  by  an  aneu- 
rysm; and  (6)  as  the  counterpart  of  the  round  or  peptic  ulcer  of  the 
stomach.  The  treatment  of  the  condition,  which,  however,  is  rarely 
recognized,  is  that  of  a  causative  factor,  or  of  gastric  ulcer. 


606  DISEASES  OF  THE  (ESOPHAGUS 

Varices. — ^Varices  of  the  oesophagus,  usually  situated  at  the  lower 
end  of  the  gullet,  and  somethnes  of  enormous  size,  may  occur  in  cirrhosis 
of  the  liver  and  in  chronic  heart  disease.  The  mucous  membrane  is 
the  seat  of  chronic  inflammation,  and  the  patient  may  eject  considerable 
mucus,  but  usually  the  condition  is  not  recognized  until  a  large,  and 
sometimes  fatal,  hemorrhage  occurs. 

Rupture. — ^Rupture  of  the  oesophagus  rarely  results  from  the 
excessive  strain  of  prolonged  vomiting,  or  from  weakness  of  the  wall 
due  to  an  ulcer. 

Dilatation. — Dilatation  of  the  oesophagus  is  rare.  Exceptionally  it 
is  primary — ^w^hen  it  is  usually  congenital,  but  it  is  said  to  have  developed 
in  consequence  of  weakness  and  dilatation  of  the  wall.  In  most  cases 
the  dilatation  is  secondary  to,  and  develops  above,  a  constriction.  The 
dilatation  may  be  fusiform  or  cylindrical.  The  chief  symptoms  are 
dysphagia,  regurgitation  of  food,  and  loss  of  weight  from  insufficient 
nourishment.  The  chief  aid  in  the  diagnosis  results  from  radiographic 
examination  after  the  injection  of  bismuth  or  iron  oxide  pastes.  When 
the  patient  can  no  longer  get  food  into  the  stomach,  he  may  be  assisted 
with  the  stomach  tube.  Eventually  rectal  enemas  and  possibly  gas- 
trostomy will  be  demanded. 

Diverticula. — Diverticula  of  the  oesophagus  (pharyngoceles)  are  of 
three  kinds:  (1)  Congenital.  (2)  Pressure  or  pulsion  diverticula,  which 
are  rare,  arise  from  pressure  within  the  oesophagus  (the  swallowing  of  large 
boluses  of  food),  are  usually  situated  on  the  posterior  wall  of  the  pharynx 
at  the  junction  of  the  pharynx  and  oesophagus,  are  rarely  long,  and  occur 
usually  in  adults.  (3)  Traction  diverticula,  which  are  not  so  rare,  arise 
from  external  traction  of  the  oesophageal  wall  (contraction  of  a  cicatrix  fol- 
lowing inflammation  of  a  mediastinal  lymph  node),  are  usually  situated 
on  the  anterior  wall  of  the  oesophagus  at  the  bifurcation  of  the  trachea, 
are  usually  quite  short,  and  occur  usually  in  children.  Traction  diver- 
ticula rarely  occasion  symptoms.  Pressure  diverticula  when  large  may 
give  rise  to  dysphagia,  fetor  of  the  breath  (on  account  of  decomposition 
of  retained  food  particles,  etc.),  nausea,  vomiting,  and  rarely  a  bulging 
on  one  side  of  the  neck.  The  diagnosis  is  best  made  by  radiographic 
examination  after  the  injection  of  bismuth  or  iron  oxide  pastes. 

Spasm. — Spasm  of  the  oesophagus  (oesophagismus,  spasmodic 
stricture  of  the  oesophagus)  is  observed  in  neurotic,  especially  hysterical, 
subjects,  and  is  more  common  in  women,  although  it  occurs  in  men. 
It  is  sometimes  present  during  pregnancy,  epilepsy,  chorea,  and  hydro- 
phobia. The  attack  may  develop  suddenly,  being  provoked  by  violent 
emotional  or  other  excitement.  The  chief  complaint  is  of  inability  to 
swallow  food,  sometimes  even  liquids  being  rejected.  An  oesophageal 
bougie  may  be  passed — sometimes  immediately,  sometimes  after  waiting 
a  little  for  the  spasm  to  relax  and  exerting  slight  pressure.  This  of 
itself  may  effect  a  lasting  cure.  The  condition  is  readily  recognized,  as 
a  rule,  but  in  elderly  subjects  care  must  be  taken  not  to  overlook  malignant 
stricture.    The  neurotic  basis  of  the  condition  demands  treatment. 


CARCINOMA   OF  THE  (ESOPHAGUS  607 

Paralysis.— Paralysis  of  the  oesophagus  occurs  in  certain  diseases  of  the 
nervous  system,  functional  (hysteria)  as  well  as  organic  (bulbar  paralysis, 
general  paresis,  diphtheritic  paralysis,  etc.).  The  main  sym'ptom  is 
dysphagia;  usually  also  there  are  regurgitation  of  food  and  emaciation. 

Stenosis. — Stenosis  (organic  stricture)  of  the  oesophagus  may  be 
congenital  or  acquired.  Acquired  stenosis  may  be  due  to:  (1)  Swelling 
and  thickening  of  the  oesophageal  wall,  such  as  is  occasioned  by  inflam- 
matory (especially  phlegmonous)  swellings,  tumors,  etc.;  (2)  cicatriza- 
tion of  ulcers  produced  by  corrosive  poisons,  syphilis,  typhoid  fever, 
diphtheria,  and  the  peptic  or  round  ulcer,  etc. ;  and  (3)  external  pressure 
produced  by  an  aneurysm,  pericardial  effusion,  mediastinal  tumors, 
enlarged  lymph  nodes,  goitre,  etc.  Stenosis  is  more  common  in  males 
than  in  females.  It  may  occur  anywhere  throughout  the  oesophagus, 
but  is  more  common  in  the  lower  third  or  the  upper  third.  It  may  be 
moderate  or  extreme,  and  annular  or  vertical,  and  if  vertical,  it  may 
involve  a  small  portion  or  almost,  if  not  quite,  all  of  the  oesophagus. 
The  symptoms  consist  of  gradually  increasing  dysphagia  and  regurgita- 
tion of  food.  At  first  there  is  perhaps  mere  discomfort  on  swallowing, 
but  later  sometimes  inability  to  swallow  even  liquids.  Regurgitation 
of  food  follows  immediately,  or  after  a  short  time,  depending  upon  the 
situation  of  the  stenosis.  When  the  stenosis  is  near  the  stomach  and  the 
oesophagus  is  dilated,  the  delay  in  regurgitating  the  food  may  suggest 
that  it  has  been  vomited,  but  its  alkalinity  and  the  absence  of  gastric 
odor  disprove  this.  Hunger  and  thirst  are  usually  marked  and  anemia 
and  emaciation  soon  develop.  The  dilatation  and  degree  of  the  stenosis 
may  be  determined  by  the  use  of  radiography  or  an  oesophageal  bougie, 
or  by  cesophagoscopy.  It  is  said  also  that  in  the  event  of  stricture, 
auscultation  over  the  eighth  or  ninth  thoracic  vertebra  will  reveal  a 
deglutition  murmur  (when  the  patient  swallows),  longer  than  the 
normal  seven  seconds.  The  treatment  in  benign  cases  consists  in  gradual 
dilatation  with  bougies.  In  some  cases  a  tube  has  been  inserted  and 
left  in  situ  indefinitely,  the  patient  being  fed  through  it.  Gastrostomy 
may  be  resorted  to  in  malignant  cases,  as  well  as  in  some  that  follow 
corrosive  poisons. 

Carcinoma. — Carcinoma  of  the  oesophagus  occurs  especially  in 
men  beyond  the  fortieth  year.  It  is  usually  situated  in  the  middle  and 
lower  thirds,  especially  at  the  bifurcation  of  the  trachea.  It  usually 
develops  from  the  surface  epithelium  (squamous-cell  variety),  rarely 
from  the  cells  of  the  mucous  glands  (adenocarcinoma).  It  usually 
encircles  the  oesophagus,  occasioning  an  annular  constriction,  and 
it  may  extend  throughout  a  considerable  portion  of  the  oesophagus. 
Above  the  growth  the  oesophagus  usually  dilates  and  its  wall  hyper- 
trophies. As  a  rule,  the  carcinoma  soon  ulcerates,  and  a  considerable 
portion  of  the  necrotic  tissue  may  be  vomited,  thus  increasing  the  lumen 
again.  Metastasis  to  the  regional  lymph  nodes  and  to  the  nodes  just 
above  the  clavicle,  as  well  as  extension  to  adjacent  tissue  (the  mediastinum, 
lung,  pleura,  pericardium,  vertebrie,  etc.),  are  common,  and  perforation  of 


60S  DISEASES   OF   THE  STOMACH 

a  bronchus,  or  the  aorta,  etc.,  is  not  unknown.  The  symptoms  consist  of 
substernal  pain  or  discomfort,  gradually  increasing  dysphagia,  regurgi- 
tation of  food,  and  progressive  emaciation  with  the  development  of  the 
cancerous  cachexia.  The  regurgitated  material  is  frequently  fetid, 
and  may  contain  blood  and  pus  from  ulceration,  and  sometimes  portions 
of  the  carcinoma  itself.  The  development  of  certain  pressure  symp- 
toms, such  as  paralysis  of  the  recurrent  larvmgeal  nerve,  oculopupillary 
phenomena,  or  a  bronchial  cough  in  association  with  oesophageal  symp- 
toms, are  of  extreme  diagnostic  importance.  The  affection  must  be 
differentiated  from  pressure  from  without,  as  by  an  aneurysm,  and  until 
this  be  excluded  the  oesophageal  bougie  should  not  be  used.  The 
bougie  may  dislodge  a  portion  of  the  growth,  examination  of  which 
will  facilitate  the  diagnosis.  The  treatment  is  merely  supportive  and 
palliative,  as  the  disease  is  usually  fatal  within  a  year.  Gastrostomy  is 
sometimes  of  service. 


DISEASES  OF  THE  STOMACH. 

Pathological  Physiology. — ^The  stomach,  the  most  widely  dilated 
portion  of  the  digestive  tract,  has  an  average  capacity  in  the  adult  of 
about  1600  c.c.  (Ewald),  with  a  normal  maximum  of  about  2000  c.c. 
It  is  designed  for  the  reception,  at  one  time,  of  a  considerable  amount 
of  food  and  to  effect  certain  digestive  and  other  changes  in  this  food 
so  as  to  render  it  suitable  for  further  alterations  in  the  intestine.  The 
important  changes,  aside  from  the  digestive,  that  the  food  undergoes 
in  the  stomach,  comprise  its  conversion  into  a  more  or  less  fluid  consist- 
ency, its  being  brought  to  a  proper  temperature  (since  the  intestine 
is  more  sensitive  to  temperature  variation,  especially  cold,  than  the 
stomach),  and  its  partial  sterilization  by  free  hydrochloric  acid. 

The  chief  functions  of  the  stomach  are  secretory  and  motor  in  nature. 
The  secretory  activity  is  expressed  in  the  gastric  juice,  which  results 
from  the  influence  of  psychic  and  chemical  stimuli.  ^lechanical  stimuli, 
as  a  rule,  induce  only  an  increased  secretion  of  alkaline  mucus,  which 
is  designed  primarily  to  protect  the  lining  of  the  stomach  from  mechanical 
insults;  the  frec|uent  repetition  of  these  insults  (bolting  of  large  masses 
of  unchewed  and  non-insalivated  food)  by  irritating  the  stomach  and 
impeding  digestion,  may  ultimately  lead  to  chronic  gastritis.  The 
psychic  stimuli  that  promote  the  secretion  of  gastric  juice  comprise  the 
pleasurable  sensations  of  the  sight,  odor,  and  anticipation  of  food, 
often  enhanced  by  agreeable  companions  and  other  environment — all  of 
which  suffice,  even  when  the  stomach  is  empty,  to  inaugurate  a  flow 
of  gastric  juice — of  appetite  juice  as  Pawlow  has  expressed  it.  The 
chemical  stimuli  comprise  the  chemical  constituents  of  certain  foods 
and  condiments,  such  as  hors  d'anivre,  meat  extracts  represented  in 
soups,  other  proteins,  etc.  The  customary  arrangement  of  the  courses 
at  dinner  thus  finds  justification  in  the  normal  physiological  activities 


DISEASES  OF  THE  STOMACH  609 

of  the  stomach.  Starches  and  other  carbohydrates  (later  courses  at 
dinner)  do  not  promote  any  noteworthy  flow  of  gastric  juice;  they  are, 
therefore,  indicated  in  cases  of  excessive  gastric  secretion,  whereas  the 
aforementioned  excitors  of  gastric  juice  are  indicated  in  cases  of  deficient 
secretion;  and  it  is  a  matter  of  common  knowledge  that  an  invalid  with 
poor  appetite  can  be  made  to  eat  and  to  digest  by  such  environment 
as  well  arranged  and  tastefully  served  food.  The  secretion  of  gastric 
juice  begins  usually  before  food  has  entered  the  stomach  and  it  continues, 
as  a  rule,  for  an  hour  or  two  thereafter,  whereupon  it  gradually  lessens. 
Variations  in  this,  however,  are  common,  being  due  to  individual  pecu- 
liarities, the  amount  and  character  of  the  food,  etc.,  and  in  diseased 
states  too  much  or  too  little  gastric  juice  may  be  secreted — ^hypersecre- 
tion and  h}^osecretion,  respectively. 

The  normal  gastric  juice  is  a  thin,  colorless  (or  almost  colorless) 
fluid;  it  has  a  characteristic  odor,  is  strongly  acid  in  reaction,  and  has 
a  specific  gravity  of  1002  to  1003.  Its  essential  constituents  are  hydro- 
chloric acid,  pepsin  (a  proteolytic  enzyme),  rennin  (lab-ferment,  a  milk- 
curdling  enzyme),  and,  in  small  amount,  lipase  (a  fat-splitting  enzyme); 
in  addition,  mucin,  inorganic  salts,  and  water  are  found.  The  hydro- 
chloric acid  is  a  product  of  certain  so-called  border  or  cover  cells  present 
in  the  fundic  glands,  which  are  especially  numerous  in  the  midportion 
or  prepyloric  region  of  the  stomach.  Normally  hydrochloric  acid  is 
present  in  the  gastric  juice  in  the  proportion  of  0.3  per  cent.,  although 
it  may  reach  higher  values.  Expressed  in  terms  of  the  amount  in  cubic 
centimeters  of  decinormal  sodium  hydrate  solution  required  to  neutralize 
it  (the  method  commonly  employed  in  clinical  work),  the  free  hydro- 
chloric acid  content  of  the  gastric  juice  normally  varies  between  20  and 
40  per  hundred  (which  figures  multiplied  by  0.00365  give  the  actual 
hydrochloric  acid  percentage).  The  total  acidity  of  the  gastric  juice, 
that  is,  the  free  hydrochloric  acid,  plus  the  combined  hydrochloric  acid, 
acid  salts,  and  organic  acids,  normally  varies  between  30  and  50,  with 
60  as  a  normal  maximum.  These  values  may  be  notably  increased  or 
decreased  in  disease,  and  hydrochloric  acid  may  be  entirely  absent 
(see  secretory  disorders). 

Pepsin,  the  proteolytic  enzyme  of  the  stomach  that  breaks  down 
proteins  into  albumoses  and  peptones,  is  active  only  in  an  acid  medium ; 
and  since  pepsinogen  or  propepsin  is  activated  by  the  hydrochloric 
acid,  the  acidity  of  the  gastric  juice  and  peptic  activity  usually  run 
parallel.  At  all  events  if  the  hydrochloric  acid  of  the  gastric  juice  is 
normal  or  increased,  it  is  usually  unnecessary  to  determine  the  peptic 
activity.  In  chronic  gastritis  with  subacidity  the  peptic  activity  may 
be  lessened;  but  even  in  this  event  if  the  mobility  of  the  stomach  remains 
effective  the  patient  may  suffer  no  noteworthy  ill  consequences.  Rennin 
(lab-ferment,  milk-curdling  enzyme)  is  sometimes  found  deficient 
or  absent  in  achylia  gastrica,  certain  forms  of  chronic  gastritis,  car- 
cinoma, etc.  Lipase  (fat-splitting  enzyme)  also  may  be  found  absent 
in  like  circumstances. 
39 


610  DISEASES  OF  THE  STOMACH 

As  food  is  taken  into  the  stomach,  it  is  received  in  the  fundus,  the  chief 
function  of  which  is  to  act  as  a  reservoir,  gradually  to  mix  the  gastric 
juice  with  the  food,  and  to  pass  the  mixed  food  on  to  the  pyloric  portion 
of  the  stomach.  The  later  portions  of  a  large  meal  are  received  into  the 
mid-portion  of  the  mass  of  food  already  in  the  stomach;  and  since  the 
movements  of  the  fundus  are  not  very  active,  contact  with  the  gastric 
juice  is  only  gradually  effected  and  salivary  digestion  thus  may  continue 
for  some  time.  The  pyloric  end  is  separated  from  the  rest  of  the  stomach 
by  a  more  or  less  well-defined  muscular  band,  which  serves  to  prevent 
mixing  of  the  food  in  these  two  portions  of  the  organ.  Food  is  gradually 
received  into  the  pyloric  portion  through  the  intermediation  of  a  pre- 
pyloric (pre-antral)  or  middle  portion,  the  seat  of  regularly  recurring 
contractions  (every  fifteen  or  twenty  seconds).  In  the  pylorus  the 
muscular  movements  are  much  more  active  than  elsewhere;  here  the 
food  is  finely  comminuted,  converted  into  a  more  or  less  fluid  consist- 
ency, intimately  comingled  with  the  gastric  juice,  and  passed  on  to  the 
duodenum.  The  cause  of  the  movements  of  the  stomach  has  not  been 
definitely  determined;  they  have  been  ascribed  to  the  hydrochloric  acid, 
but  since  they  occur  in  the  entire  absence  of  hydrochloric  acid,  it  is  not 
unlikely  that  they  are  due  to  the  presence  of  the  food  itself;  they  seem 
to  be  myogenic  in  origin,  but  they  are  doubtless  under  the  control  of 
the  nervous  system.  The  intermittent  opening  of  the  pylorus  and  the 
discharge  of  the  gastric  contents  into  the  duodenum  also  have  been 
attributed  to  the  hydrochloric  acid,  and  the  closing,  to  the  alkalinity  of 
the  duodenum  (Cannon).  Doubtless  this  is  a  factor,  but  not  the  sole 
factor,  since  it  occurs  in  the  absence  of  hydrochloric  acid  and  h}"per- 
chlorhydria  appears  to  be  an  important  factor  in  producing  pylorospasm. 
Disorders  of  the  motility  of  the  stomach  are  discussed  under  a  separate 
heading. 

SYMPTOMATIC  DISORDERS  OF  THE  STOMACH. 

Disorders  of  the  functions  of  the  stomach,  notably  epigastric  pain, 
nausea,  and  vomiting,  are  the  natural  consecjuence  of  definite  anatomical 
lesions  of  the  stomach  of  the  most  diverse  nature,  and  as  such  they  are 
usually  recognized  and  correctly  referred  to  a  more  or  less  obvious  cause. 
In  other  cases,  they  are  manifestations  of  disease  of  adjacent  or  other 
abdominal  viscera,  especially  the  gall-bladder,  the  duodenum,  the 
pancreas,  the  vermiform  appendix,  and  the  intestine  (obstruction); 
in  other  cases  they  are  due  to,  or  are  part  and  parcel  of,  some  general 
neurosis,  such  as  hysteria  or  neurasthenia;  whereas  in  other  cases,  the 
gastric  symptoms  seem  to  be  due  entirely  to  some  perversion  of  the  func- 
tional activity  of  the  gastric  nervous  mechanism,  and  are  not  associated 
with  discoverable  anatomical  lesions;  in  other  words,  the  condition 
is  a  neurosis. 

The  Appetite. — Loss  or  impairment  of  appetite  (anorexia)  is  a  sjTuptom 
of  the  most  diverse  disorders.    It  is  common  in  all  diseases  of  the  stomach. 


SYMPTOMATIC  DISORDERS  OF  THE  STOMACH  611 

although,  on  the  contrary,  even  serious  diseases  of  the  stomach  may  exist 
with  httle  or  no  impairment  of  the  appetite.  Anorexia  is  a  character- 
istic symptom  of  the  chronic  alcoholic  subject  (chronic  gastritis),  and 
is  common  in  many  dyspeptics  who,  for  one  reason  or  another,  have 
gradually  but  progressively  restricted  their  dietary.  Furthermore,  the 
appetite  is  impaired  in  all  fever  states,  in  debilitated  conditions  (carci- 
noma, tuberculosis,  prolonged  suppuration),  in  anemic  states  (chlorosis, 
pernicious  anemia),  in  nervous  disorders,  such  as  hysteria,  and  following 
grip,  worry,  excitement,  etc.,  and  it  may  itself  be  a  neuroses  (nervous 
anorexia).  Increase  of  appetite  (boulimia)  is  common  in  convalescents 
from  acute  infectious  diseases,  especially  typhoid  fever;  it  occurs  in 
certain  cases  of  diabetes;  in  pertussis  (on  account  of  the  large  amount 
of  food  often  lost  by  vomiting) ;  in  certain  cases  of  gastritis  (after  the 
anorexia  passes  away);  and  it  is  a  manifestation  of  certain  neurotic  condi- 
tions (see  sensory  disorders  of  the  stomach). 

Thirst. — Increased  thirst  is  a  common  symptom  of  the  most  diverse 
disorders.  It  is  found  especially  during  the  summer  and  after  profuse 
sweating;  in  all  febrile  states;  in  xerostomia  (dry  mouth),  arrest  of 
salivary  secretion;  in  many  diseases  of  the  stomach,  especially  in  those 
attendedby  much  vomiting;  in  diseases  of  the  intestines  characterized  by 
profuse  watery  discharges  (certain  diarrhoeas,  cholera,  hemorrhage,  etc.); 
and  in  diabetes.  Persistent,  increased  thirst  should  suggest  diabetes  and 
lead  to  appropriate  examinations.  The  contrary  condition,  absence  of 
thirst,  sometimes  more  apparent  than  real,  is  found  in  some  adynamic 
febrile  disorders  attended  by  stupor,  especially  typhoid  fever.  In  view 
of  its  importance,  large  amounts  of  water  should  be  given  to  such 
patients. 

Flatulence. — The  presence  of  an  excessive  amount  of  gases  in  the 
stomach  may  be  due  to  several  factors:  (1)  It  may  be  due  to  the  intake 
of  air  when  eating  (aerophagia).  This  is  very  common,  and  occurs 
especially  in  those  who  eat  rapidly  and  bolt  their  food;  and  in  nervous 
and  hysterical  subjects.  The  gases  are  largely  those  of  the  atmosphere, 
oxygen  and  nitrogen.  (2)  It  may  be  due  to  gases  taken  with  the  food 
and  drink — carbonated  waters  and  wines,  beers,  etc.  (3)  It  may 
result  from  fermentation  of  the  food,  which  is  likely  to  occur  in  the 
event  of  a  deficiency  or  an  absence  of  free  hydrochloric  acid,  and  when 
the  food  is  retained  for  some  time  in  the  stomach,  especially  in  passive 
congestion,  chronic  catarrhal  gastritis,  carcinoma  and  dilatation  of  the 
stomach,  etc.  In  these  cases  one  may  find  not  only  oxygen  and  nitro- 
gen, but  also  sulphuretted  hydrogen,  carbon  dioxide,  and  aromatic 
products  of  acetic,  lactic,  butyric,  and  other  forms  of  fermentation. 
(4)  It  is  a  common  symptom  in  many  cases  of  pylorospasm,  often  associ- 
ated with  hyperchlorhydria.  The  condition  is  manifested  by  epigastric 
distress,  pain,  and  distention;  the  pain  may  be  quite  severe  and  even 
colicky  in  nature.  Relief  follows  belching  of  the  gas.  The  treatment 
must  be  based  upon  the  etiological  factors;  and  comprises  also  the 
exclusion  of  fermentable  foods,  especially  milk,  buttermilk,  potatoes, 


612  DISEASES  OF  THE  STOMACH 

rare  meat,  etc.,  and  the  use  of  antifermentatives  mentioned  under  the 
different  types  of  chronic  gastritis,  dilatation  of  the  stomach,  etc. 

Nausea  and  Vomiting. — Nausea  and  vomiting  are  exceedingly 
common  symptomatic  complaints,  and  may  be  due  to  many  causes. 
Usually  they  occur  together,  the  nausea  preceding  the  vomiting,  but 
either  may  occur  alone — the  most  distressing  and  persistent  nausea  with 
inability  to  vomit,  and  sudden  vomiting  without  antecedent  nausea. 

Etiology. — ^Vomiting  may  be  due  to:  (1)  Disease  of  the  stomach;  (2) 
disease  of  the  abdominal  viscera;  (3)  disease  of  the  nervous  system;  (4) 
intoxications;  (5)  reflex  disturbances;  and  (6)  it  may  occur  as  a  pure 
neuroses. 

1.  The  diseases  of  the  stomach  occasioning  vomiting  are  acute  and 
chronic  catarrh,  perigastric  adhesions,  ulcer,  carcinoma,  and  dilatation. 
The  vomiting  of  acute  gastritis  is  often  related  immediately  to  the  etio- 
logical factor,  and  is  accompanied  by  epigastric  pain  and  nausea.  The 
vomited  matter  consists  first  of  the  gastric  contents  (which  may  reveal 
the  cause  of  the  attack),  then  mucus,  and  later  bile;  sometimes  it  is 
streaked  with  blood.  Vomiting  is  a  conspicuous  feature  of  some  cases 
of  chronic  gastric  catarrh,  and  usually  occurs  in  from  one-half  to  one  and 
one-half  or  two  hours  after  eating.  The  vomited  matter  consists  of  partly 
digested  food  and  mucus,  which,  being  ejected,  usually  relieves  the  at- 
tendant epigastric  distress  and  nausea.  Vomiting  is  common  in  ulcer 
of  the  stomach,  often  occurs  immediately  on  taking  food,  but  may  be 
delayed  for  two  hours  or  thereabout;  usually  it  relieves  the  pain  which  the 
taking  of  food  may  provoke,  but  it  possesses  no  especial  diagnostic  signifi- 
cance unless  accompanied  by  hematemesis.  Vomiting  is  rarely  missed 
in  carcinoma  of  the  stomach,  but  possesses  no  characteristic  features, 
unless  it  is  persistently  of  the  "  coffee-ground"  characters.  In  dilatation 
of  the  stomach,  vomiting  is  common;  it  occurs  several  hours  after  taking 
food,  or  at  intervals  of  several  days,  is  profuse,  and  contains  stagnant 
and  putrefying  food. 

2.  Disease  of  other  abdominal  viscera  is  a  common  cause  of  vomiting 
often  believed  to  be  due  to  disease  of  the  stomach,  especially  cholecystitis 
with  or  without  cholelithiasis,  disease  of  the  duodenum,  pericholecystic, 
periduodenal,  and  pericolonic  adhesions,  acute  and  chronic  pancreatitis, 
appendicitis,  inflammatory  and  obstructive  disorders  of  the  intestine, 
acute  and  chronic  peritonitis,  etc. 

3.  Diseases  of  the  nervous  system  frequently  give  rise  to  vomiting, 
especially  (a)  meningitis  (with  or  without  hydrocephalus),  brain  tumor, 
brain  abscess,  and  embolism,  thrombosis,  or  hemorrhage;  (b)  errors  of 
refraction  (especially  astigmatism)  and  of  muscle  balance,  and  Meniere's 
disease;  (c)  locomotor  ataxia — gastric  crisis;  and  (d)  hysteria. 

4.  Intoxications  are  a  common  cause  of  vomiting,  of  which  the  most 
important  are  the  acute  infectious  diseases,  such  as  scarlet  fever,  yellow 
fever,  smallpox,  etc.;  exogenous  intoxications,  such  as  ptomaine  poison- 
ing, acute  alcoholism,  sewer-gas  poisoning,  apomorphine,  ipecac,  ether, 
chloroform,  and  other  drug  intoxications,  etc.;  and  autogenic  intoxica- 


SYMPTOMATIC  DISORDERS  OF  THE  STOMACH  613 

tions,  such  as  the  toxemia  of  pregnancy,  uremia,  or  cholemia  (diseases 
of  the  hver),  acid  intoxications  that  accompany  diabetes  and  the  cyhc 
vomiting  of  children  associated  with  ketonuria,  aberrant  gout,  etc. 

5.  Reflex  vomiting  is  common  and  due  to  a  wide  variety  of  causes, 
such  as  disease  of  any  of  the  thoracic  or  abdominal  viscera,  those  already 
mentioned  as  well  as  renal  colic,  gallstone  colic,  intestinal  colic,  unpleas- 
ant odors,  sights,  or  thoughts  (in  some  neurotic  subjects),  etc. 

Vomiting  without  nausea  is  found  in  certain  disorders  of  the  brain, 
such  as  tumor  or  abscess  and  premonitory  to  apoplexy,  in  uremia  and 
other  autogenic  poisonings,  in  hysteria,  and  as  a  neurosis  of  the  stomach. 

The  vomit  consists  at  first  of  the  contents  of  the  stomach.  In  catarrh 
there  is  often  undigested  food,  and  there  is  often  much  mucus.  The 
vomiting  of  watery  fluid  and  mucus  occurs  also  in  certain  nervous  dis- 
orders. Bile  in  the  vomit  (bilious  vomiting)  occurs  after  repeated  and 
violent  vomitings,  and,  as  a  rule,  has  no  other  significance,  but  occasion- 
ally when  appearing  independently  of  repeated  vomiting  efforts  it  is  a 
precursor  of  fecal  vomiting.  Fecal  (stercoraceous)  vomiting  is  significant 
of  intestinal  obstruction,  but  has  rarely  been  observed  in  other  conditions, 
such  as  gastrocolic  fistula,  and  even  in  neurotic  conditions.  Purulent 
vomiting  occurs  in  phlegmonous  gastritis,  or  after  rupture  of  an  abscess 
into  the  stomach  or  oesophagus.  Profuse  vomiting  occurs  in  gastric 
dilatation.  Parasites  are  occasionally  observed  in  the  vomit.  Blood 
is  of  frequent  occurrence,  and  of  varying  significance. 

Hematemesis  (Gastrorrhagia;  Hemorrhage  from  the  Stomach). — 
Etiology. — Hematemesis  is  of  common  occurrence  and  of  varying 
import.  The  general  causes,  alike  to  those  that  occasion  hemorrhage 
from  the  intestine,  are  such  as  determine  hemorrhage  in  other  parts  of 
the  body — purpura,  scurvy,  malignant  (or  hemorrhagic)  forms  of  certain 
specific  infections  (smallpox,  yellow  fever,  cholera,  malaria,  measles, 
scarlatina,  diphtheria,  etc.),  leukemia,  pernicious  anemia,  etc.;  and  it 
is  rarely  a  manifestation  of  vicarious  menstruation,  and  other  neurotic 
conditions,  such  as  hysteria,  vasomotor  ataxia,  etc.  The  local  causes 
are:  (a)  Hyperemia  of  the  gastric  vessels  (or  of  the  oesophageal  plexus 
of  veins),  common  in  advanced  cirrhosis  of  the  liver,  heart  disease,  pri- 
mary splenomegaly,  etc.  (b)  Inflammation,  erosion,  and  ulceration  of 
the  gastric  mucosa,  such  as  may  be  provoked  by  irritant  poisons,  etc. 
(c)  Peptic  or  other  ulceration  of  the  stomach  or  duodenum,  including 
tuberculous,  syphilitic,  and  especially  carcinomatous  ulceration,  (r/) 
C'hanges  in  the  vessel  walls,  such  as  occur  in  amyloid  disease,  nephritis, 
etc.,  may  occasion  hemorrhage,  in  some  cases  in  consequence  of  the 
formation  and  rupture  of  small  aneurysms,  (e)  Trauma,  external  blows 
or  internal  injuries,  provoked  by  diverse  kinds  of  foreign  bodies  (chicken 
bones,  oyster  shells,  etc.).  (f)  Hematemesis  may  also  be  due  to  rupture 
of  an  aneurysm,  or  to  the  swallowing  of  blood  coming  from  the  nose, 
throat,  (rsophagus,  or  lungs  (hemoptysis). 

Symptoms. — Minor  hemorrhages  into  the  stomach  doubtless  fre- 
quently pass  unnoticed,  the  blood  being  conveyed  into  the  intestine  with 


614  DISEASES  OF  THE  STOMACH 

the  food.  When  large  the  blood  is  usually  vomited,  though  some  of  it 
usually  passes  into  the  intestine,  and,  being  discharged  with  the  feces, 
may  discolor  the  stools.  As  vomited  the  blood  is  usually  dark  in  color, 
clotted,  though  some  is  fluid,  is  acid  in  reaction,  and  often  mixed  with 
food.  When  the  hemorrhage  occurs  slowly,  characteristic  dark  granular 
particles  (coffee  grounds)  are  likely  to  appear;  when  it  has  occurred 
suddenly  and  in  large  amount  it  is  usually  immediately  ejected  and 
may  be  quite  red,  though  some  of  it  is  likely  to  be  clotted.  The  amount 
of  blood  vomited  varies  within  wide  limits  from  a  scarcely  perceptible 
tinge  to  several  quarts;  and  the  hemorrhage  may  be  single  or  repeated, 
either  in  quick  succession  or  extend  over  a  period  of  days.  Attending 
the  hemorrhage  are  the  usual  evidences  of  internal  bleeding,  faintness, 
weakness,  pallor,  dimness  of  sight,  and  often  collapse.  Occasionally 
severe  and  even  fatal  collapse  has  occurred  without  the  discharge  of  any 
blood  by  the  mouth  or  anus. 

Diagnosis. — The  many  causes  of  hematemesis  should  be  borne  in  mind, 
as  well  as  the  fact  that  some  patients  practise  deception;  in  case  of  doubt 
it  is  wisest  to  see  the  blood  before  committing  one's  self  to  the  belief 
of  its  having  occurred.  Small  bleedings  that  readily  pass  unnoticed 
or  cannot  be  seen  by  the  unaided  eye,  may  be  detected  by  tests  for 
occult  blood  in  the  vomit  or  the  gastric  contents  after  a  test  meal,  or  in 
the  feces.  Differentiating  hemoptysis  may  sometimes  cause  anxiety,  but 
in  hematemesis  sensations  of  faintness  and  of  warmth  in  the  epigastrium 
often  proceed  the  vomiting;  the  blood  is  usually  dark  in  color,  clotted, 
acid  in  reaction,  and  often  mixed  with  food;  the  symptoms  and  signs 
point  to  disease  of  the  abdominal  viscera;  and  blood  may  be  discharged 
by  the  bowel;  whereas  in  hemoptysis  a  sensation  of  tickling  in  the  throat 
often  precedes  the  hemorrhage,  faintness  if  it  occurs  follows  the  hemor- 
rhage, and  vomiting  does  not  occur  until  later;  the  blood  is  bright  red, 
frothy,  fluid,  alkaline  in  reaction,  and  may  be  mixed  with  mucus  or 
purulent  expectorations;  the  symptoms  and  signs  point  to  disease  of  the 
thoracic  viscera;  and  the  sputiun,  if  there  is  any,  may  be  blood-tinged 
for  several  days. 

Treatment. — ^The  treatment  of  hematemesis  depends  upon  the  cause. 
In  general  it  is  similar  to  that  of  hemorrhage  occurring  in  typhoid  fever 
(page  59). 

Motor  Disorders. — The  motor  disorders  of  the  stomach  may 
be  irritative  or  depressive:  on  the  one  hand,  hypermotility,  peri- 
staltic unrest,  spasm,  and  vomiting;  on  the  other  hand,  atony,  insuffi- 
ciency of  the  pylorus  or  of  the  cardia,  rumination,  and  regurgi- 
tation. 

Hypermotility  or  hyperkinesis  is  an  increased  activity  of  the  motor 
functions  of  the  stomach  whereby  the  chyme  is  discharged  into  the 
intestine  too  soon.  It  may  occur  as  a  primary  neurosis,  but  is  usually 
associated  with  hyperacidity,  and  with  some  forms  of  achylia  gastrica. 
The  condition  rarely  occasions  any  symptoms,  and  the  diagnosis  is 
to  be  made  only  by  attempts  to  remove  the  gastric  contents. 


SYMPTOMATIC  DISORDERS  OF   THE  STOMACH  615 

Peristaltic  unrest  of  the  stomach  is  a  term  originally  applied  by  Kuss- 
maul  to  exaggerated  peristaltic  action  on  the  stomach.  It  is  especially 
common  in  nervous  and  hysterical  subjects,  and  is  often  associated  with 
like  disorders  of  the  intestine.  The  exaggerated  peristaltic  movements 
which  often  begin  soon  after  eating,  and  are  sometimes  induced  by 
emotional  disturbances,  give  rise  to  loud  rolling  and  gurgling  sounds, 
which  may  even  be  heard  at  a  distance  from  the  patient,  and  occasion 
corresponding  annoyance  and  discomfort.  The  movements  are  some- 
times visible  through  a  thin  abdominal  wall.  The  rapid  emptying  of 
the  stomach  often  leads  to  marked  hunger,  and  the  advent  of  ill-prepared 
chyme  into  the  intestine  often  provokes  diarrhoea.  Occasionally  the 
direction  of  the  movement  is  the  reverse  of  the  normal — antiperistalsis, 
and  the  gastric  contents  (rarely  even  the  intestinal  contents)  may  be 
ejected  by  the  mouth.  The  condition  must  be  differentiated  from  the 
visible  peristalsis  of  pyloric  obstruction. 

Spasm  of  the  cardia  sometimes  occurs  in  regional  ulceration  or  carci- 
noma; and  it  may  be  provoked  by  the  introduction  of  a  stomach  tube, 
and  too  hasty  swallowing  of  food  or  drink,  especially  if  too  hot  or  too  cold. 
Apparently  as  a  pure  neurosis  it  is  sometimes  observed  in  neuropathic 
subjects,  and  may  be  acute,  recurring  periodically,  or  chronic,  developing 
after  the  ingestion  of  food.  In  air  swallowers  (aerophagia)  who  ordin- 
arily would  discharge  the  air,  cardiospasm  is  not  uncommon,  and  if 
associated  with  spasm  of  the  pylorus,  sometimes  leads  to  considerable 
painful  distention  of  the  stomach  (pneumatosis),  which,  with  the  sub- 
sidence of  the  spasm,  rapidly  subsides  with  the  occurrence  of  the  gaseous 
eructations. 

Spasm  of  the  pylorus  is  a  common  associate  of  irritative  lesions  of  the 
pyloric  end  of  the  stomach  (hyperacidity,  hypersecretion,  ulcer,  etc.), 
and  is  a  contributing  factor  in  the  production  of  pneumatosis.  Whether 
it  occurs  as  a  primary  disorder  is  still  debated.  The  symptoms  are 
pain,  increased  peristalsis,  gastric  dilatation,  and  vomiting.  Pyloric 
spasm  has  been  found  also  in  children  the  subjects  of  persistent 
vomiting. 

Nervous  belching  or  eructation  is  usually  noisy,  and,  occurring  par- 
oxysmally  and  sometimes  persisting  for  hours,  has  been  observed  in 
neuropathic  subjects  (women  and  children).  The  expelled  gas  is  usually 
the  atmospheric  air  which  had  been  previously  swallowed  or  aspirated, 
and  may  be  distinguished  from  the  eructations  of  gastric  disorders  by  the 
absence  of  unpleasant  odor. 

Nervous  vomiting  is  sometimes  observed  in  hysterical  subjects,  being 
rather  a  regurgitation  of  the  food  and  unattended  by  preliminary  nausea 
and  the  ordinary  straining  efforts.  Von  Leyden  has  described  a  primary 
periodic  vomiting  characterized  by  sudden  onset,  recurrence  at  irregular 
intervals,  and  persistence  for  from  several  hours  to  several  days,  which 
he  regards  as  a  neurosis.  A  cyclic  or  periodic  vomiting  in  children  has 
also  been  described,  and  is  believed  to  be  due  to  acid  (auto-)  intoxication. 


616  DISEASES  OF  THE  STOMACH 

Of  interest  in  this  connection  is  the  vomiting  of  blood  sometimes  observed 
in  hysterical  subjects  without  organic  disease  of  the  stomach. 

Atony  of  the  stomach  (gastroparesis,  mechanical  or  motor  insufficiency, 
myasthenia  gastrica)  sometimes  results  from  a  variety  of  disorders  which 
need  not  be  discussed  here  (see  dilatation  of  the  stomach),  and  is 
possibly,  in  unusual  cases,  a  pure  neurosis.  The  symptoms  are  those 
of  dilatation,  which  soon  develops. 

Insufficiency  or  incontinence  of  the  cardia  may  result  from  organic 
disease  or  from  nervous  disorder,  and  is  recognized  by  involuntary 
regurgitation  of  food,  or  by  rumination  (merycismus) — the  regurgitation 
and  chewing  of  food  as  ruminants  chew  their  cud.  The  last  named, 
as  a  neurosis,  is  sometimes  observed  in  neuropathic  subjects — hysteria, 
idiocy,  insanity,  epilepsy,  etc. 

Insufficiency  or  incontinence  of  the  pylorus  may  be  due  to  organic 
disease  or  nervous  disorders.  The  condition  is  rare  and  scarcely  gives 
rise  to  destructive  symptoms,  but  may  be  recognized  by  finding  bile  and 
intestinal  contents  in  the  stomach,  and  by  the  rapid  passage  into  the 
intestine  of  gas  or  water  introduced  into  the  stomach. 

Treatment. — The  treatment  of  the  motor  disorders  of  the  stomach  is 
primarily  that  of  any  local  anatomical  disease  with  which  they  may 
be  associated,  but  attention  must  also  be  paid  to  the  common  under- 
lying neuropathic  condition.  In  many  cases  greatest  benefit  attends  a 
modified  rest  cure,  with  subsequent  change  of  climate,  if  possible.  A 
"  cure"  at  some  one  of  the  well-known  health  resorts  is  often  of  much  benefit 
on  account  of  the  habits  of  regularity  there  enforced,  and  the  attention 
directed  to  detail.  In  general  the  diet  must  be  regulated  to  suit  each 
individual  patient;  the  bowels  must  be  moved  once  daily;  and  rest  and 
exercise  in  proper  proportion  must  be  enjoined.  Mild  hydropathic 
measures,  massage,  and  electricity  are  useful  adjuvants.  In  cases  due 
to  irritability  of  the  motor  apparatus  sedatives  conjoined  with  the  general 
measures  mentioned  are  of  service,  especially  the  bromides,  belladonna, 
and  hyoscyamus,  and  sometimes  such  simple  medicinal  measures  as 
Hoffmann's  anodyne,  etc.  In  conditions  due  to  diminished  irritability 
of  the  motor  apparatus,  the  best  results  attend  the  use  of  the  general 
measures  mentioned,  but  in  some  cases  excellent  results  follow  the  use 
of  strychnine,  but  especially  tincture  of  nux  vomica,  beginning  with 
15  minims  (1  c.c.)  and  gradually  increasing  to  60  to  90  minims  (4 
to  6  c.c.)  three  times  a  day.  One  must  not,  however,  mistake  mere 
atony  for  the  weakness  of  overuse.  Iron  and  arsenic  are  valuable  in 
many  cases. 

Sensory  Disorders. — ^The  sensibility  of  the  stomach  may  be  increased 
(hyperesthesia),  diminished  (anesthesia),  or  perverted  (paresthesia). 

Hyperesthesia  of  the  stomach,  increased  sensitiveness  of  the  sensory 
nerves  of  the  stomach,  is  sometimes  observed  in  hysterical  and  neuras- 
thenic subjects,  and  is  manifest  by  the  development  of  epigastric  distress, 
a  sense  of  weight,  burning  pain,  etc. — symptoms  common  to  many  gastric 
disorders,  and  still  the  gastric  functions  seem  to  be  performed  normally. 


SYMPTOMATIC  DISORDERS  OF  THE  STOMACH  617 

Sometimes  extreme  pain  seems  to  be  provoked  by  the  smallest  amount 
of  food,  and  the  patient  may  in  consequence  of  a  voluntary  starvation 
emaciate  considerably. 

Gastralgia  (gastrodynia,  cardialgia),  an  aggravated  hyperesthesia, 
may  be  due  to  organic  disorders  of  the  stomach,  such  as  ulcer  or  car- 
cinoma; it  may  be  part  of  the  gastric  crisis  of  tabes  dorsalis;  and  it 
may  occur  as  a  neurosis,  independently  of  organic  diseases.  The  last 
mentioned  may  occur  in  men  or  women,  but  is  much  more  common  in 
hysterical,  neurasthenic,  and  anemic  women,  and  is  often  associated 
with  disorders  of  menstruation.  It  consists  of  the  sudden  occurrence  of 
extremely  severe  pains  in  the  epigastrium  which  radiate  toward  the  back, 
and  are  likely  to  recur  at  certain  intervals  (in  some  cases  at  night),  and 
are  independent  of  the  taking  of  food  or  other  demonstrable  cause.  The 
attack  may  last  from  a  few  minutes  to  an  hour  or  more,  and  belching, 
nausea,  hiccough,  etc.,  may  be  associated;  but,  as  a  rule,  the  functions 
of  the  stomach  appear  to  be  well  performed:  the  taking  of  food  often, 
indeed,  affords  temporary  relief  from  the  pain.  Mental  depression  and 
hypochondriasis  not  infrequently  result.  Care  must  be  taken  to  exclude 
gastric  ulcer,  gastric  carcinoma,  biliary  colic,  and  the  gastric  crises  of 
tabes. 

Anorexia,  or  loss  of  appetite,  as  previously  mentioned,  sometimes 
occurs  as  a  pure  neurosis,  and  is  sometimes  associated  with  an 
absence  of  the  sense  of  hunger.  This  nervous  anorexia  may  occur 
suddenly  after  psychic  and  emotional  disturbances  (shock,  fright,  un- 
pleasant odors,  etc.),  and  soon  passes  away.  A  more  or  less  chronic 
anorexia  is  observed  in  many  neurotic  subjects — in  young  girls  who,  fear- 
ing to  become  stout,  from  the  habit  of  eating  little  engender  the  impossi- 
bility of  eating  much;  and  in  certain  elderly  and  rather  rotund  women 
in  whom  extreme  emaciation  sometimes  results. 

Akoria,  an  absence  of  the  sense  of  satiety,  is  occasionally  observed 
in  hysterical  and  neurasthenic  subjects,  and  may  or  may  not  be  associated 
with  hyperorexia. 

Hyperorexia  (boulimia,  polyphagia),  in  addition  to  the  conditions 
mentioned  under  disorders  of  the  appetite,  is  sometimes  seen  as  a  pure 
neuroses  in  certain  neuropathic  subjects,  hysteria,  neurasthenia.  Graves' 
disease,  epilepsy,  insanity,  idiocy,  etc.  In  consequence  of  the  inordinate 
consumption  of  food,  gastritis  and  gastric  dilatation  not  infrequently 
result. 

Parorexia  (perverted  appetite,  pica),  a  craving  for  unusual  articles 
for  food,  is  seen  in  minor  grades  (capriciousness)  in  some  young  children, 
in  chlorosis,  hysteria,  pregnancy,  etc.  In  exaggerated  degree,  amomiting 
almost  to  coprophagy,  it  is  occasionally  seen  in  dementia,  mania,  idiocy, 
epilepsy,  etc. 

Treatment. — The  treatment  of  the  sensory  disorders  is  determined 
l)y  their  nature  and  manifestations.  As  in  the  management  of  motor 
disorders,  attention  must  always  be  directed  to  the  underlying  basic  dis- 
order.    In  some  cases  of  persistent  gastrodynia  the  full  rest  treatment 


618  DISEASES  OF  THE  STOMACH 

must  be  carried  out.  Milder  cases  may  be  relieved  by  external  applica- 
tions, such  as  a  mustard  plaster,  a  spice  poultice,  or  a  hot-water  bag, 
cold  compresses  and  other  hydropathic  applications,  and  remedies 
such  as  bismuth  subnitrate  or  subcarbonate,  Hoffmann's  anodyne, 
chloroform  water,  aromatic  spirit  of  ammonia,  bromides,  and  valerian 
internally.  Cocaine  or  carbolic  acid  are  useful  in  some  cases.  In  cases 
associated  with  hyperacidity  (rather  common)  silver  nitrate  and 
belladonna,  and  other  remedies  mentioned  under  hyperchlorhydria,  are 
very  useful.  Morphine  should  be  avoided,  but  if  necessary  an  occa- 
sional dose  of  codeine  may  be  given. 

Secretory  Disorders. — ^Although  the  secretion  of  the  gastric  juice  is 
directly  under  the  control  of  the  nervous  system,  perversions  of  this  secre- 
tion may  not  be  ascribed  to  nervous  influences  alone.  Variations  in 
the  amount  and  quality  of  the  gastric  juice  are  among  the  most  impor- 
tant manifestations  of  functional  and  organic  disease  of  the  stomach  of 
the  most  diverse  nature;  and  they  may  occur  also  as  a  pure  neurosis. 
The  gastric  juice  may  be  increased  or  diminished  in  total  quantity  or 
in  the  quantity  of  some  one  or  more  of  its  constituent  elements — ^whence 
we  may  distinguish  the  following: 

Hyperchlorhydria  (hyperacidity,  superacidity),  the  secretion  of  an 
abnormally  abundant  and  abnormally  acid  (HCl)  juice  during  digestion, 
is  a  manifestation  of  certain  organic  diseases  of  the  stomach,  especially 
some  cases  of  chronic  gastritis  (more  particularly  the  cases  of  so-called 
dyspepsia  occurring  in  young  subjects),  and  almost  all  cases  of  gastric 
ulcer  (in  which  it  is  quite  characteristic);  it  is  common  in  chlorosis;  and 
it  sometimes  occurs  as  a  pure  neurosis  in  neuropathic  subjects,  in  whom 
it  may  be  induced  by  emotional  disturbances,  shock,  etc.  The  ferments 
of  the  stomach  are  believed  to  be  usually  increased  with  hydrochloric 
acid.  The  hyperchlorhydria  of  organic  disease  of  the  stomach,  notably 
ulcer,  is  likely  to  be  more  or  less  persistent,  whereas  that  due  to  neurotic 
influences  varies  much  from  time  to  time,  and  is  often  aggravated  by 
emotional  disturbances.  Thesymptoms  are  variable;  hyperacidity  may  not 
produce  symptoms,  and  symptoms  commonly  attributed  to  hyperacidity 
may  occur  when  the  hydrochloric  acid  is  normal  or  even  diminished. 
Other  factors  seem  to  be — hypersecretion,  gastric  atony  (or  other  organic 
condition),  or  hypersensitiveness  (hyperesthesia)  of  the  gastric  mucosa 
(often  associated  with  general  neurasthenia).  Usually  there  is  epigastric 
distress  and  burning  (perhaps  extremely  severe),  often  associated  with  acid 
eructations,  coming  on  in  from  one  to  three  hours  after  taking  food  (at  the 
height  of  digestion),  and  disappearing  with  the  discharge  of  the  chyme 
into  the  intestine  or  after  vomiting  (which  is  rare).  The  epigastric  dis- 
tress is  often  associated  with  distention  and  flatulence,  commonly  due 
to  pylorospasm.  The  appetite  is  usually  good  and  the  patient  appears 
well  nourished.  Constipation  is  the  rule,  but  the  attacks  of  diarrhoea 
are  rather  common,  and  are  due  to  the  irritation  caused  by  the  discharge 
into  the  intestine  of  a  chyme  too  acid  to  be  neutralized  by  the  bile  and 
the  pancreatic  juice.     The  motor  function  of  the  stomach  is  usually 


SYMPTOMATIC  DISORDERS  OF  THE  STOMACH  619 

unimpaired  (empty  six  liom"S  after  a  meal),  but  atony  and  dilatation  may 
develop.  Examination  of  the  gastric  contents  after  an  Ewald  test  break- 
fast reveals,  instead  of  the  normal  20  to  40  hydrochloric-acid  content 
and  30  to  50  total  acidity,  values  as  high  as  60  to  100  or  more  hydro- 
chloric-acid content  and  80  to  130  or  more  total  acidity.  Albiunin  is 
digesed  rapidly;  starch  slowly. 

Gastrosuccorrhoea  (hypersecretion;  supersecretion ;  Reichmann's  dis- 
ease; gastroxynsis,  Rossbach),  or  an  increased  flow  of  (usually  highly 
acid)  gastric  juice,  is  a  perversion  of  the  secretory  function  of  the  stomach, 
whereby  the  gastric  juice  is  secreted  independently  of  the  presence  of 
food  in  the  stomach.  To  the  hypersecretion  and  hyperchlorhydria  a 
motor  insufficiency  is  not  infrequently  added.  In  many  cases  the  condi- 
tion is  a  pure  neurosis,  but  it  may  also  be  caused  by  persistent  irritation 
of  the  gastric  mucosa — ^whence  the  term  acid  catarrh  of  the  stomach, 
proposed  by  Jaworski  and  Gulzinski,  may  not  be  altogether  inappropri- 
ate. The  condition  is  usually  found  in  neuropathic  subjects,  hysteria, 
neurasthenia,  locomotor  ataxia,  etc.  The  increased  flow  may  be  inter- 
mittent or  continuous.  The  intermittent  form  (gastroxynsis,  Rossbach) 
is  the  rarest.  The  attacks  occur  at  irregular  intervals,  and  are  charac- 
terized by  severe,  often  colicky  pain  in  the  epigastrium,  headache,  and 
the  vomiting  of  a  considerable  quantity  of  clear  (or  yellowish),  watery, 
highly  acid  fluid.  The  attacks  usually  occur  quite  independently  of 
the  taking  of  food,  last  for  from  several  hours  to  a  day  or  more,  and  disap- 
pear rather  rapidly.  In  the  intervals  the  patient  may  be  quite  well,  or  some- 
times complain  of  indefinite  dyspeptic  complaints.  Continuous  gastro- 
succorrhoea is  the  more  common  disorder.  The  patient  complains  of 
epigastric  distress  and  burning,  with  belching,  acid  eructations,  and 
vomiting  of  highly  acid,  watery  fluid,  mixed  or  not  with  particles  of 
food.  In  the  beginning  the  appetite  is  good,  but  later  becomes  impaired; 
thirst  is  usually  increased,  and  constipation  is  the  rule,  although  attacks 
of  diarrhoea  occur.  The  continuation  of  the  hypersecretion  when  the 
stomach  contains  no  food  often  occasions  increased  distress  and  vomiting 
during  the  night  and  the  early  morning — ^which  are  quite  characteristic. 
In  consequence  of  the  pyloric  spasm  (and  consequent  obstruction) 
induced  by  the  highly  acid  gastric  contents,  considerable  dilatation  of 
the  stomach  results,  and  in  long-standing  cases,  marked  emaciation, 
even  suggesting  carcinoma,  may  ensue.  The  diagnosis  is  confirmed  by 
washing  and  emptying  the  stomach  in  the  evening,  and,  in  the  morning 
before  the  patient  has  had  any  food,  again  introducing  the  stomach  tube 
and  securing  a  clear  fluid,  acid  in  reaction  and  rapidly  digesting  albumin. 

Ilypochlorhydria  (hyposecretion;  subacidity;  anacidity;  hypochylia 
gastrica;  achylia  gastrica). — Inasmuch  as  the  secretion  of  gastric  juice, 
or  of  its  hydrochloric  acid  content  may  be  increased,  so  also  jnay  it  be 
diminished.  In  the  majority  of  cases  there  is  both  a  diminution  in  the 
total  amount  of  gastric  juice  as  well  as  of  the  hydrochloric  acid  content, 
but  the  hydrochloric-acid  content  may  be  disproportionately  diminished 
or  even  absent,  while  gastric  juice  is  still  secreted;  pepsin  and  the  curdling 


620  DISEASES  OF  THE  STOMACH 

ferment  or  their  zymogens  are  usually  present.  Subacidity  is  a  feature 
of  most  cases  of  gastric  catarrh,  and  is  present  from  time  to  time  in 
many  cases  of  nervous  dyspepsia.  Anacidity,  even  an  absence  of 
hydrochloric  acid,  is  found  in  some  cases  of  chronic  gastric  catarrh,  and 
in  nervous  dyspepsia,  and  it  is  a  noteworthy  feature  of  almost  all  cases 
of  gastric  carcinoma.  Total  absence  of  the  gastric  juice,  achylia  gastrica 
(Einhorn),  was  originally  considered  significant  of  complete  atrophy  of  the 
gastric  mucosa,  but  is  now  known  to  occur  as  a  pure  neurosis,  and  to  be 
susceptible  of  cure.  The  symptoms  vary  much  in  different  cases.  Gener- 
ally they  are  those  of  chronic  catarrh  of  the  stomach  with  fermentation, 
but  symptoms  may  be  absent  if  the  motor  activity  of  the  stomach  remains 
normal.  The  condition  is  susceptible  of  accurate  diagnosis  only  by 
analyzing  the  gastric  contents  after  a  test  meal  (absence  of  hydrochloric 
acid,  of  pepsin,  and  of  rennin).  In  many  cases  despite  the  notable 
deficiency  of  gastric  juice,  the  digestive  functions  seem  to  be  well 
performed,  a  fact  compatible  with  the  demonstration  recently  that  the 
intestine  is  able  vicariously  to  perform  the  functions  of  the  stomach 
when  the  hydrochloric-acid  deficit  is  marked;  but  lienteric  diarrhoea  is 
not  infrequent. 

Treatment. — The  treatment  of  the  secretory  disorders  of  the  stomach 
is  primarily  that  of  the  underlying  disease — anatomical,  neurotic,  or  both. 
In  addition,  in  cases  of  hyperacidity,  regulation  of  the  diet  is  of  the  utmost 
importance.  This  should  be  largely  albuminous  (meat,  eggs,  fish,  etc.), 
and  non-irritating;  starches  should  be  given  in  small  amounts,  in  view 
of  the  marked  reduction  in  the  time  of  amylolytic  digestion  in  the  stomach 
caused  by  the  prompt  and  excessive  secretion  of  hydrochloric  acid;  fats 
are  fairly  well  tolerated,  as  a  rule.  The  drinking  of  moderate,  and 
sometimes  of  considerable,  amounts  of  water  at  and  between  meals 
is  often  of  service — serving  to  dilute  the  highly  acid  gastric  juice;  but 
discretion  must  be  used  in  advising  this,  bearing  in  mind  its  influence 
in  gastric  atony  and  dilatation,  which  may  be  present.  Alkaline  mineral 
waters  are  especially  serviceable.  Alcohol,  tea,  coffee,  and  stimulating- 
condiments,  and  too  much  table  salt,  must  be  avoided.  The  adminis- 
tration of  alkalies,  such  as  sodium  bicarbonate,  magnesia,  etc.,  at  the 
height  of  digestion,  seems  to  neutralize  the  excessive  acidity,  but  they 
should  not  be  given  when  the  stomach  is  empty,  since  thus  they  may  only 
serve  to  increase  the  acidity.  In  •  many  cases  the  hyperchlorhydria  may 
be  controlled  by  sedatives,  of  which  the  bromides  serve  as  a  type,  but 
especially  silver  nitrate  and  belladonna  or  hyoscyamus.  Cocaine  and 
codeine  may  prove  useful  in  some  cases.  Large  doses  of  nux  vomica 
are  often  useful  in  cases  associated  with  neurasthenia. 

Ill  gastrosuccorrhcea,  similar  regulation  of  the  diet  is  called  for:  the 
amount  of  water  should  be  reduced;  the  meals  should  be  reduced  in 
number  (as  compared  with  hyperchlorhydria),  but  one  should  bear  in 
mind  that  a  small  amount  of  food  will  sometimes  almost  immediately 
relieve  the  subjective  complaints.  Lavage  is  of  the  greatest  service; 
one  may  use  alkaline  solutions  or  silver  nitrate  1  to  1000.     The  treatment 


NERVOUS  DYSPEPSIA  621 

is  otherwise  similar  to  that  of  hyperchlorhydria.     Atropine  has  rendered 
excellent  service  in  some  cases. 

In  subacidity  and  anacidity  the  treatment  is  largely  that  of  the  under- 
lying condition — gastric  catarrh,  carcinoma,  etc.  The  diet  should  be 
carefully  regulated  and  mixed,  and  should  contain  articles  likely  to 
excite  secretion,  condiments,  etc.  Meat  is  ill  borne  in  many  of  these 
cases,  and  usually  must  be  reduced  to  a  minimum,  for  a  time  at  least. 
Dilute  hydrochloric  acid  and  nux  vomica  (in  large  doses)  are  of 
especial  value.  Bitter  tonics  are  also  useful.  In  achylia  gastrica  the 
use  of  hydrochloric  acid,  nux  vomica,  bitter  tonics,  hydrotherapy, 
massage,  and  electricity  are  indicated. 


NERVOUS  DYSPEPSIA. 

(Nervous  Dyspepsia,  Leube;  Gastric  Neurasthenia,  Eivakl.) 

Nervous  dyspepsia  is  a  syndrome  made  up  of  varying  combinations 
of  the  gastric  neuroses,  a  condition,  however,  in  which  the  subjective 
complaints  are  altogether  disproportionate  to  the  anomalies  of  gastric 
motility  and  secretion. 

Etiology. — Nervous  dyspepsia  is  ascribed  to  undue  irritability  of 
the  gastric  nerves,  but  in  some  cases  the  gastric  condition  is  depressive 
rather  than  irritative.  It  sometimes  appears  as  an  apparently  inde- 
pendent disorder;  usually  it  is  associated  with  other  neurotic  manifesta- 
tions, such  as  hysteria,  neurasthenia,  etc. ;  and  it  may  be  induced  in  neuro- 
pathic subjects  by  overwork,  anxiety,  sexual  excesses,  chronic  alcoholism, 
etc.  It  sometimes  arises  reflexly  from  disease  of  other  organs,  especially 
the  eye  (eye  strain),  and  the  female  genitalia;  it  appears  occasionally 
to  follow  infections,  such  as  malaria;  and  it  may  develop  in  anemic  and 
chlorotic  conditions. 

Symptoms. — ^The  symptoms  are  extremely  variable,  and  this  is  a  char- 
acteristic feature.  The  appetite  varies  considerably:  sometimes  it  is 
normal,  sometimes  increased,  sometimes  diminished,  sometimes  capri- 
cious or  perverted.  The  tongue  is  usually  clean.  Epigastric  distress  is 
the  chief  complaint.  Usually  it  is  present  or  at  least  most  marked  during 
digestion;  it  varies  in  intensity  from  slight  discomfort  to  extreme  agony; 
it  may  come  on  early  or  not  for  an  hour  after  taking  food,  and  it  may  or 
may  not  be  dependent  upon  the  character  of  the  food.  The  pain  is 
most  marked  when  there  is  hyperacidity.  Occasionally  there  is  epi- 
gastric tenderness;  usually  cutaneous  hyperesthesia.  Evidences  of 
motor  disturbances,  such  as  belching,  pyrosis,  peristaltic  unrest,  etc., 
are  not  uncommon.  Nausea,  rarely  vomiting,  and  referred  symptoms 
such  as  headache,  somnolence,  palpitation  of  the  heart,  etc.,  may  be 
present.  When  the  stomach  is  empty  there  may  be  complaint  of  weak- 
ness, headache,  vertigo,  tinnitus  aurium,  etc.,  and  sometimes  even  of 
severe  pain  (gastralgokenosis),  which  fact  has  led  Boas  to  distinguish 
a  special  form  of  gastric  neurasthenia.     The  motor  power  of  the  stomach 


622  DISEASES  OF  THE  STOMACH 

usually  suffers  no  noteworthy  deterioration,  since  the  stomach  is  usually 
found  empty  six  hours  after  a  meal.  Not  infrequently  there  are  evidences 
of  neurotic  disorders  of  the  intestine — flatulence,  peristaltic  unrest, 
colic,  constipation  alternating  with  diarrhoea,  etc.  All  of  the  symptoms 
are  extremely  irregular;  they  vary  much  from  time  to  time;  they  develop 
slowly  or  suddenly,  and  disappear  equally  slowly  or  suddenly;  and  the 
attacks  which  may  be  induced  by  emotional  or  other  disturbances  (even 
ill  hiunor)  last  varying  periods.  Equally  variable  is  the  condition  of 
the  gastric  juice — subacidity,  hyperacidity,  and  normal  acidity,  occurring 
from  time  to  time,  although  independently  of  discoverable  cause.  The 
general  health  of  the  patient,  despite  the  marked  complaints,  is  often 
wonderfully  preserved;  but  some  aggravated  cases  are  seen  in  lean  and 
quite  marantic  subjects.  A  general  hypochondriacal  and  neurasthenic 
habitus  is  common. 

Diagnosis. — ^The  marked  variability  in  the  complaints  and  in  the  condi- 
tion of  the  gastric  juice,  the  not  uncommon  association  of  other  evidences 
of  neurasthenia,  the  long  duration  of  the  symptoms  with  intervals  of 
good  health,  the  dependence  of  attacks  upon  well-known  emotional 
disturbances,  and  the  absence  of  specific  symptoms,  serve  to  exclude 
chronic  gastric  catarrh,  gastric  ulcer,  and  gastric  carcinoma.  Frequently, 
however,  serious  organic  disease  is  manifested  first  by  evidences  of 
nervous  dyspepsia. 

Treatment. — ^The  treatment  is  practically  that  of  neurasthenia.  Great 
difficulty  is  often  experienced  by  convincing  the  patient  that  his  stomach 
is  capable  of  digesting  a  generous  meal — which,  when  once  accomplished, 
is  soon  followed  by  dissipation  of  many  of  the  subjective  complaints. 
Change  of  scene,  of  climate,  and  sometimes  of  association,  are  of  much 
benefit  in  most  cases.  In  other  cases  the  complete  or  modified  Weir 
Mitchell  rest  cure  must  be  employed.  Outdoor  exercise,  hydrothera- 
peutic  measures,  and  nux  vomica  are  very  useful  in  other  cases. 


ACUTE  CATARRHAL  GASTRITIS. 

(Acute  Gastritis;  Acute  Gastric  Catarrh;  Simple  Gastritis;  Acute  Dyspepsia.) 

Acute  catarrhal  gastritis  is  an  acute  inflammation  of  the  gastric 
mucous  membrane,  characterized  by  local  pain  and  tenderness,  nausea, 
vomiting,  and  sometimes  fever. 

Etiology. — ^The  affection  occurs  at  all  ages,  and  in  both  sexes.  An 
inherited  predisposition  is  suggested  by  the  expression  "weak  stomach," 
but  the  "weak  stomach"  is  frequently  acquired  rather  than  inherited. 
The  gouty,  the  debilitated,  and  the  subjects  of  chronic  congestion  of  the 
stomach  (liver  cirrhosis,  heart  disease)  are  also  predisposed  to  the  dis- 
ease. The  exciting  cause  of  the  disorder  is  summed  up  in  the  term 
dietetic  indiscretions.  These  may  consist  of  the  eating  of  improper 
food,  such  as  tainted  meats,  unripe  fruit,  etc.;  of  overloading  the  stomach 
with  too  much  food  and  drink,  even  of  good  quality;  of  defective  masti- 


ACUTE  CATARRHAL  GASTRITIS  623 

cation,  often  due  to  hurried  eating,  "quick  luncheons,"  imperfect  teeth, 
etc.;  of  overindulgence  in  alcohol,  periodical  debauches,  etc.  Acute 
gastric  catarrh  may  be  provoked  also  by  the  use  of  certain  drugs,  such 
as  the  iodides,  salicylates,  mercury,  etc.,  and  it  is  common  also  in  many 
infective  diseases,  and  may  be  aggravated  by  injudicious  dieting. 

Pathology. — The  lesions  are  those  of  catarrhal  inflammation  in 
general — swelling  and  hyperemia,  and  increase  of  mucous  secretion. 
Later  there  may  be  small  submucous  hemorrhages  and  superficial  ero- 
sions. The  cells  of  the  mucous  and  peptic  glands  show  cloudy  swelling, 
and  between  them  there  is  a  small  amount  of  round-cell  infiltration. 
The  gastric  juice  is  deficient,  and  lactic  and  fatty  acids,  the  consequence 
of  decomposition,  may  be  present. 

Symptoms. — In  the  ordinary  cure  of  acute  indigestion  the  symptoms 
are  relatively  mild,  and  consist  of  epigastric  distress  and  tenderness, 
soon  succeeded  by  nausea  and  vomiting,  with  some  relief.  The  tongue 
is  flabby  and  coated  with  a  thick,  brownish-yellow  fur;  there  is  an 
unpleasant  taste  in  the  mouth,  and  perhaps  headache  and  constipation 
(biliousness).  In  children  there  may  be  diarrhoea,  and  even  mild 
intestinal  colic.  The  attack  usually  subsides  within  twenty-four  hours. 
In  severer  cases  the  onset  may  be  quite  acute,  sometimes  with  a  chill 
and  moderate  fever.  The  epigastric  pain  and  tenderness  are  more 
marked,  and  the  vomiting  may  be  repeated  and  persistent,  and  bile 
may  appear  in  the  vomited  matter.  There  may  be  acid  eructations 
without  vomiting.  The  appetite  is  lost.  Thirst  is  usually  marked,  and 
when  quenched  by  water  is  often  immediately  followed  by  vomiting. 
The  headache  is  usually  well  marked,  the  tongue  coated,  the  breath 
fetid,  and  there  is  much  prostration,  and  usually  constipation.  The 
urine  is  concentrated  and  may  contain  indican.  The  attack  usually 
subsides  within  three  or  four  days,  but  may  last  longer  in  debilitated 
subjects. 

Diagnosis. — Mild  cases  present  no  diagnostic  difficulties.  Some 
of  the  severer  cases,  simulating  an  infection  at  first,  may  be  mistaken 
for  typhoid  fever  when  they  occur  independently  of  known  dietetic  indis- 
cretions; diagnostic  difficulties  are  sometimes  maintained  by  persistence 
in  the  use  of  the  term  "gastric  fever."  From  typhoid  fever  these  cases 
may  be  distinguished  by  the  abrupt  onset,  relatively  marked  remissions, 
and  sudden  fall  of  the  temperature,  the  absence  of  epistaxis,  of  enlarged 
spleen,  of  initial  bronchitis,  of  roseola,  and  of  the  Gruber-Widal  reaction. 
It  may  simulate  meningitis.  In  children  confusion  Avith  the  exanthemas 
may  occur,  but  the  detecting  of  a  rash  clears  the  diagnosis. 

Prognosis. — The  prognosis  is  good,  but  in  debilitated  subjects  the 
disease  may  be  unduly  protracted,  and  as  a  complication  of  certain 
infectious  diseases,  heart  diseases,  etc.,  it  may  prove  serious,  even  fatal. 
Recovery  is  usually  complete,  but  repeated  attacks  may  result  in  subacute 
or  chronic  gastritis. 

Treatment. — Mild  cases  require  no  special  treatment,  aside  from 
abstention  from  food,  and  a  purge  of  castor  oil,  calomel,  or  blue  mass, 


624  DISEASES  OF    THE  STOMACH 

followed  by  a  saline  cathartic.  If  there  be  discomfort  without  vomiting, 
vomiting  may  be  promoted  by  warm  water,  or  emetics  like  wine  of  ipecac 
or  mustard,  or  lavage  may  be  resorted  too.  In  severe  cases  the  patient 
should  be  confined  to  bed,  food  withdrawn  for  a  day,  and  an  initial  dose  of 
blue  mass  (5  grains,  0.3  gram),  or  calomel  in  ^  grain  (0.008  gram) 
every  fifteen  minutes  for  eight  doses,  given.  The  epigastric  distress  and 
tenderness,  as  w^ell  as  acid  eructations,  may  be  relieved  by  bismuth  sub- 
carbonate  and  sodimn  bicarbonate,  10  grains  (0.06  gram)  of  each,  every 
two  hours;  or  bismuth  subnitrate  (10  grains,  0.06  gram)  and  carbolic 
acid  (1  minim,  0.06  c.c.)  every  two  hours.  A  spice  poultice  to  the 
epigastrium  is  often  grateful.  If  the  vomiting  is  severe  and  prolonged,  it 
may  be  relieved  by  cocaine  (|  grain,  0.01  gram)  in  lime  water  every 
hour  or  two,  if  required.  Morphine  had  best  be  withheld.  On  the  second 
day  peptonized  milk  may  be  commenced,  in  small  amounts,  a  tablespoon- 
ful  (15  c.c.)  every  fifteen  minutes.  Later,  the  amount  may  be  increased 
and  the  intervals  lengthened,  and  other  articles  of  diet  added. 


PHLEGMONOUS  GASTRITIS. 

(Acute  Suppuratire  Gastritis.) 

Etiology. — Phlegmonous  gastritis  is  a  rare  disease,  characterized  by 
suppurative  inflammation  of  the  submucous  and  muscular  coats  of  the 
stomach.  It  appears  occasionally  ,to  be  idiopathic,  but  is  more  common 
in  association  with  pyemic  processes,  such  as  puerperal  infection,  etc. ;  it 
may  follow  trauma,  and  may  be  associated  with  gastric  carcinoma  (Osier's 
cases). 

Pathology. — The  purulent  collection  may  be  circumscribed  (abscess) 
or  difi^use  (phlegmon).  Rarely  the  abscess  ruptures  into  the  stomach 
cavity  or  the  peritoneum. 

Symptoms.— The  local  symptoms  are  those  of  severe  gastritis — epigas- 
tric pain,  tenderness,  nausea,  vomiting;  the  general  symptoms,  those  of 
sepsis — repeated  chills,  high  fever  (104°  to  105°  F.),  sweats,  prostration, 
delirium,  feeble  pulse,  leukocytosis,  etc.  Rarely,  the  pus  has  occasioned 
an  epigastric  prominence,  and  it  may  appear  in  the  vomit. 

The  diagnosis  is  scarcely  possible,  and  treatment  is  unavailing. 


TOXIC  GASTRITIS. 

Etiology. — Toxic  gastritis  results  from  the  ingestion  (often  with 
suicidal  intent)  of  corrosive  poisons,  such  as  strong  acids  and  alkalies, 
as  well  as  certain  non-corrosive  poisons,  such  as  phosphorus,  arsenic, 
mercury,  antimony,  iodine,  hydrocyanic  acid,  alcohol,  etc. 

Pathology. — In  some  relatively  mild  cases  the  lesions  are  those  of  a 
severe  acute  gastritis.  The  lesions  due  to  non-corrosive  poisons  consist 
of  fatty  degeneration  of  the  gastric  tubules,  with  round-cell  infiltration,  and 


INFECTIOUS  GASTRITIS  625 

foci  of  hemorrhage.  Following  the  ingestion  of  the  corrosive  poisons  the 
lesions  vary,  depending  upon  the  concentration  of  the  poison,  from  foci 
of  necrosis  surrounded  by  areas  of  inflammatory  reaction,  to  the  most 
severe  and  widespread  destruction  of  the  stomach  wall,  amounting  in 
some  cases  to  conversion  of  a  large  portion  of  the  stomach  into  a  dis- 
colored eschar,  and  perforation  into  the  peritoneum.  Similar  lesions  are 
usually  found  also  in  the  mouth,  pharynx,  and  oesophagus,  and  rarely 
in  the  duodenum.  Should  the  patient  survive,  ulceration  is  followed 
by  cicatrization  and  atrophy  of  the  gastric  mucosa;  sometimes  by  hour- 
glass contraction  of  the  stomach,  stenosis  of  the  oesophagus,  etc. 

Symptoms. — In  severe  cases  the  ingestion  of  the  poison  is  followed  by 
extreme  abdominal  pain,  immediate  collapse,  and  speedy  death.  In 
less  severe  cases  the  symptoms  consist  of  severe  burning  pain  in  the 
mouth,  oesophagus,  and  stomach;  swallowing  is  almost,  if  not  quite, 
impossible,  and  vomiting  and  retching  almost  constant.  The  vomit 
is  bloody,  and  sometimes  contains  sloughs  of  the  stomach  wall.  The 
abdomen  is  tender  and  tympanitic;  the  urine  may  contain  albumin  and 
casts.  Subcutaneous  hemorrhage  and  delirium  and  convulsions  may 
develop,  and  the  patient  may  die  in  a  few  days  from  the  intoxication, 
or  later,  from  perforation  of  the  stomach  or  inanition.  In  mild  cases 
recovery  may  ensue. 

Diagnosis. — ^The  diagnosis  is  quite  apparent  from  the  history  of  the 
case,  and  an  inspection  of  the  mouth,  thi'oat,  and  vomit. 

Treatment. — ^The  treatment  is  that  appropriate  in  the  different  poison- 
ings to  which  the  condition  may  be  due,  especially  the  use  of  magnesia 
with  milk  or  egg-albumen  in  acid  poisonings,  and  dilute  acids  in  strong 
alkali  poisonings,  etc.  Lavage  may  prove  useful.  Morphine  should  be 
given  for  the  pain.     In  severe  cases  treatment  is  usually  unavailing. 


INFECTIOUS  GASTRITIS. 

The  term  infectious  gastritis  is  sometimes  employed  to  distinguish 
affections  of  the  stomach  due  to  certain  microorganisms,  and  occurring 
usually  in  the  course  of  certain  infective  diseases.  In  a  broad  sense,  some 
of  the  cases  of  acute  catarrhal  gastritis  are  doubtless  infective ;  phlegmon- 
ous gastritis  is,  of  course,  infective.  Usage,  however,  has  tended  to  restrict 
the  term  to  diseases  of  the  stomach  caused  by  microorganisms,  such  as  the 
diphtheria  bacillus,  tubercle  bacillus,  pneumococcus,  the  t}^hoid  bacillus, 
colon  bacillus,  streptococcus,  etc.  Occasionally,  especially  in  diphtheria, 
pneumonia,  pyemia,  typhus  fever,  smallpox,  etc.,  the  lesions  go  on  to  the 
formation  of  a  pseudomembrane — sometimes  called  membranous  gas- 
tritis. Rarely  fungi,  such  as  yeast  fungi,  Saccharomyces  albicans,  the 
favus  fungus,  etc.,  excite  a  gastritis — so-called  mycotic  or  parasitic  gas- 
tritis. The  symptoms  are  not  distinctive,  and  the  nature  of  the  lesions 
is  not  to  be  recognized  unless,  perchance,  the  fungus  or  a  portion  of  the 
pseudomembrane  is  detected  in  the  vomit. 
40 


626  DISEASES  OF  THE  STOMACH 

CHRONIC  GASTRITIS. 

(Chronic  Catarrhal  Gastritis;  Chronic  Gastric  Catarrh;  Chronic  Dyspepsia.) 

Chronic  gastritis  is  a  chronic  inflammation  of  the  gastric  mucosa 
attended  by  increased  secretion  of  mncus  and  alterations  in  the  gastric 
juice,  and  sometimes  associated  with  impairment  of  the  motor  power, 
and  different  structural  changes  in  the  wall  of  the  stomach. 

Etiology. — Chronic  gastritis  may  follow  directly  on  an  acute  attack, 
but  it  is  more  commonly  due  to  the  continuous  or  frequently  repeated 
action  of  minor  irritants,  especially  in  those  predisposed  by  constitu- 
tional or  local  factors.  The  general  predisposing  factors  comprise  anemia 
(chlorosis,  pernicious  anemia)  and  the  toxic  conditions  and  vitiation  of 
the  blood,  inseparable  from  tuberculosis,  gout,  nephritis,  diabetes,  etc. 
The  local  predisposing  factors  comprise  the  congestive  conditions 
found  in  cirrhosis  of  the  liver,  chronic  heart  disease,  etc.,  and  different 
diseases  of  the  stomach  itself,  such  as  carcinoma,  ulceration,  dilatation,  etc. 
The  exciting  cause  of  the  condition  comprises  dietetic  indiscretions  in  a 
broad  sense,  such  as  persistent  hurried  and  irregular  eating,  insufficient 
mastication,  too  highly  seasoned  food,  pastry,  overindulgence  in  alcohol, 
tea,  tobacco,  iced  dr.nks,  soda  water,  etc.  It  is  sometimes  induced  also 
by  the  long-continued  use  of  certain  drugs,  such  as  arsenic,  mercury, 
iodine,  and  drastic  cathartics. 

Pathology,. — The  lesions  vary  considerably  in  different  cases.  In  cases, 
mild  and  of  short  standing,  so-called  simple  chronic  gastritis,  the  mucous 
'membrane  is  thickened,  pale  gray  in  color,  somewhat  congested,  though 
less  so  than  in  acute  gastritis,  and  covered  by  a  tenacious  mucus,  which 
sometimes  is  so  worked  as  to  warrant  the  term  mucous  gastritis.  Many 
dilated  and  enlarged  veins  may  be  visible,  especially  in  the  gastritis  of 
portal  obstruction,  and  there  are  frequently  small  areas  of  hemorrhage 
and  pigmentation — occasionally  of  superficial  erosion.  The  glands  are 
usually  choked  with  retained  secretion  and  may  enlarge  to  form  small 
cysts.  In  more  aggravated  cases,  almost,  if  not  quite,  the  entire  wall 
of  the  stomach  participates  in  the  process,  and  the  mucous  membrane 
may  be  thrown  up  into  small  polyp-like  projections — gastritis  polyposa. 
Histologically  the  lesions  are  those  of  interstitial  inflammation  with 
parenchymatous  degeneration.  In  most  cases,  after  the  lapse  of  time, 
atrophic  alterations,  and  more  or  less  dilatation  of  the  stomach,  result — 
so-called  atrophic  gastritis.  The  mucous  membrane,  as  well  as  the  entire 
wall  of  the  stomach,  becomes  much  thinned,  the  gastric  tubules  atrophy 
and  may  eventually  disappear  and  be  replaced  by  sclerotic  fibrous 
connective  tissue,  giving  to  the  mucous  membrane  an  exceedingly  smooth 
appearance,  which  may  be  interrupted  here  and  there  by  a  small  cyst. 
In  rare  cases  the  stomach  becomes  much  diminished  in  size  (so  that  its 
capacity  may  be  only  a  few  ounces),  and  its  wall  very  much  thickened 
(2  to  3  cm.)  in  consequence  of  hyperplasia  of  the  submucosa  and 
muscularis  (sclerosis  of  the  stomach).     The  condition  may  resemble  a 


A 


CHRONIC  GASTRITIS  627 

diffuse  infiltrating  carcinoma.  This  and  the  atrophic  gastritis  are  some- 
times spoken  of  as  two  varieties  of  sclerotic  gastritis — the  one  as  phthisis 
ventriculi,  the  other  as  cirrhosis  (sclerosis)  ventriculi. 

Symptoms. — The  symptoms  vary  much  in  different  cases,  and  in  the 
same  case  from  time  to  time.  Usually  the  appetite  is  poor  and  eating 
is  followed  by  epigastric  distress  and  a  sense  of  weight  and  fulness 
which  sometimes  amounts  to  severe  pain,  and  the  epigastrium  may  be 
tender  on  pressure.  In  some  cases  the  appetite  is  good;  in  other  cases 
there  is  marked  distress  when  the  stomach  is  empty,  and  eating  only 
augments  it.  Acid  eructations  and  flatulence  are  frequently  present 
(flatulent  dyspepsia).  Nausea  is  common,  but  vomiting  is  rather 
unusual  except  in  aggravated  cases,  in  alcoholic  subjects  (the  morning 
vomiting  of  alcoholics),  and  in  the  event  of  serious  gastric  disease, 
such  as  carcinoma,  ulcer,  pyloric  obstruction,  tlilatation,  etc.  Associ- 
ated with  the  gastritis  there  is  usually  more  or  less  catarrh  of  the  mouth 
and  the  intestine:  the  tongue  is  coated  and  its  tip  and  margin  red;  there 
is  an  unpleasant  taste  in  the  mouth,  the  breath  is  malodorous,  the 
oral  and  pharyngeal  secretions  are  often  increased,  and  constipation 
(due  to  deficient  activity  of  the  intestinal  muscularis)  is  the  rule,  although 
diarrhoea,  sometimes  associated  with  tympanites  and  colic  (due  to  the 
propulsion  into  the  intestine  of  undigested  and  fermenting  food)  may 
occur.  Headache,  irritability,  languor,  and  vertigo,  manifestations  of 
auto-intoxication,  and  palpitation  of  the  heart,  due  also  to  pressure  on 
the  heart  by  the  distended  stomach,  are  common  concomitants. 

In  the  event  of  vomiting,  the  ejected  matter  consists  of  partly  digested 
and  sometimes  fermenting  food,  considerable  mucus,  and  different 
aromatic  acids  (butyric,  lactic,  and  acetic),  which  partly  or  completely 
replace  the  normal  hydrochloric  acid.  The  presence  of  considerable 
mucus  suggests  the  term  mucous  gastritis.  Analysis  of  a  test  breakfast 
reveals  variations  in  the  hydrochloric  acid — hyperacidity  (uncommon), 
subacidity  (common),  or  anacidity  (rare).  Absorption  from  the  stomach 
is  slow — potassium  iodide  given  in  a  capsule  does  not  appear  in  the 
saliva  until  considerably  after  fifteen  minutes,  the  average  time  in 
normal  individuals;  and  the  motility  of  the  stomach  is  impaired — food 
may  be  found  in  the  stomach  as  much  as  seven  hours  after  the  last  eating. 

Atrophic  or  sclerotic  gastritis  gives  rise  to  no  characteristic  symptoms. 
The  symptoms  are  severe,  as  a  rule,  and  the  patient  may  emaciate 
rapidly.  Pernicious  anemia  or  carcinoma  is  frequently  simulated, 
particularly  as,  in  some  cases,  the  small,  thickened,  and  sclerotic  stomach 
gives  rise  to  a  palpable  mass  in  the  epigastrium,  and  hydrochloric 
acid  may  be  entirely  absent  from  the  gastric  contents. 

Diagnosis. — ^^Phe  diagnosis  is  usually  quite  apparent;  but  it  is  impor- 
tant to  bear  in  mind  that  the  great  majority  of  cases  of  supposed  chronic 
dyspepsia  or  gastritis  that  are  not  improved  by  several  months  of  well- 
dii-ected  therapy  have  an  anatomical  basis.  Most  of  them  are  cases  of 
gastric  or  duodenal  ulcer,  gastric  carcinoma,  cholecystitis  with  or  without 
gallstone,  perigastric,  pericholecystic,  or  periduodenal  adhesions,  clironic 


628  DISEASES  OF  THE  STOMACH 

pancreatitis,  chronic  appendicitis,  cirrhosis  of  the  Hver,  etc.  In  protracted 
cases  it  may  be  difficult  to  exclude  carcinoma,  especia  ly  as  carcinoma 
may  be  preceded  for  years  by  chronic  gastritis  or  ulcer.  Rapid  course, 
marked  emaciation,  hematemesis,  severe  epigastric  pain,  a  palpable 
tumor,  glandular  enlargement,  absence  of  hydrochloric  acid,  and  the 
presence  of  lactic  acid  (after  a  Boas  test  meal),  and  the  Oppler-Boas 
bacillus,  characterize  carcinoma.  When  a  palpable  tumor  is  present  the  rare 
cirrhotic  stomach  may  be  distinguished  from  carcinoma  by  the  fact  that 
in  the  one  the  stomach  is  small,  whereas  in  carcinoma  it  is  usually  con- 
siderably dilated. 

Prognosis. — In  many  cases  the  outlook  is  good — ^with  regulation 
of  the  diet  and  proper  hygiene.  Atrophy  of  the  mucosa,  however,  since 
it  cannot  be  repaired,  may  lead  to  grave  anemia  and  death. 

Treatment. — ^The  special  etiological  factors  in  each  case  must  be  cor- 
rected. Food  must  be  taken  at  regular  intervals;  it  must  be  eaten 
slowly  and  thoroughly  masticated;  tea,  coffee,  alcohol,  tobacco,  pastry, 
hot  bread,  hot  cakes,  fats,  sweets,  pork,  veal,  etc.,  must  be  prohibited. 
In  some  cases  mere  regulation  of  the  diet  suffices  to  dissipate  all  the 
symptoms.  In  other  cases  a  strict  dietetic  regimen  is  imperative,  for 
a  time  at  least;  in  some  cases,  especially  those  occurring  in  liver  cir- 
rhosis, Bright's  disease,  etc.,  a  milk  diet  for  several  weeks  may  be  tried. 
The  milk  should  be  given  in  stated  amounts  at  regular  intervals  and 
about  2  liters  in  the  twenty-four  hours.  It  may  be  diluted  with  Vichy 
or  lime  water,  or,  especially  in  the  event  of  nausea,  sodium  bicarbonate 
(5  to  10  grains  0.3  to  0.6  gram)  may  be  added  to  each  glassful.  For  a 
short  time  the  milk  may  be  peptonized,  or  buttermilk  may  be  substituted. 
In  most  cases  it  is  unnecessary  to  restrict  the  diet  to  milk;  most  patients 
can  d'gest,  in  addition  to  milk,  dry  toast,  chicken,  and  roasted  or  broiled 
red  meats.  Farinaceous  foods,  especially  potatoes,  and  coarse  vegetables 
are  a  fruitful  source  of  trouble  and  must  be  interdicted,  especially 
in  the  event  of  flatulence  or  acid  eructations.  As  the  patient  improves, 
the  diet  may  be  made  more  liberal  by  the  addition  of  eggs,  broths,  and  rice; 
and  green  vegetables,  such  as  spinach,  lettuce,  fruits,  etc.,  may  be 
allowed;  but  pastry,  fried  foods,  coarse  vegetables,  strong  condiments, 
and  meats,  such  as  pork  and  veal,  must  be  prohibited.  In  general, 
fluids  taken  with  a  meal  should  be  moderate  in  amount;  one  should 
strive  for  the  happy  medium  between  the  senselessness  of  the  absolutely 
dry  diet  and  the  perniciousness  of  the  excessive  amounts  of  fluid.  Plain 
water  is  the  best  fluid.    It  should  be  partaken  of  freely  between  meals. 

The  medicinal  treatment  should  be  based  upon  the  state  of  the  gastric 
secretion.  In  conditions  of  subacidity,  dilute  hydrochloric  acid  (15 
minims,  1  c.c),  in  a  glassful  of  water,  should  be  given  with  each  meal. 
In  many  cases,  however,  instead  of  supplying  the  deficient  hydro- 
chloric acid,  we  can  stimulate  the  secretion  and  improve  the  motor  power 
of  the  stomach  with  tincture  of  nux  vomica,  beginning  with  15  minims 
(1  c.c.)  three  times  a  day  and  gradually  increasing  the  dose  to  60  minims 
(4  c.c.)  or  more.    The  bitter  tonics,  gentian,  cinchona,  quassia,  calumba, 


ACUTE  DILATATION  OF  THE  STOMACH  629 

condurango,  cardamoms,  etc.,  are  extensively  used,  and  are  of  value  in 
improving  the  appetite  and  stimulating  the  secretion  and  motor  power 
of  the  stomach.  Digestive  ferments  (pepsin,  pancreatic  preparations, 
etc.)  may  be  of  service  in  supplying  a  deficient  digestive  ferment  pending 
the  restoration  of  the  gastric  functions,  but  they  are  less  important  than 
was  formerly  believed,  the  hydrochloric  acid  being  the  more  important 
factor  and  activating  the  zymogens  already  present.  In  protracted  cases 
silver  nitrate,  ^  grain  (0.008  gram)  combined  with  extract  of  belladonna 
or  hyoscyamus,  ^  grain  (0.008  gram),  three  times  daily,  if  there  is  much 
pain  and  hyperacidity,  is  of  value. 

In  many  cases  lavage,  preferably  in  the  morning  before  breakfast, 
is  serviceable.  In  ordinary  cases,  plain  lukewarm  water,  or  1  per  cent, 
sodium  chloride  solution,  may  be  used.  In  case  there  is  much  mucus,  a 
5  per  cent,  sodium  bicarbonate  solution  may  be  used,  and  in  case  of 
fermentation,  a  3  per  cent,  boric-acid  solution  or  a  2  per  cent,  salicylic- 
acid  solution,  may  be  used — depending  upon  the  exigencies  of  the  case. 
The  lavage  may  be  done  daily  or  every  other  day,  but  its  use  should  not 
be  persisted  in  too  long,  lest  the  ''stomach-tube  habit"  be  acquired.  In 
some  cases  the  drinking  of  a  glassful  of  hot  water  before  breakfast,  or 
before  each  meal,  is  a  more  or  less  satisfactory  substitute  for  lavage. 

Excessive  flatulence  may  be  relieved  by  the  use  of  bismuth,  sodium 
bicarbonate,  soda-mint,  aromatic  spirit  of  ammonia,  chloroform  water, 
magnesium  oxide,  carbonate,  or  salicylate,  carbolic  acid,  creosote,  resorcin, 
charcoal,  etc.  Vomiting,  if  marked,  may  be  relieved  by  carbolic  acid, 
dilute  hydrocyanic  acid,  cerium  oxalate,  bismuth  subnitrate  or  sub- 
carbonate,  cocaine,  lavage,  etc. 


ACUTE  DILATATION  OF  THE  STOMACH. 

Acute  dilatation  of  the  stomach  results  usually  from  the  rapid  over- 
filling of  the  stomach  with  excessive  amounts  of  food  and  drink  (espe- 
cially effervescing  fluids) — the  development  of  the  condition  being  some- 
what favored  by  acute  and  chronic  catarrh  of  the  stomach.  Aggravated 
cases  merit  the  designation  acute  paralytic  distention  of  the  stomach 
(Fagge),  and  not  infrequently  terminate  fatally.  Another  and  large 
series  of  cases  follow  operations  and  general  anesthetization.  Minor 
grades  sometimes  occur  during  or  after  certain  of  the  infectious  diseases 
— in  consequence  of  parenchymatous  degeneration  of  the  gastric  muscu- 
lature. A  majority  of  all  cases  have  been  found  to  be  due  to  obstruc- 
tions of  the  lower  end  of  the  duodenum  by  the  root  of  the  mesentery. 
The  symptoms  are  sudden  in  onset,  and  consist  of  abdominal  pain  and 
distention,  the  vomiting  of  a  large  amount  of  bile-stained  non-fecal 
fluid,  collapse,  and  frequently  death.  The  treatment  of  the  aggravated 
cases  consists  of  emptying  the  stomach  by  means  of  the  stomach  tube, 
placing  the  patient  in  the  anterior  prone  or  knee-chest  position,  sub- 
sequent restriction  of  the  diet,  and  the  use  of  tonics. 


630  DISEASES  OF  THE  STOMACH 

CHRONIC  DILITATION  OF  THE  STOMACH. 

(Gastrectasis.) 

Etiology. — Chronic  dilatation  of  the  stomach — an  increase  in  the 
capacity  of  the  stomach  associated  with  motor  insufficiency — is  especially 
common  in  adult  life,  but  is  not  rare  in  rachitic  children.  It  may  be 
obstructive  or  non-obstructive.  The  causes  of  obstructive  dilatation  are : 
(1)  Pyloric  obstruction,  which  may  be  due  to  (a)  intragastric  factors,  such 
as  cicatrization  of  a  gastric  ulcer,  carcinoma  or  other  tumor,  non-malig- 
nant hypertrophic  stenosis  of  the  pylorus,  pyloric  spasm;  or  (6)  extra- 
gastric  factors,  such  as  compression  by  a  tumor  of  the  gall-bladder,  liver, 
pancreas,  or  neighboring  lymph  nodes,  or  adhesions  about  the  pylorus, 
and  other  causes  (such  as  displaced  right  kidney)  exerting  traction  and 
causing  twisting  or  angulation  of  the  pylorus.  Similar  factors  operating 
on  the  duodenum  may  also  cause  dilatation  of  the  stomach.  Non- 
obstructive dilatation  is  due  to  atony  of  the  muscular  coat  of  the  stomach; 
this  may  be  (a)  congenital,  or  (b)  acquired,  in  consequence  of  re- 
peated overfilling  of  the  stomach  (beer  drinkers,  gluttons,  the  insane, 
diabetics,  etc.),  chronic  catarrh,  and  other  organic  (especially  degenera- 
tive) diseases  of  the  stomach.  It  is  common  in  tuberculosis,  carcinoma, 
anemia,  and  other  general  disturbances  of  nutrit'on,  disorders  of  inner- 
vation, etc. 

Pathology.  —  The  capacity  of  the  average  normal  adult  stomach  is 
about  1600  c.c.  (Ewald),  though  this  is  subject  to  individual  variations, 
and  doubtless  varies  in  the  same  individual  from  time  to  time."  Some 
persons  normally  have  an  abnormally  large  stomach — ^megastria.  In 
disease,  however,  the  dilatation  may  be  so  extreme  that  the  stomach 
occupies  almost  the  entire  abdominal  cavity  and  attains  a  capacity  of 
10  or  more  liters,  especially  in  the  obstructive  forms.  In  obstructive 
dilatation  the  stomach  wall  is  thickened  in  consequence  of  hj^ertroph}^; 
in  the  non-obstructive  form  it  is  usually  thinned  in  consequence  of 
atrophy  of  the  muscular  coat.  There  are  also  the  evidences  of  catarrhal 
or  other  alterations. 

Symptoms. — ^The  symptoms  vary  with  the  cause  and  the  degree  of  the 
dilatation.  Minor  grades,  especially  those  due  to  muscular  atony,  may 
be  symptomless.  The  symptoms  of  chronic  gastric  catarrh  are  present 
in  the  majority  of  cases,  and  should  the  dilatation  be  associated  with 
carcinoma,  the  specific  symptoms  of  carcinoma  may  be  present.  The 
dilatation  itself  is  suggested  by  loss  of  appetite  alternafing  with  exces- 
sive appetite  and  thirst,  acid  eructations,  constipation,  and  the  vomiting 
at  long  intervals  of  large  amounts  of  fluid  and  partially  digested  and 
stagnant  food.  Vomiting  sometimes  occurs  daily,  but  not  infrequently 
at  longer  intervals  —  three  days  or  more;  and  the  amount  ejected 
at  once  may  be  as  much  as  3  liters  or  more.  The  epigastric  distress, 
which  often  has  been  gradually  increasing,  is  usually  much  relieved 
hj  the  vomiting.  The  vomit  is  malodorous  and  acid  (due  to  aromatic 
acids,  lactic,  acetic,  and  butyric),  and  on  stand  ng  separates  into  three 


Chronic  dilatation  of  the  stomach  63i 

layers  —  the  lowermost  consisting  of  decomposing  food  remnants 
(food  that  may  have  been  taken  days,  even  weeks,  previously);  the 
middle,  of  a  dirty,  yellowish,  light  brownish,  or  grayish  fluid;  and 
the  uppermost,  of  a  dirty  brown  frothy  mass.  The  hydrochloric  acid 
content  varies  much,  depending  largely  upon  the  associated  conditions; 
it  is  usually  diminished  or  absent,  rarely  increased.  In  consequence  of 
the  absorption  of  but  little  fluid,  constipation,  lessening  of  the  amount 
of  urine,  and  a  dry  skin  result;  in  consequence  of  deficient  nourish- 
ment the  patient  loses  weight  and  strength  and  becomes  anemic;  and 
in  consequence  of  auto-intoxication,  the  absorption  of  fermentation 
products,  divers  nervous  disorders,  such  as  headache,  vertigo,  insomnia, 
neuralgiform  pains,  mental  depression,  hypochondriasis,  etc.,  result. 

Physical  Signs. — Physical  examination  often  reveals  a  prominent 
and  distended  abdomen  (often  most  marked  about  or  below  the  umbili- 
cus), and  the  outline  of  the  enlarged  stomach  can  often  be  perceived — 
the  greater  curvature  usually  below  the  umbilicus,  often  near  the  pubes. 
Peristaltic  (occasionally  antiperistaltic)  waves  are  sometimes  visible  — 
and  may  even  be  palpable.  Splashing  sounds  (clapotage)  may  usually 
be  elicited,  and  sometimes  even  by  the  patient  (by  suddenly  contracting 
the  diaphragm)  or  other  sudden  motion.  Percussion  and  auscultatory 
percussion  yield  definite  information  as  to  the  size  of  the  stomach.  The 
most  trustworthy  results  are  obtained  by  inflating  the  empty  stomach 
(by  means  of  a  stomach  tube  and  a  hand-bulb  syringe  or  other  pump). 
A  stomach  may  be  considered  dilated  when  the  vertical  diameter  of  gas- 
tric tympany  is  more  than  12  to  14  cm.  The  lower  border  of  the  stomach 
when  it  is  dilated  is  at  or  below  the  umbilicus,  but  one  must  not 
mistake  a  displaced  for  a  dilated  stomach.  Frequently,  however,  the 
two  conditions  are  associated. 

Diagnosis. — The  diagnosis  is  usually  quite  obvious  from  the  recurrent 
vomiting  of  large  amounts  of  fluid  and  the  results  of  inspection  and  of 
percussion,  especially  after  inflation  of  the  stomach.  Gastroptosis  may 
usually  be  excluded  by  the  results  of  physical  examination  and  the 
presence  of  vomiting  of  stagnant  food. 

Piognos  s. — ^The  prognosis  is  favorable  in  most  cases  except  those  due 
to  malignant  obstruction  of  the  pylorus. 

Treatment. — The  most  particular  attention  must  be  paid  to  the  diet, 
which  should  be  concentrated  and  readily  assimilated,  such  as  eggs,  chops, 
steak,  roast  beef,  chicken,  lamb,  and  mutton  (no  coarse  meats),  well- 
toasted  bread  or  Zw'eback,  rice,  etc.,  for  a  time,  at  least.  Fluids  should 
be  reduced  to  a  minimum,  and  the  food  should  be  taken  in  small  amounts 
at  rather  frecjuent  intervals,  rather  than  larger  amounts  less  frequently. 
The  digestive  processes  may  be  aided  and  the  comfort  of  the  patient 
promoted  by  the  recumbent  posture  for  an  hour  or  so  after  partaking  of 
food.  Gradually  a  more  lil)eral  diet  may  be  permitted.  In  aggravated 
cases  it  may  be  necessary  to  put  the  patient  to  bed  and  give  only  small 
amounts  of  egg-albumen,  peptonized  milk,  scraped  beef,  etc.,  for  several 
days  or  a  week. 


632  DISEASES  OF  THE  STOMACH 

Lavage  is  a  useful  adjuvant  in  many  cases,  and  is  of  unquestionable 
service  in  the  beginning  of  the  treatment.  Warm  water,  a  saline  solu- 
tion, or  a  mild  antiseptic  solution  (boric  acid,  salicylic  acid)  may  be  used. 
It  serves  to  remove  the  stagnating  and  fermenting  food,  to  cleanse  the 
mucous  membrane  (removing  sometimes  large  amounts  of  mucus — in 
associated  catarrh),  and  it  relieves  the  overloaded  stomach  of  a  great 
weight.  It  is  wise  to  discontinue  the  lavage  as  soon  as  possible,  since  the 
stomach-tube  habit  is  not  without  attendant  evil  consequences. 

Medicinal  measures  comprise  the  use  of  tincture  of  nux  vomica,  which 
is  of  the  very  greatest  service  in  increasing  the  motor  power  of  the 
stomach,  if  given  in  doses  of  15  minims  (1  c.c),  three  times  daily,  and 
gradually  increased  until  as  much  as  60  minims  (4  c.c.)  or  more  is 
given  three  times  daily.  Strychnine  may  be  used,  but  it  appears  to  be 
not  so  useful  as  the  tincture  of  nux  vomica.  When  hydrochloric  acid  is 
deficient,  it  should  be  supplied  for  a  time  at  least.  Occasionally  antifer- 
mentatives,  such  as  carbolic  acid,  creosote,  salicylic  acid,  resorcin, 
charcoal,  magnesia,  etc.,  may  be  called  for. 

In  dilatation  due  to  benign  or  malignant  obstruction  of  the  pylorus, 
perigastric  adhesions,  and  similar  conditions,  resort  should  be  had  to 
surgical  procedures. 


ULCER  OF  THE  STOMACH  AND  DUODENUM. 

(Simple,  Round,  Peptic,  or  Perforating  Ulcer  of  the  Stomach  and  Duodenum.) 

The  term  ulcer  of  the  stomach  or  duodenum  is  somewhat  inaptly 
used  to  designate  a  localized  area  of  necrosis  of  the  wall  of  the  stomach 
or  duodenum,  resulting  from  lessening  of  vitality  and  consequent  diges- 
tion by  the  gastric  juice. 

Etiology. — Gastric  and  duodenal  ulcer  may  occur  in  both  sexes,  and 
at  all  ages,  even  in  the  very  young  and  the  aged.  Formerly  about  60 
per  cent,  of  the  cases  were  believed  to  occur  in  women,  but  surgical 
statistics  have  shown  that  the  condition  is  just  as  common  if  not  more 
common  in  men.  In  women  it  occurs  especially  between  the  twentieth 
and  the  thirtieth  year,  particularly  in  servants,  in  whom  it  is  attributed  to 
anemia  and  their  injudicious  mode  of  eating  and  tasting  very  hot  food 
(of  the  truth  of  which  there  is  little  trustworthy  data).  In  men  it  is 
most  common  between  the  thirtieth  and  the  fiftieth  year,  especially  in 
shoemakers,  tailors,  and  weavers,  etc.,  in  whom,  with  little  reason,  it  has 
been  attributed  in  part  to  pressure  on  the  epigastrium. 

The  exact  cause  of  the  necrosis  is  ill  understood.  It  has  been  attrib- 
uted to  trauma  —  external,  internal,  and  that  resulting  from  violent 
vomiting  (whence,  as  sometimes  in  uremia,  hemorrhagic  erosion  and 
ulceration  may  result);  by  Virchow  to  thrombosis  or  embolism  of  a 
nutrient  artery,  infarction,  and  consequent  necrosis;  by  Pavy  and 
Cohnheim  to  diminished  alkalescence  of  the  blood  (common  in  anemias), 
supplemented  by  gastric  hyperacidity  and  local  injury  to  the  gastric 


ULCER  OF  THE  STOMACH  AND  DUODENUM  633 

mucosa;  by  Dallavedova  to  disturbances  of  the  celiac  plexus  and  the 
splanchnics;  by  Talma  to  disease  of  the  pneumogastric  nerve,  occa- 
sioning undue  muscular  contraction;  and  by  Letulle,  Nauwerck,  and 
Sidney  Martin  to  bacterial  infection  and  toxic  necrosis  of  the  gastric 
mucosa.  Recently  it  has  been  suggested  that  in  health  the  cells  of  the 
gastric  mucosa  produce  an  anti-enzyme  that  resists  peptic  digestion  of  the 
cells,  and  that  this  anti-enzyme  may  be  deficient  or  absent  in  disease. 
And  it  has  also  been  supposed  that  the  system  may  contain  a  poison 
which,  being  eliminated^  injures  the  gastric  cells.  Experimentally,  ulcers 
may  be  produced  by  injecting  into  the  stomach  a  gastrotoxic  serum  pre- 
pared by  immunizing  a  goat,  cat,  or  other  animal  to  the  gastric  cells  of 
another  animal  Ewald  insists  upon  the  importance  of  anemia  and  gas- 
tric hyperacidity,  which  are  assuredly  present  clinically  in  most  of  the 
cases. 

The  analogous  duodenal  ulcer  is  attributable  to  like  factors.  In 
addition,  ulceration  of  the  duodenum  is  often  observed  after  burns  of  the 
skin,  especially  of  the  abdomen;  it  is  attributable  to  the  action  of  toxins 
formed  in  the  burned  skin  (or,  perhaps,  retained  on  account  of  functional 
incapacity  of  the  burned  skin),  and  eliminated  by  the  duodenal  mucosa. 

Peptic  ulceration  of  the  jejunum  is  occasionally  observed  after  gastro- 
enterostomy, and  is  attributed  to  the  influence  of  acid  chyme,  which  finds 
its  way  directly  into  the  intestine. 

Pathology. — Small  abrasions  or  hemorrhagic  erosions  of  the  gastric 
mucosa  are  rather  common.  They  are  perhaps  not  essentially  different 
from  the  more  obvious  ulceration  (so-called),  although  they  usually 
heal.  The  gastric  ulcer  itself  may  be  acute  or  chronic.  Usually  (80 
per  cent,  of  cases)  there  is  a  single  ulcer  (chronic  form);  sometimes 
there  are  several,  and  rarely  there  are  many  ulcers  (acute  and  chronic 
forms) :  I  have  seen  more  than  twenty  in  one  case.  The  single  chronic 
ulcer  is  usually  situated  in  the  posterior  wall  toward  the  pylorus  and 
at  or  near  the  lesser  curvature  (more  than  80  per  cent,  of  the  cases); 
in  some  cases  it  involves  and  may  even  straddle  the  pylorus.  The 
acute  ulcer  is  usually  small,  rounded,  well  defined  (punched  out),  with  a 
smooth  floor,  and  without  associated  induration.  The  chronic  ulcer  is 
often  much  larger,  sometimes  very  large,  5,  10,  or  15  cm.  in  diameter, 
irregular  in  shape,  with  sloping  or  terraced  margins  (funnel-like);  its 
floor  may  be  the  submucous,  muscular,  or  peritoneal  coats  of  the 
stomach — in  some  cases  even  adjacent  viscera,  such  as  the  pancreas 
or  liver,  to  which  it  may  have  become  adherent.  Cicatrization  usually 
results,  the  resulting  scar  being  smooth  if  the  mucous  membrane  only  is 
involved;  but  the  cicatrization  of  deeper  ulcers  is  attended  by  the  devel- 
opment of  a  puckered  and  stellate  scar  and  consequent  damage  to  the 
stomach,  such  as  pyloric  stenosis  and  dilatation  of  the  stomach.  The 
cicatrization  of  a  so-called  girdle  ulcer  may  lead  to  hour-glass  con- 
traction of  the  stomach;  and  perigastric  adhesions  may  result  in  other 
deformities  of  the  stomach,  interference  with  its  function,  and  persistent 
pain.    Perigastric,  especially  posterior,   adhesions,  however,    in   many 


634  DISEASES  OF  THE  STOMACH 

cases  are  a  fortunate  provision  of  nature,  since  they  anticipate,  and 
sometimes  prevent,  a  not  uncommon  and  frequently  fatal  accident — 
perforation.  Perforation,  when  it  occurs,  is  usually  into  the  adhesions 
and  the  related  organs,  where  it  gives  rise  to  an  abscess,  or  into  the 
lesser  peritoneal  cavity,  where  it  occasions  what  is  known  as  a  sub- 
phrenic pyopneumothorax;  or,  as  sometimes  happens,  sinuses  may  form 
between  the  stomach  and  the  colon,  duodenum,  pericardium,  pleura,  oi* 
externally.  Perforation  of  ulcers  on  the  anterior  sm'face  of  the  stomach, 
where  adhesions  rarely  form,  usually  gives  rise  to  an  extensive  and 
rapidly  fatal  peritonitis.  Extensive  and  rarely  fatal  hemorrhage  may 
occur  usually  from  a  branch  or  the  main  artery  of  the  lesser  curvature, 
sometimes  from  rupture  of  an  aneurysmal  dilatation  of  an  artery  in  the 
floor  of  the  ulcer,  rarely  from  erosion  of  the  splenic  artery,  etc.  More 
common  bleeding  is  doubtless  prevented  by  antecedent  thrombosis. 
Some  ulcers  persist  for  years;  recmTences  are  common;  and  carcinoma 
sometimes  develops  from  an  ulcer  or  its  cicatrix. 

The  analogous  duodenal  ulcer  is  found  above  the  papilla.  In  more 
than  one-half  of  the  cases  it  reaches  to  v/ithin  three-fourths  inch  of  the 
pylorus,  and  in  20  per  cent,  of  the  cases  it  involves  the  margin  of  the 
pylorus.  The  appearances  and  the  accidents,  especially  hemorrhage, 
perforation,  and  adhesions  to  adjacent  tissues  are  quite  analogous  to 
those  of  gastric  ulcer. 

Symptoms. — ^The  symptoms  are  extremely  variable.  In  a  few  cases 
(lament  gastric  ulcer)  there  are  no  symptoms,  the  ulcer  being  an  acci- 
dental finding  at  the  necropsy;  rarely  a  profuse  hemorrhage  or  a  per- 
foration is  the  initial  manifestation.  In  the  majority  of  cases,  however, 
definite  symptoms  suggesting  ulcer  are  preceded  for  months  or  years 
by  the  ordinary  evidences  of  chronic  gastritis :  but  many  of  these  are 
cases  of  already  existing,  that  is,  chronic  ulcer.  Ulcer  is  suggested  by 
pain,  tenderness,  undue  vomiting,  pylorospasm,  and  hyperchlorhydria. 
Gaseous  and  acid  fluid  eructations,  headache,  faintness,  and  constipa- 
tion, occasionally  diarrhoea,  may  also  be  present.  Pain  is  a  constant 
and  characteristic  symptom,  although  it  varies  much  in  dift'erent  cases. 
It  is  usually  severe,  and  may  be  extreme  and  paroxysmal  (character- 
istic). It  may  be  localized  to  a  small  spot,  which  is  often  exquisitely 
tender,  near  the  median  line  in  the  epigastrium;  it  often  radiates  to  the 
side  and  back,  and  may  be  associated  with  a  spot  of  tenderness  near  the 
tenth  thoracic  vertebra  (Boas'  point).  Taking  food  often  induces  or 
aggravates  the  pain,  either  immediately,  or  after  a  short  time,  and  the 
pain  persists  until  the  stomach  is  relieved  of  food,  either  by  vomiting  or 
by  its  passage  into  the  intestine;  it  is  sometimes  very  severe  two  or  three 
hom'S  after  eating,  when  the  acid  chyme  begins  to  pass  into  the  intes- 
tine, thus  irritating  an  ulcer  situated  at  the  pylorus.  The  pain  is  some- 
times relieved  by  firm  pressure  or  by  change  of  posture — permitting 
the  gastric  contents  to  gravitate  away  from  the  site  of  the  ulcer.  The 
pain  is  thus  due  to  direct  irritation  of  the  ulcer  by  the  gastric  contents, 
to  the  peristaltic  movements  of  the  stomach,  and  to  the  hyperchlorhydria 


ULCER  OF   THE  STOMACH  AND  DUODENUM  635 

(usually,  though  not  always,  present).  In  some  cases  it  may  also  result 
from  an  intermittent  or  more  or  less  continuous  pylorospasm,  which 
leading  of  retention  of  intragastric  gases  may  cause  stretching  of  the 
stomach  or  increased  intragastric  tension. 

^^omitino■  is  rather  common,  and  occurs  usually  at  the  height  of  the 
paroxysm  of  pain  (from  one-quarter  to  two  hours  after  eating).  It  is  not 
iufrequently  provoked  voluntarily  by  the  patient  to  relieve  the  intense 
pain.  AMien  perigastric  adhesions  have  formed,  vomiting  may  occur  in 
the  intervals  between  eating,  and  when  dilatation  (a  late  phenomenon) 
ensues,  the  characteristic  vomiting  of  this  condition  results.  In  the  ab- 
sence of  dilatation,  gastric  digestion  is  usually  hastened  rather  than 
retarded,  and  the  vomited  matter  is  usually  small  in  amount,  well  digested, 
and  has  an  acid  taste  and  odor.  It  also,  as  well  as  a  test  meal,  usually  but 
not  invariably  reveals  marked  hyperacidity  (increased  hydrochloric  acid). 

Hematemesis  is  common — occurring  clinically  in  about  50  per  cent, 
of  the  cases.  Some  bleeding  probably  occurs  in  all  cases,  from  irritation 
and  congestion  provoked  by  the  food,  distention  and  stretching  of  the 
stomach  by  gases  (Moynihan),  severe  vomiting,  etc.,  but  the  blood  may  not 
be  visible  macroscopically  in  the  vomit  or  the  stools.  As  a  rule,  the  bleed- 
ing is  moderate  in  amount,  but  it  may  be  extreme  (and  followed  by 
syncope),  and  it  is  rarely  immediately  fatal.  The  extravasation  of  the 
blood  being,  as  a  rule,  rather  slow,  the  blood  may  remain  in  the  stomach 
for  some  time,  and,  being  altered  by  the  gastric  juice,  appear  in  the  vomit 
as  black,  tarry  masses  resembling  liver,  or  smaller  particles  resembling 
coffee  grounds.  The  vomiting  of  a  large  amount  of  bright  blood,  how- 
ever, is  quite  significant  of  gastric  ulcer,  inhered  blood  often  appears  in 
the  stools;  and  in  a  few  cases,  when  the  hemorrhage  is  small,  it  may 
appear  in  the  stools  and  not  in  the  vomit.  In  many  cases  recourse 
must  be  had  to  tests  for  occult  blood  to  detect  small  amounts  in  the 
vomit  or  the  feces.  In  most  cases  a  posthemorrhagic  anemia  develops, 
and  in  some  cases  may  become  extreme. 

In  some  cases  one  may  be  able  to  palpate,  through  the  abdominal 
wall,  a  mass,  which  may  be  a  thickening  about  the  ulcer,  perigastric 
exudation  and  adhesions,  enlarged  regional  lymph  nodes,  or  the  li}-per- 
trophied  pylorus  resulting  from  long-continued  spasmodic  contractions. 
Loss  of  weight  may  occur  in  protracted  cases  and  following  large  hemor- 
rhages (when  it  is  associated  with  marked  anemia),  but  many  subjects 
appear  fairly  well  nourished. 

The  onset  of  perforation,  which  occurs  in  about  (i  per  cent,  of  the 
cases,  is  manifested  by  severe  abdominal,  usually  epigastric,  pain,  and 
sliock,  and  the  rapid  development  of  peritonitis,  usually  of  the  u])per 
half  of  the  alxlomen,  aUhough  it  may  become  general. 

Diagnosis. —  Dyspeptic  symptoms,  with  local  pain  occurring  par- 
oxysmally  and  provoked  by  food,  circumscribed  tenderness,  li\per- 
chlorhydria,  and  hematemesis  in  a  young  woman,  are  unmistakable; 
but  dyspeptic  symptoms,  without  hematemesis,  in  a  chlorotic  girl  or  in 
a  man  may  be  difficult  to  interpret.    The  greatest  diagnostic  siguilicance 


636  DISEASES  OF  THE  STOMACH 

should  be  attached  to  the  persistence  of  symptoms,  especially  of  pain, 
tenderness,  pylorospasm,  and  hyperchlorhydria,  despite  several  months 
of  well-directed  therapy:  such  cases  often  believed  to  be  merely  "chronic 
indigestion,"  usually  have  an  anatomical  basis,  which  is  often  ulcer. 
The  pain  of  ulcer,  as  contrasted  with  other  conditions,  may  sometimes 
be  relieved  by  orthoform,  10  to  30  grains  (0.6  to  2  grams)  at  once,  or 
smaller  doses  before  meals.  Some  diagnostic  significance  has  been 
attached  to  this.  It  may  be  difficult  or  impossible  (and  is  usually  unne- 
cessary since  the  treatment  is  similar)  to  differentiate  duodenal  from 
gastric  ulcer,  but  duodenal  ulcer  is  suggested  by  the  male  sex,  later  life, 
pain  to  the  right  rather  than  to  the  left  of  the  median  line,  delayed  after 
taking  food,  little  or  no  vomiting,  and  blood  in  the  stools  rather  than 
hematemesis.  In  gastralgia,  as  contrasted  with  ulcer,  the  pain  is  less 
circumscribed,  occurs  independently  of  or  is  relieved  by  food  (this 
occasionally  occurs  in  ulcer),  there  is  less  circumscribed  epigastric  and 
post-thoracic  tenderness,  there  is  no  hematemesis,  vomiting  is  uncom- 
mon, the  general  nutrition  of  the  patient  suffers  little  if  at  all,  and  there 
are  periods  of  entire  relief  from  symptoms.  The  pain  of  biliary  colic 
may  be  distinguished  by  its  sudden  onset,  usually  extreme  severity,  short 
duration,  and  sudden  cessation,  enlargement  and  tenderness  of  the  liver 
and  gall-bladder,  and  possible  jaundice,  fever,  and  leukocytosis.  The 
hematemesis  of  cirrhosis  of  the  liver  maybe  distinguished  by  its  marked 
preference  for  the  male  sex,  certain  etiological  factors  (especially  alco- 
hol), and  associated  liver  conditions.  The  hematemesis  of  chronic 
gastric  catarrh,  especially  that  occurring  in  the  aged,  and  that  attrib- 
uted to  gastric  erosions,  is  usually  difficult  of  differentiation,  but  in 
erosions  hematemesis  is  less  marked,  the  pain  is  less  severe  and  burning 
in  character,  subacidity  rather  than  hyperacidity  is  likely  to  be  present, 
and,  as  maintained  by  Einhorn,  shreds  of  the  gastric  mucosa  may  be 
found  in  the  vomit  or  the  washings  after  lavage.  Attempts  have  been 
made  to  determine  the  site  of  the  ulcer  by  noting  the  influence  of 
posture  on  the  pain  (different  postures  causing  the  food  to  come  in 
contact  with  and  irritate  the  ulcer,  or  to  gravitate  away  from  it);  and 
a  palpable  induration  has  been  deemed  significant  of  ulcer  on  the 
anterior  wall,  and  pain  in  the  back  significant  of  ulcer  of  the  posterior 
wall — but  these  signs  are  untrustworthy. 

Prognosis. — Most  patients  recover,  but  the  disease  usually  runs  a 
protracted  course,  relapses  are  common,  and  large  hemorrhages  and  per- 
forations are  to  be  dreaded;  cicatrization  of  an  ulcer  may  cause  pyloric 
obstruction  and  dilatation  or  hour-glass  contracture  of  the  stomach, 
or  may  be  followed  by  carcinoma;  and  perigastric  adhesions  may  be  a 
source  of  continued  pain  and  ill  health. 

Treatment. — Absolute  rest  in  bed  for  the  patient  for  at  least  four 
weeks,  and  rest  for  the  stomach  secured  by  rectal  feeding  for  at  least 
seven  days,  are  of  prime  importance.  Rarely  it  may  be  deemed 
desirable  to  begin  feeding  by  the  stomach  at  the  end  of  three  or  four 
days.     The  rectal  enemas  may  consist  of  peptonized  milk,  4  ounces 


ULCER  OF  THE  STOMACH  AND  DUODENUM  637 

(120  c.c),  the  whites  of  one  or  two  eggs,  a  pinch  of  salt,  and  5  minims 
(0.3  c.c.)  of  deodorized  tincture  of  opium.  This  may  be  injected  high 
up  in  the  rectum  or  in  the  sigmoid  every  six  or  eight  hours,  and  should 
be  preceded  by  a  cleansing  enema.  When  feeding  by  the  mouth  is 
commenced  the  food  must  be  very  bland,  and  neither  too  hot  nor  too 
cold.  Milk  is  the  best  food.  At  first  it  should  be  peptonized  or 
pancreatinized,  and  given  in  small  amounts  at  regular  intervals — in 
ordinary  cases,  2  to  4  ounces,  and  later  4  to  6  ounces,  every  three  hours. 
To  counteract  the  hyperacidity,  sodium  bicarbonate  or  calcined  mag- 
nesia may  be  added  to  the  milk.  Buttermilk  is  sometimes  an  excellent 
substitute.  Soon  two  to  four  or  six  raw  eggs  daily  may  be  added  to  the 
milk,  and  beef  juice,  thin  gruels,  arrowroot,  strained  broths,  potato 
puree,  etc.,  may  be  given.  In  the  early  days  of  the  treatment  undue 
thirst  may  be  relieved  by  enteroclysis.  At  the  end  of  three  or  four 
weeks  from  the  time  of  beginning  feeding  by  the  mouth,  scraped  beef, 
sweetbread,  tender  chicken,  and  similar  articles  of  diet  may  be  allowed ; 
but  care  and  discretion  must  be  enjoined  for  at  least  three  months. 

An  essential  feature  of  the  treatment  is  regulation  of  the  bowels, 
which  should  be  opened  once  daily — ^preferably  by  the  use  of  saline 
cathartics.  These  do  good  not  only  by  clearing  the  bowel,  but  also 
(and  this  is  the  philosophy  of  their  use  in  large  amounts)  by  counter- 
acting the  hyperacidity,  and  by  their  depurative  action  relieving  the 
commonly  associated  gastro-intestinal  catarrh. 

In  many  cases,  aside  from  the  foregoing,  no  medicines  are  required — ■ 
unless  pain  is  severe.  Leube  speaks  highly  of  the  local  use  (to  the  epi- 
gastrium) of  boric-acid  ointment  and  hot  flaxseed  poultices  (changed 
every  fifteen  minutes)  during  the  day,  and  a  cold-water  compress  during 
the  night — in  relieving  the  epigastric  pain  and  distress.  Hemorrhage 
(blood  in  the  bowels,  as  well  as  hematemesis)  is  a  contra-indication  to  the 
use  of  the  poultices.  In  cases  of  severe  pain,  however,  I  am  rather  partial 
to  the  use  for  a  short  time  of  opium,  which  should  be  combined  with 
silver  nitrate,  giving  three  times  daily  a  pill  of  silver  nitrate,  |  grain 
(0.015  gram),  and  extract  of  opium,  i  to  |-  grain  (0.008  to  0.015  gram). 
If  the  pain  is  not  severe,  I  substitute  hyoscyamus  or  belladonna  for  the 
opium.  The  bromides  also  are  useful  in  relieving  the  pain  and  in 
checking  hyperacidity.  Codeine  or  cocaine  may  be  used  for  the  same 
purpose;  and  these,  as  well  as  cerium  oxalate,  hydrocyanic  acid,  chloro- 
form, ether,  etc.,  are  useful  in  protracted  vomiting.  Bismuth  in  large 
doses  (30  to  60  grains,  2  to  4  grams,  three  times  daily)  has  been  highly 
recommended,  but  it  probably  exerts  more  beneficial  influence  on 
the  associated  catarrh  than  on  the  ulcer,  and  it  often  gives  rise  to  the 
most  annoying  constipation.  Olive  oil  in  large  doses  has  been  recom- 
mended by  Cohnheim. 

In  the  event  of  severe  hemorrhage  the  patient  must  be  confined  to 
bed  absolutely  at  rest;  an  ice  bag  may  be  applied  lightly  to  the  epi- 
gastrium, and  morphine,  ^  grain  (0.015  gram),  should  be  administered 
hypodermically.     Tannic  acid,  gallic  acid,  lead  acetate,  ergot,  Monsel's 


638  DISEASES  OF  THE  STOMACH 

solution  of  iron  sulphate,  are  of  doubtful  utility;  but  30  minims  (2  c.c.) 
of  adrenalin  chloride  (1  to  1000)  may  be  administered  with  the  hope 
that  it  may  do  good.  Hypodermoclysis  should  be  resorted  to  in  large 
hemorrhages  to  restore  the  volume  of  fluid  lost. 

The  surgical  treatment  of  gastric  ulcer  has  to  be  considered  in  many 
cases.  Operation  may  be  said  to  be  indicated :  (1)  In  recurring  hemor- 
rhages uncontrolled  by  medicinal  measures;  (2)  in  intractable  cases  with 
severe  pain,  persistent  vomiting,  hematemesis,  and  resulting  emaciation; 
(3)  when  perforation  has  occurred;  and  (4)  for  the  relief  of  perigastric 
adhesions,  and  the  less  common  perigastric,  subphrenic,  or  other  peri- 
toneal suppurations. 

CARCINOMA  OF  THE  STOMACH. 

Etiology. — Carcinoma  of  the  stomach  is  somewhat  more  common  in 
males  than  in  females;  and  occurs  especially  after  the  fortieth  year  (80 
per  cent,  of  the  cases);  but  it  has  been  observed  in  subjects  less  than 
twenty-five  years  of  age,  and  rarely  even  in  children.  The  etiological 
factors  are  the  same  as  those  of  carcinoma  in  general,  and  are  as  ill 
understood.  Some  influence  is  attributed  to  heredity.  The  affection  is 
more  common  in  the  white  race  than  in  the  negro,  and  in  some 
countries  (England)  rather  than  others  (America).  A  history  of  a 
previous  ulcer  may  be  obtained  in  some  cases. 

Pathology. — Carcinoma  may  involve  any  part  of  the  stomach,  even 
the  entire  organ,  but  the  lesser  curvature  and  the  pylorus  are  the  favorite 
seats.  Welch's  analysis  of  1300  cases  showed  the  pylorus  to  be  the 
seat  in  791  (60.8  per  cent.),  the  lesser  curvature  in  148  (11.4  per  cent.), 
the  cardia  in  104  (8  per  cent.),  the  posterior  wall  in  68  (5.2  per  cent.), 
the  whole  or  greater  part  of  the  stomach  in  61  (4.7  per  cent.),  the  greater 
curvature  in  34  (2.6  per  cent.),  the  anterior  wall  in  30  (2.3  per  cent.), 
the  fundus  in  19  (1.5  per  cent.),  and  multiple  tumors  in  45  (3.5  per  cent.). 
The  carcinoma  develops  from  the  mucous  membrane,  and,  as  a  rule, 
speedily  involves  the  submucous  and  even  the  muscular  and  the  serous 
coats  of  the  stomach,  and  it  may  spread  to  adjacent  tissues  and  give  rise 
to  metastases.  The  primary  growth  varies  much  in  size  in  different 
cases — from  a  small  tumor,  2  to  3  cm.  in  diameter,  to  involvement 
of  the  entire  stomach.  It  may  appear  as  an  annular  growth  about  the 
pylorus;  as  a  circumscribed  flat  elevation,  round,  ovoid,  or  irregular  in 
outline;  as  a  more  or  less  exuberant  cauliflower  or  pol}^oid  groAvth 
prone  to  necrosis;  or  as  a  diffuse  infiltration  of  almost  if  not  all  of  the 
stomach.  Extension  to  adjacent  tissues  by  continuity  of  structure  may 
ensue;  and  metastases  (usually  by  way  of  the  lymphatics)  to  the  liver, 
regional  lymph  nodes,  omentum,  and  to  more  distant  organs,  occur 
frecjuently.  Welch's  analysis  of  1574  cases  showed  metastasis  to  the 
lymph  nodes  in  551  cases,  to  the  liver  in  475,  to  the  peritoneum,  omen- 
tum, and  intestine  in  357,  to  the  pancreas  in  122,  to  the  pleura  and  lung 
in  98,  to  th?  spleen  in  26,  to  the  brain  and  meninges  in  9,  and  to  other 


I 


CARCINOMA   OF  THE  STOMACH  639 

parts  of  the  body  in  92.  Necrosis  and  ulceration  are  common.  Por- 
tions of  the  growth  may  be  found  in  the  vomit,  and,  being  subjected  to 
microscopic  examination,  facihtate  the  diagnosis  in  a  doubtful  case. 
Perforation  occurs  in  4  per  cent,  of  the  cases,  but  it  is  usually  preceded 
and  frequently  prevented  by  dense  adhesions  that  bind  the  stomach  to 
the  liver,  gall-bladder,  colon,  al)dominal  wall,  etc.  In  one  of  my  cases 
a  large  portion  (about  10  cm.  in  diameter)  of  what  at  first  appeared  to 
be  the  wall  of  the  stomach  was  made  up  of  the  ulcerating  and  necrotic 
left  lobe  of  the  liver — the  stomach  wall  at  this  place  having  entirely 
disappeared.  Rarely  fistulous  communications  between  the  stomach 
and  the  intestines,  lungs,  pleura,  the  exterior,  etc.,  may  become  estab- 
lished. In  carcinoma  of  the  pylorus  with  annular  constriction  the 
stomach  is  usually  dilated  from  obstruction,  and  in  some  cases  it  is 
much  distorted  and  displaced;  in  diffuse  carcinoma  the  stomach  wall 
may  be  greatly  thickened  and  the  organ  reduced  in  capacity;  whereas 
in  carcinoma  of  the  cardia  the  esophagus  is  usually  dilated  and  the 
stomach  sometimes  atrophied. 

The  common  carcinoma  of  the  stomach  is  the  cylindrical-cell  epi- 
thelioma, which  may  be  of  the  scirrhus,  medullary,  or  colloid  variety. 
The  so-called  malignant  adenoma  (adenocarcinoma),  or  adenoma 
destruens,  is  less  common;  and  the  squamous  epithelioma  occurring 
at  the  cardia,  and  usually  associated  with  carcinoma  of  the  esophagus, 
is  the  rarest.  Scirrhus  carcinoma  may  involve  the  pylorus,  causing 
an  annular  constriction  and  consequent  dilatation  of  the  stomach,  or 
it  may  involve  almost  if  not  quite  all  of  the  stomach,  causing  an  appear- 
ance much  resembling  sclerosis  of  the  stomach  and  exhibiting  little 
tendency  toward  ulceration.  Medullary  carcinoma  occurs  as  a  soft 
cauliflower-like  mass  that  grows  with  rapidity  and  commonly  ulcerates, 
causing  hemorrhage,  and  may  give  rise  to  perforation.  Colloid  (or 
mucoid)  carcinoma  occurs  as  a  more  or  less  diffusely  infiltrating  gela- 
tinous mass  that  grows  with  rapidity  and  involves  all  the  coats  of  the 
stomach.  Malignant  adenoma  for  a  time  presents  a  fairly  typical 
histological  appearance,  but  exhibits  malignant  characteristics  by  its 
diffusely  infiltrating  tendencies.  Secondary  carcinoma  of  the  stomach 
has  been  observed,  but  is  rare.. 

Symptoms. — The  symptoms  of  carcinoma  of  the  stomach  vary  much  in 
different  cases.  Several  of  the  most  extensive  carcinomas  of  the  stomach 
that  I  have  seen  gave  rise  to  no  suggestive  symptoms  during  the  life 
of  the  patient,  and  this  latency  is  by  no  means  uncommon.  In  other 
cases  the  symptoms  suggest  and  are  sometimes  mistaken  for  pernicious 
anemia;  or  secondary  manifestations,  metastases  in  the  liver,  superficial 
lymph  nodes,  etc.,  attract  attention,  and  the  primary  growth  is  overlooked. 
In  the  majority  of  cases,  however,  the  diagnosis  is  readily  made,  although 
not  always  in  the  early  stages.  In  many  cases  evidences  of  cln-onic 
gastritis  precede  and  they  usually  accompany  the  symptoms  character- 
istic of  carcinoma.  In  Osier's  series  of  150  cases  the  symptoms  at  the 
onset  were:  Pain  in  48,  dyspepsia  iji  44,  vomiting  in  21,  loss  of  weight  in 


640  DISEASES  OF  THE  STOMACH 

13,  difficulty  in  swallowing  in  3,  and  tumor  in  1;  in  7  the  symptoms 
suggested  pernicious  anemia,  and  in  37  the  onset  was  acute.  The  most 
suggestive  symptoms  are  chronic  indigestion  with  persistent  epigastric 
pain,  and  loss  of  weight  and  strength,  occurring  in  a  person  past  middle 
life.  The  epigastric  pain  is  burning  or  gnawing  in  character,  often 
severe,  more  or  less  constant,  frequently  increased  by  food  (sometimes 
not  for  several  hours),  and  may  radiate  to  the  back  or  shoulders.  Anor- 
exia, nausea,  vomiting,  and  constipation  are  features  of  almost  all  cases, 
but  they  may  be  missed.  In  the  early  stages  the  vomiting  is  not  marked, 
but  later,  especially  if  either  orifice  is  involved,  it  becomes  a  conspicuous 
symptom  and  may  recur  several  times  a  day.  In  carcinoma  of  the  pylorus 
the  vomiting  may  be  delayed  for  several  hours  after  the  taking  of  food;  in 
carcinoma  of  the  cardia  it  usually  occurs  soon;  whereas  in  carcinoma  of 
the  body  of  the  stomach  it  may  occur  rarely  if  at  all.  The  vomited 
matter  varies  somewhat  in  different  cases.  If  there  be  associated  dilata- 
tion of  the  stomach  the  vomit  partakes  of  the  characteristics  of  this 
condition.  Usually  it  consists  of  undigested,  or  partially  digested,  and 
often  fermenting  foods,  mucus,  and  sometimes  blood.  Blood  occurs  in 
one-half  or  more  of  the  cases.  In  most  cases  the  blood  is  small  in  amount, 
and  partakes  of  the  general  characters  of  coftee  grounds — the  result  of 
the  action  of  the  gastric  juice  on  the  hemoglobin.  In  some  cases  the 
hemorrhage  is  profuse  and  the  blood  as  ejected  is  either  bright  red  or 
dark  red  and  clotted,  depending  upon  the  length  of  time  it  has  remained 
in  the  stomach.  Blood  may  also  appear  in  the  stools,  with  or  without 
associated  hematemesis. 

The  loss  of  weight  and  strength,  while  in  the  main  progressive,  is 
subject  to  interruptions — ^marked  temporary  improvement  often  attend- 
ing the  removal  of  the  patient  to  a  hospital,  the  advent  of  a  new  physi- 
cian, regulation  of  the  diet,  attention  to  the  appetite,  and  treatment  of  the 
co-existing  gastritis.  Well-marked  anemia  is  a  prominent  feature  of  the 
disease  and  usually  progresses  concurrently  with  the  loss  of  weight; 
but  it  is  sometimes  so  extreme  and  disproportionate  to  the  other  features 
of  the  disease  as  to  suggest  pernicious  anemia.  Usually,  however,  the 
blood  is  of  the  chloranemic  type — the  erythrocytes  2,500,000  to  3,500,000 
(being  rarely  less  than  2,000,000,  as  is  common  in  pernicious  anemia) ; 
the  hemoglobin  varies,  but  in  well-marked  cases  it  is  less  than  50  per 
cent.;  and  the  leukocytes  are  sometimes  slightly  increased,  12,000  to 
18,000.  The  anemia,  emaciation,  prostration,  and  certain  attendant 
phenomena,  such  as  a  peculiar  sallowness  and  sometimes  pigmenta- 
tion of  the  skin,  a  distressed  countenance,  etc.,  comprise  the  well-known 
cachexia.  In  some  cases  there  is  slight  irregular  fever  (101°  F.),  attrib- 
utable to  the  anemia  or  to  infection  and  suppuration  about  the  car- 
cinoma. 

Examination  of  the  abdomen  reveals  a  visible  and  palpable  mass  in  at 
least  80  per  cent,  of  the  cases  some  time  during  their  course.  This  varies 
much  in  position  in  different  cases,  but  is  usually  in  the  epigastrium, 
hard,  nodular,  and  tender.     In  many  cases,  especially  if  it  has  formed 


CARCINOMA   OF  THE  STOMACH  641 

adhesioiis  with  the  liver  or  gall-bladder,  it  descends  on  inspiration,  and 
it  is  often  extremely  mobile,  susceptible  of  displacement  over  a  wide  area. 
On  account  of  the  anatomical  conditions,  as  a  rule,  only  tumors  of  the 
pyloric  end  of  the  stomach  are  palpable.  In  some  cases,  especially  of 
pyloric  obstruction,  visible  peristalsis  may  be  apparent,  or  if  the  tumor 
sufficiently  large  or  the  patient  sufficiently  emaciated,  a  pulsation  be 
transmitted  from  the  aorta  may  be  visible. 

Examination  of  an  Ewald  test  breakfast  reveals  absence  of  free  hydro- 
chloric acid  in  a  large  proportion  (90  per  cent.)  of  cases,  and  diminution 
in  the  amount  of  combined  hydrochloric  acid;  but  the  total  acidity, 
attributable  to  aromatic  (lactic  and  other)  acids,  is  often  high.  The 
presence  of  lactic  acid,  especially  following  preliminary  lavage  and  a  Boas' 
test  meal,  possesses  much  diagnostic  value.  The  presence  of  a  consider- 
able or  normal  amount  of  free  hydrochloric  acid  in  the  presence  of  symp- 
toms suggesting  carcinoma  is  sometimes  believed  to  indicate  ulcus  carcino- 
matosum.  Microscopicly  the  most  important  ingredients  of  the  gastric 
contents  are  undigested  food,  yeast  fungi,  sarcinse,  blood  (corpuscular 
or  crystalline  forms),  and  the  Oppler-Boas  bacillus — a  long  non-motile 
organism,  usually  of  much  diagnostic  value,  and  answerable  for  the 
formation  of  the  lactic  acid.  The  milk-curdling  ferment  is  usually 
reduced  in  amount,  and  the  motor  power  of  the  stomach  is  deficient. 
The  stools  may  contain  large  numbers  of  Gram-positive  (Oppler-Boas) 
bacilli,  in  contrast  to  other  conditions  in  which  the  stools  are  Gram- 
negative. 

As  the  disease  advances  cachexia  increases  and  metastatic  nodules 
develop  in  different  organs.  Some  of  these  are  accessible  to  clinical 
observation  and  sometimes  give  a  clue  to  the  diagnosis — thus  nodules  in 
the  liver,  about  the  umbilicus,  or  in  the  left  supraclavicular  lymph  nodes 
just  external  to  the  attachment  of  the  sternomastoid  muscle,  etc.  Perfora- 
tion of  the  wall  of  the  stomach  with  consequent  peritonitis,  or  fistulous 
communications  with  different  organs,  may  occur.  Ascites  due  to  carci- 
nomatous involvement  of  the  peritoneum  or  to  compression  of  the  portal 
vein  by  enlarged  lymph  nodes,  jaundice  due  to  obstruction  of  the  bile 
ducts,  and  oedema  of  the  legs  due  to  anemia  or  thrombosis  of  the  veins, 
may  develop. 

Diagnosis. — In  the  early  stages  the  diagnosis  is  often  in  doubt,  but 
chronic  indigestion,  persistent  epigastric  pain,  loss  of  flesh  and  strength, 
absence  of  free  hydrochloric  acid  and  the  presence  of  lactic  acid  in  a  test 
meal,  occurring  in  a  person  past  middle  life,  are  extremely  suggestive  of 
carcinoma.  After  the  occurrence  of  hematemesis  and  a  palpable  tumor 
the  diagnosis  is  no  longer  in  doubt;  but  at  this  time  the  disease  has 
advanced  to  such  a  stage  that  hope  of  lasting  benefit  can  no  longer  be 
entertained :  the  growth  has  made  much  local  progress,  and  metastases 
undoubtedly  have  occurred.  Chronic  gastritis  may  be  distinguished  by 
the  absence  of  cachexia,  of  profound  anemia,  of  leukocytosis,  and  of 
lactic  acid,  the  presence  of  free  hydrochloric  acid  (although  it  may  be 
temporarily  absent),  and  the  persisting  improvement  following  treat- 
41 


642  DISEASES  OF  THE  STOMACH 

ment.  Gastric  ulcer  may  usually  be  distinguished  by  its  occurrence  in 
younger  subjects,  by  gastralgic  paroxysms  (pylorospasm),  epigastric  pain 
often  augmented  immediately  by  taking  food  and  relieved  by  vomiting, 
persistent  hyperchlorhydria,  often  profuse  hematemesis  (occurring  in 
apparent  health,  as  contrasted  with  the  hematemesis  of  carcinoma  which 
occurs  in  weakened  and  emaciated  subjects),  absence  of  cachexia,  and 
absence  of  tumor  (although  it  is  sometimes  almost  if  not  quite  impossible 
to  differentiate  between  the  induration  and  cicatrization  of  an  ulcer  and  a 
carcinoma).  Pernicious  anemia  may  usually  be  excluded  by  the  predom- 
inance of  the  gastric  symptoms;  by  the  fact  that  the  erythrocyte  count 
is  rarely  less  than  2,000,000,  and  there  may  be  a  slight  leukocytosis; 
and  the  characteristic  blood  picture  of  pernicious  anemia  (megalocytes, 
megaloblasts,  etc.)  is  absent.  Hypertrophic  stenosis  of  the  pylorus 
sometimes  gives  rise  to  confusion  because  of  a  mass  in  the  epigastrium, 
but  it  occurs  in  younger  subjects,  there  is  no  cachexia  and  no  hema- 
temesis, and  the  free  hydrochloric  acid  is  normal  or  increased.  A  gas- 
trocolic fistula  is  suggested  by  fecal  vomiting  and  the  passage  through 
the  rectum  of  unaltered  food;  but  fecal  vomiting  may  be  due  to  reversed 
peristalsis,  and  an  extremely  foul  vomiting,  scarcely  to  be  distinguished 
from  fecal  vomiting,  may  be  due  to  ulceration  or  gangrene  of  the 
carcinoma. 

Prognosis. — Carcinoma  of  the  stomach  leads  inevitably  to  a  fatal 
termination— usually  within  a  year  from  the  time  the  disease  is  recog- 
nized. Some  patients  die  within  three  months,  and  occasionally  a 
patient  lives  two  years  from  the  time  the  disease  is  recognized. 

Treatment. — ^The  physician's  chief  concern,  since  he  is  unable  to  cure 
carcinoma  of  the  stomach,  should  be  to  recognize  it  at  the  earliest  pos- 
sible moment,  in  the  hope  that  prompt  resort  to  surgical  intervention 
may  prove  of  lasting  benefit.  And  since  it  is  impossible  in  most  cases  to 
diagnose  the  disorder  until  such  time  that  all  hope  of  permanent  relief 
has  passed,  he  should  suspect  it  in  all  cases  of  persisting  indigestion, 
with  lessened  or  absent  hydrochloric  acid  and  loss  of  flesh  and  strength, 
occurring  especially  about  the  fortieth  year.  In  these  cases,  unless  some 
other  organic  disorder  can  be  found  to  explain  the  symptoms,  the  physi- 
cian should  advise  an  exploratory  operation.  This  will  enable  the  sur- 
geon to  make  a  positive  diagnosis,  and  should  the  condition  prove  to  be 
carcinoma,  operation  may  be  undertaken  at  a  time  when  hope  of  success 
can  be  reasonably  entertained.  Aside  from  operative  intervention,  we 
are  limited  to  relieving  the  patient's  suffering,  to  feeding  him,  and  pro- 
longing his  life.  In  many  cases  milk  is  the  best  diet;  in  other  cases  a 
mixed  diet — milk,  animal,  and  vegetable.  Lavage  is  serviceable  in  per- 
sistent vomiting  and  in  pyloric  obstruction.  Pain  must  be  relieved  by 
external  applications,  and  by  the  internal  use  of  alkalies,  lime  water, 
codeine,  cocaine,  morphine,  or  cannabis  indica,  and  by  the  use  of  anti- 
fermentatives,  such  as  carbolic  acid,  creosote,  resorcin,  salicylic  acid, 
bismuth,  and  hydrochloric  acid.  The  appetite  may  be  stimulated  by 
nux  vomica  and  the  bitter  tonics  (gentian,  quassia,  condurango,  etc.). 


DISEASES  OF  THE  INTESTINE  G43 


NON-CARCINOMATOUS  TUMORS. 

Non-carcinomatous  tumors  of  the  stomach  are  rare  and  of  pathological 
rather  than  clinical  interest.  Lipomas,  fibromas,  leiomyomas,  sarcomas, 
cysts,  and  polyps  (polyadenomas)  have  been  described.  Foreign  bodies, 
of  which  the  most  curious  and  remarkable  are  hair  balls,  or  hair  tumors, 
occurring  in  hysterical  women,  have  been  mistaken  for  carcinoma. 

HYPERTROPHIC  STENOSIS  OF  THE  PYLORUS. 

Hypertrophic  stenosis  of  the  pylorus  may  occur  as  a  congenital  or  an 
acquired  condition.  The  congenital  cases  are  sometimes  due  to  ulcer- 
ation or  fissures  at  the  pylorus;  in  other  cases  there  seems  to  be  only  a 
spasmodic  contraction  of  the  pylorus  (Thomson).  The  acquired  cases 
consist  of  hyperplasia  of  the  submucous  and  muscular  coats  of  the 
pylorus.  Some  of  these  cases  are  perhaps  developed  upon  a  congenital 
basis,  since  they  become  manifest  in  adolescence.  The  symptoms  consist 
of  pylorospasm,  pyloric  obstruction,  consequent  dilatation  of  the  stomach, 
and  vomiting.  In  some  cases  there  is  visible  peristalsis  and  a  palpable 
mass.  Some  of  the  cases  of  periodic  or  cyclic  vomiting  in  infants  and 
children  are  believed  to  be  due  to  this  hypertrophic  stenosis  of  the  pylorus, 
and  the  associated  diaceturia  to  be  the  result  of  starvation.  In  the  mild 
cases,  particularly  those  occurring  in  infants  and  children,  benefit  and 
often  cure  follows  regulation  of  the  diet,  especially  small  amounts  at 
frequent  intervals  of  a  bland  and  alkaline  diet,  and  the  use  of  alkalies  and 
sedatives,  such  as  the  bromides,  etc.  In  some  cases  resort  must  be  had 
to  operative  intervention — dilatation  of  the  pylorus,  Loretta's  operation, 
gastro-enterostomy,  etc. 


DISEASES  OF  THE  INTESTINE. 

Pathological  Physiology. — ^The  small  intestine  is  designed  for  the 
further  digestion  of  the  chyme  received  from  the  stomach  and  for  the 
absorption  of  the  final  products  of  this  digestion.  In  the  first  portion 
of  the  duodenum  the  chyme  is  still  acid  in  reaction  (free  hydrochloric 
acid) — which  is  undoubtedly  one  reason  why  the  peptic  ulcer  of  the 
duodenum  is  almost  always  found  in  close  proximity  to  the  pylorus. 
Ivower  down  the  acid  chyme  encounters  and  is  rendered  alkaline  and 
otherwise  acted  upon  by  the  bile  and  the  pancreatic  juice.  Bile,  of 
course,  is  secreted  more  or  less  continuously,  but  when  the  stomach  is 
empty  (that  is,  during  the  periods  between  digestion)  it  backs  up  in  the 
gali-])ladder,  largely  on  account  of  closure  of  the  sphincter  at  the  end  of 
the  common  })ile  duct.  The  stimulus  to  tiie  discharge  of  bile  into  the 
duodenum  seems  to  be  proteins  and  fats,  or  some  of  their  digestive 


644  DISEASES  OF  THE  INTESTINE 

products;  acids,  alkalies,  and  starches  are  ineffective  (Bruns).  There 
is  some  reason,  however,  to  believe  that  the  secretion  of  bile  may  be 
stimulated,  as  is  the  pancreatic  juice,  by  secretin.  The  proteins  and 
fats  entering  the  duodenum,  excite,  probably  by  a  reflex  action,  a  con- 
traction of  the  gall-bladder,  and  an  inhibition  of  the  sphincter  closing 
the  opening  into  the  intestine  (Howell).  Bile  is  both  an  excretion  and 
a  secretion.  As  an  excretion  it  serves  to  eliminate  some  end-products 
of  katabolism,  such  as  cholesterin,  lecithin,  bile  acids,  and  bile  pigments; 
the  bile  acids  and  the  bile  pigments,  however,  may  be  in  part  reabsorbed. 
The  chief  action  of  the  bile  as  a  secretion  is  exerted  in  the  breaking 
up  and  the  absorption  of  fats.  On  account  of  its  contained  bile  acids 
it  serves  as  a  medium  for  the  suspension  and  splitting  up  of  fats  into 
fatty  acids  and  glycerin,  a  hydrolysis  effected  by  the  lipase  of  the  pan- 
creatic juice  materially  aided  by  the  bile.  When  bile  is  absent  from 
the  intestine  the  fat  in  the  feces  is  greatly  increased  (from  the  normal 
7  to  10  per  cent,  to  as  much  as  80  per  cent.);  this  is,  in  part,  the  cause  of 
the  pale  color  of  the  feces  in  jaundice,  and  it  suggests  the  wisdom  of 
withholding  fats  from  the  feces  in  such  cases.  The  bile  also  serves  to 
neutralize  the  acidity  of  the  gastric  chyme  and  thus  enable  the  trypsin 
of  the  pancreatic  juice  to  act,  trypsin  being  active  only  in  an  alkaline 
medium.  Formerly  the  bile  was  supposed  to  exert  an  antiseptic  action 
in  the  intestine,  preventing  putrefaction;  but  these  is  little  real  proof 
of  this  (the  bile  acts  as  a  good  culture  medium  for  bacteria);  its  absence 
may  permit  of  the  putrefaction  of  proteins  and  fats  which,  were  the  bile 
present,  would  not  occur.  The  bile  was  also  thought  to  stimulate 
peristalsis,  and  to  its  absence  the  constipation  of  jaundice  was  attributed; 
but  there  is  some  doubt  regarding  the  stimulating  effect  of  the  bile  on 
peristalsis,  and  constipation  is  not  always  present  in  jaundice. 

The  secretion  of  the  pancreatic  juice  is  called  forth  by  a  chemical 
stimulus  exerted  by  the  acid  chyme  on  the  duodenal  mucosa;  this  results 
in  the  production  of  a  substance,  secretin,  the  consequence  of  activation 
of  an  antecedent  substance  (prosecretin)  by  the  acid  of  the  gastric  juice. 
Secretin  is  absorbed  by  the  blood  and  carried  to  the  pancreas,  where, 
acting  as  a  hormone,  it  stimulates  the  pancreas  to  activity.  There  is 
some  reason  to  believe  that  other  substances,  fats,  for  instance,  may 
act  as  the  efficient  stimulus,  since  the  pancreatic  juice  seems  to  be 
secreted  even  in  cases  in  which  hydrochloric  acid  may  be  absent  from 
the  gastric  juice. 

The  pancreatic  juice  contains  three  enzymes:  (1)  Trypsin,  a  pro- 
teolytic enzyme,  which,  however,  is  secreted  by  the  pancreas  as  trypsin- 
ogen  and  is  activated,  converted  into  trypsin,  by  enterokinase,  a  product 
of  the  intestinal  mucosa  and  a  constituent  of  the  intestinal  juice.  (2) 
Amylopsin  (amylase),  a  diastatic  enzyme,  the  action  of  which  is  similar 
to,  if  not  identical  with,  that  of  ptyalin  of  the  saliva;  it  serves  to  complete 
the  digestion  of  starches.  (3)  Steapsin  (lipase),  a  fat-splitting  enzyme. 
Absence  of  pancreatic  juice  from  the  intestine  results  in  deficient  pro- 
teolysis and  fat-splitting.     The  deficient  fat-splitting  leads  to  the  occur- 


i 


DISEASES  OF  THE  INTESTINE  645 

rence  of  large,  pale,  grayish,  slate-colored,  or  clay-colored,  pasty,  fetid, 
acid  stools — ^which  are  quite  characteristic. 

The  intestinal  juice  (succus  entericus)  also  is  active  in  digestive 
processes;  but  more  so  certain  enzymes  resident  in  the  cells  of  the  in- 
testinal mucosa.  These  enzymes  perhaps  may  be  secreted  into  the 
intestinal  juice,  but  some  of  them  doubtless  exert  their  activity  within 
the  epithelial  cells  themselves.  These  enzymes  are:  secretin,  the 
hormone  stimulating  the  pancreas  to  activity;  enterokinase,  which 
activates  the  trypsinogen  of  the  pancreas,  and  forms  the  proteolytic 
ferment  trypsin;  erepsin,  also  a  proteolytic  enzyme,  believed  to  assist 
in  tryptic  digestion;  nuclease,  an  enzyme  believed  to  aid  in  the  digestion 
of  nucleins;  and  certain  inverting  enzymes  (maltase,  invertase,  and 
lactase)  that  conlieict  disaccharids  (maltose,  saccharose,  and  lactose) 
into  monosaccharids  (dextrose,  levulose,  and  galactose). 

The  stimulus  calling  forth  the  secretion  of  this  succus  entericus  is 
not  definitely  known;  it  has  been  attributed  to  secretin  and  to  the 
mechanical  influence  of  the  food.  Mechanical  and  other  irritants,  such 
as  mercury,  arsenic.  Bacillus  dysenterise,  saline  cathartics,  etc.,  induce 
a  watery  secretion,  that  differs  materially  from  the  normal  intestinal 
juice;  a  similar  watery  secretion  occurs  in  chronic  passive  congestion 
of  the  intestine,  amyloid  disease,  etc. 

The  intestine  always  contain  more  or  less  gases,  especially  nitrogen, 
derived,  in  part,  from  the  swallowed  atmosphere,  in  part  from  bacterial 
decomposition  of  proteins;  carbon  dioxide,  from  carbohydrate  fermenta- 
tion and  the  interaction  of  the  gastric  acids  on  the  alkaline  hepatic, 
pancreatic,  and  intestinal  secretions;  and  hydrogen,  sulphuretted 
hydrogen,  and  marsh  gas,  largely  from  the  putrefaction  of  proteins. 

The  intestinal  contents  are  passed  along  by  peristaltic  movements, 
which  consist  of  contractions  moving  on  from  segment  to  segment, 
while  the  part  first  contracted  gradually  relaxes.  In  addition,  there  are 
movements  of  rhythmical  segmentation,  which  have  been  well  studied  by 
Cannon,  and  seem  to  subserve  the  purpose  of  thorough  and  intimate 
mixing  of  the  intestinal  contents.  The  intestinal  movements  are  not 
continuously  progressive  from  the  beginning  to  the  end  of  the  intestine, 
but  segmental  and  pendulum-like,  though  ultimately  they  serve  to 
pass  the  intestinal  contents  onward.  Readily  digestible  food  appears 
to  traverse  the  small  intestine  in  about  four  hours,  and  to  reach  the  sig- 
moid colon  in  two  or  three  hours  more  (Hertz).  Exaggeration  of  the 
intestinal  movements  gives  rise  to  borborygmi,  which  is  especially 
marked  when  the  intestine  contains  much  gas  and  little  food.  Exagger- 
ated contractions  against  a  mechanical  obstruction  or  incoordinated 
contraction  and  relaxation  give  rise  to  intestinal  colic;  stimulation  of 
the  splanchnics  (through  which  a  nervous  control  is  exerted)  may  cause 
colic  and  constipation  (as  in  lead  poisoning);  and  paresis  or  paralysis 
may  lead  to  a  form  of  nervous  diarrhoea.  Antiperistalsis  does  not  occur 
in  health,  but  may  be  observed  in  diseased  conditions,  especially  those 
attended  by  intestinal  obstruction. 


646  DISEASES  OF  THE  INTESTINE 

The  function  of  the  large  intestine  is  largely  to  absorb  water  from 
the  intestinal  contents,  and  thus  indirectly  to  cause  inspissation  of  the 
intestinal  contents.  Very  little  nutritive  matter  is  absorbed  by  the  colon, 
so  that  persons  fed  by  rectal  alimentation  soon  begin  to  suffer  from 
starvation. 

In  health,  divers  sorts  of  bacteria  are  found  in  the  intestinal  tract, 
especially  in  the  large  bowel,  notably  Bacillus  coli;  in  disease  the  number 
of  species  may  become  increased,  or  the  normal  inliabitants  may  be  over- 
come by  the  invaders.  Zooparasites  also  are  common.  It  seems  likely 
that  bacterial  activity  is  of  much  importance  in  the  orderly  performance 
of  the  intestinal  functions,  and  that  derangements  of  this  bacterial 
activity  may  lead  to  diseased  processes.  Those  to  which  chief  importance 
is  attached  are  associated  with  putrefactive  changes;  the  disorders  to 
which  they  are  supposed  to  give  rise  are  called  intestinal  auto-intoxica- 
tions, w^hich  have  already  been  discussed  (page  303). 

The  feces  consist  of:  (1)  Indigestible  material  (ligaments  of  meat, 
cellulose  from  vegetables);  (2)  undigested  material,  such  as  fragments 
of  meat,  starch,  or  fats  which  have  escaped  digestion;  (3)  products  of 
intestinal  secretions;  (4)  products  of  bacterial  growth,  especially  indol 
and  skatol,  to  which  the  odor  of  the  feces  is  largely  due;  (5)  cholesterin, 
probably  derived  from  the  bile;  (6)  purin  bases,  especially  guanin  and 
adenin;  (7)  mucus  and  epithelial  cells  thrown  off  from  the  intestinal 
wall;  (8)  pigment,  especially  urobilin  or  stercobilin,  derived  from  the 
bilirubin  of  the  bile;  (9)  inorganic  salts — salts  of  sodium,  potassium, 
calcium,  magnesium,  and  iron,  chiefly  the  last  three  together  with 
phosphoric  acid;  and  (10)  microorganisms,  usually  in  great  quantities 
(Howell).  Study  of  the  feces  is  of  much  importance  in  determining 
the  functional  efficiency  of  the  intestines.  This  is  best  done  after  the 
use  for  three  or  more  days  of  Schmidt's  test  diet  (see  intestinal  indi- 
gestion), 

SYMPTOMATIC  DISORDERS  OF  THE  INTESTINE. 

Disorders  of  the  functions  of  the  intestine  are  the  natural  consequence 
of  definite  anatomical  lesions  of  most  diverse  nature,  and  as  such  are 
usually  recognized  and  correctly  ascribed  to  a  more  or  less  obvious 
cause.  In  other  cases  intestinal  symptoms  are  due  to,  or  part  and 
parcel  of,  a  general  neurosis,  such  as  hysteria,  neurasthenia,  etc.,  or  they 
are  reflex  manifestations  of  disease  of  some  adjacent  viscera;  whereas  in 
other  cases  the  intestinal  disorder  seems  to  be  due  entirely  to  some  per- 
version of  the  functional  activity  of  the  intestinal  nervous  mechanism, 
and  is  unassociated  with  discoverable  anatomical  lesions;  in  other  words, 
the  condition  is  a  neurosis.  The  dividing  line  between  these  different 
classes  of  cases,  however,  is  by  no  means  distinct,  and  sometimes  cannot 
be  drawn  at  all.  We  may,  nevertheless,  as  in  the  stomach,  distinguish 
disorders  of  motility,  of  sensibility,  and  of  secretion,  though  they  often 
do  not  occur  alone. 


SYMPTOMATIC  DISORDERS  OF  THE  INTESTINE  647 

Motor  Disorders. — Disorders  of  motility  are  dependent  upon  in- 
creased or  decreased  irritability  of  the  motor  nerves  and  musculature: 
on  the  one  hand,  peristaltic  unrest,  nervous  diarrhoea,  or  enterospasm, 
results;  on  the  other  hand,  paresis  or  paralysis. 

Peristaltic  unrest  (intestinal  tormina),  a  condition  allied  to  peristaltic 
unrest  of  the  stomach,  is  not  infrequently  a  manifestation  of  catarrhal 
enteritis  or  intestinal  stenosis,  but  it  sometimes  occurs  also  as  an  appa- 
rently independent  affection,  especially  in  nervous,  hysterical,  and 
hypochondriacal  women,  and  rarely  even  in  persons  without  other  neuro- 
pathic manifestations.  The  condition  consists  of  rolling  and  gurgling 
sounds  in  the  intestine,  varying  much  in  intensity  from  time  to  time, 
sometimes  so  loud  as  to  be  audible  some  considerable  distance  from  the 
patient,  and  often  occasioning  extreme  annoyance  and  discomfort, 
especially  when  they  are,  as  sometimes,  loud  and  squeaking.  Pain  is 
rarely  complained  of.  The  condition  is  due  to  increased  peristalsis  of  the 
small  intestine  carrying  along  the  gaseous  and  fluid  contents  from  one 
segment  of  the  intestine  to  another.  Eructations  may  occur  in  associated 
peristaltic  unrest  of  the  stomach,  and  Rosenheim  even  reports  feculent 
vomiting  (which,  however,  must  be  exceedingly  rare).  The  peristaltic 
movements  are  not  infrequently  visible  and  even  palpable  through  thin 
abdominal  walls.  The  attacks  usually  come  on  without  noteworthy 
cause,  though  they  may  be  provoked  by  emotional  disturbances,  certain 
articles  of  diet,  etc.;  they  usually  last  for  a  few  minutes,  though  some- 
times for  hours,  and  even  during  sleep;  and  they  occur  at  irregular 
intervals. 

Nervous  diarrhoea  is  a  condition  dependent  upon  increased  peri- 
staltic movements,  on  the  one  hand,  and  an  increased  transudation  of 
fluid  into  the  intestine,  on  the  other  hand.  Allied  in  some  respects  to 
peristaltic  unrest,  it  differs  in  that,  in  at  least  some  cases,  the  increased 
peristalsis  seems  to  be  almost,  if  not  wholly,  limited  to  the  large  intes- 
tine (whence  the  intestinal  evacuations),  and  in  the  rapid  transudation  of 
fluid.  This  is  certainly  attributable  to  nervous  influences  (paresis  or 
paralysis  of  the  splanchnics) — since  there  is  no  other  evidence  of  disease 
of  the  intestine,  and  the  attack  is  almost  always  provoked  by  emotional 
disturbances,  such  as  shock  (unwelcome  news),  fright,  ordeal  of  the 
witness  stand,  public  speaking,  examinations  (students,  etc.).  A  similar 
condition  is  sometimes  observed  in  nervous  disorders  like  tabes,  and  may 
occur  as  a  reflex  manifestation  in  different  gastro-intestinal  disorders, 
disorders  of  the  female  genitalia,  e  c.  The  stools  vary  in  number  from 
three  or  four  to  a  dozen  or  more,  are  often  passed  in  rapid  succession, 
and  consist  of  thin  liquid  material.  Sometimes  the  flrst  evacuation  is 
of  more  or  less  well-formed  fecal  matter,  whereas  the  subsequent  stools 
are  very  thin  and  serous.  Peristaltic  unrest  (rolling  and  gurgling  sounds) 
sometimes  accompanies  the  evacuations.  A  somewhat  similar  condition 
is  occasionally  observed  in  persons  generally  constipated,  who  when  they 
become  "nervous"  from  any  cause,  have  an  almost  immediate  evacuation 
of  the  bowels.     Diarrhoea  is  also  a  common  symptom  of  many  diseases 


648  DISEASES  OF  THE  INTESTINE 

of  the  intestine,  notably  acute  and  chronic  enteritis,  under  which  head- 
ings it  is  discussed. 

Spasm  of  the  intestine  (enterospasm)  is  a  term  appHed  to  tonic  con- 
tracture of  the  muscular  fibers  (longitudinal  and  circular)  of  the  intes- 
tine, resulting  in  lessening  or  complete  though  temporary  occlusion  of 
the  lumen.  The  very  rare  occurrence  of  a  primary  or  idiopathic  entero- 
spasm may  be  conceded,  the  subjects  being  neuropathic  or  hysterical 
individuals;  the  condition,  however,  is  almost  always  secondary  or 
symptomatic.  It  may  be  a  manifestation  of  local  inflammatory  or  other 
diseases  of  the  intestine;  it  is  a  common  manifestation  of  lead  intoxication; 
and  is  not  uncommon  in  diseases  of  the  brain,  especially  meningitis, 
in  which  the  intestinal  contractures  may  be  associated  with  scaphoid 
retraction  of  the  abdomen.  The  spasm  may  be  more  or  less  diffuse, 
involving  large  sections  of  the  small  or  large  intestine,  or  both;  or  it  may 
be  quite  circumscribed — of  which  variety,  proctospasm  (usually  asso- 
ciated with  other  diseases  of  the  rectum  or  anus)  is  a  well-known 
example.  Clinically  the  condition  resembles  enteralgia  (of  which  it  is 
really  often  the  anatomical  basis),  and  constipation  is  common;  but 
neither  pain  nor  constipation  is  essential.  Local  tympany  or  meteorism 
is  not  infrequent.  When  confined  to  the  lower  bowel,  the  feces  may  be 
narrow  or  ribbon-like,  or  resemble  sheep's  dung. 

Paralysis  of  the  intestine  may  be  due  to  a  variety  of  causes.  It  is 
common  in  peritonitis  from  whatever  cause  arisen;  it  may  be  a  concomi- 
tant of  intestinal  obstruction;  it  is  associated  with  a  form  of  chronic 
atony  with  consequent  constipation;  and  it  is  sometimes  observed  in 
hysterical  subjects  who  suffer  much  from  meteorism.  Constipation  is  the 
conspicuous  clinical  feature.  Paralysis  of  the  anal  sphincter  is  found  in 
divers  disorders  of  the  brain  associated  with  stupor  and  coma,  especially 
infectious  diseases  like  typhoid  fever,  various  intoxications,  and  more 
purely  local  diseases  of  the  brain  associated  with  coma;  it  is  a  charac- 
teristic symptom  of  certain  organic  diseases  of  the  spinal  cord;  and  it 
sometimes  develops  after  the  persistence  of  irritating  diseases  of  the 
rectum  associated  with  long-standing  tenesmus  which  ultimately  leads  to 
fatigue,  paresis,  and  paralysis  of  the  muscles.  Paresis  usually  precedes 
paralysis,  so  that  at  first  the  patient  by  an  effort  can  control  the  evacua- 
tions; later,  the  slightest  disturbance  or  undue  pressure  results  in  the 
discharge  of  gas  or  fecal  matter;  and  ultimately,  when  paralysis  is  com- 
plete, the  intestinal  contents  are  altogether  beyond  the  control  of  the 
patient  and  may  be  discharged  immediately  they  enter  the  rectum. 

Treatment. — ^The  treatment  of  the  motor  disorders  of  the  intestine  is 
similar  to  that  of  similar  disorders  of  the  stomach.  Especial  attention 
should  be  directed  to  the  underlying  conditions,  whether  neuropathic 
or  local  anatomical  factors  that  may  determine  the  onset,  or  augment 
an  attack.  The  diet  must  be  regulated  and  the  bowels  must  be  opened 
regularly  and  daily.  Hydrotherapeutic  measures,  electricity,  a  course 
of  treatment  at  certain  health  resorts,  etc.,  are  of  benefit  in  many 
cases.    Drugs,  such  as  arsenic  and  the  bromides,  and  sometimes  strych- 


SYMPTOMATIC  DISORDERS  OF  THE  INTESTINE  649 

nine  and  iron  (in  anemic  conditions),  may  subserve  a  useful  purpose. 
Belladonna  or  hyoscyamus  may  be  useful  in  spasm;  and  physostigma 
or  eserine  may  be  useful  in  overcoming  constipation  due  to  atony. 

Sensory  Disorders.— The  sensibility  of  the  intestinal  tract  may  be 
increased  (hyperesthesia,  pain),  diminished  (anesthesia),  or  perverted 
(paresthesia). 

Intestinal  pain  (enterodynia)  may  be  due  to  one  of  several  causes :  (1) 
It  may  be  a  manifestation  of  inflammation  of  any  portion  of  the  intestine 
and  of  its  peritoneal  covering  (to  be  discussed  under  appropriate  head- 
ings). (2)  It  may  be  the  so-called  intestinal  colic.  (3)  It  may  be  a  true 
intestinal  neuralgia. 

Intestinal  colic,  the  pain  produced  by  violent  tetanic  contractions  of 
the  muscular  coat  of  the  intestine,  may  be  due  to:  (1)  Sudden  chilling 
of  the  surface  of  the  body,  which  of  itself  seems  to  provoke  intestinal 
colic  in  certain  susceptible  persons;  (2)  dietetic  indiscretions — coarse, 
indigestible,  unripe,  or  decomposed  food,  especially  unripe  fruit  and 
overripe  fish,  and  cold  drinks;  (3)  foreign  bodies,  such  as  gallstones, 
enteroliths,  scybalous  masses,  large  amounts  of  mucus  (mucous  colic), 
etc.;  (4)  drastic  cathartics  and  other  medicines;  (5)  infections  and 
intoxications,  such  as  certain  infectious  diseases  (cholera),  lead  poisoning, 
etc.;  (6)  zooparasitic  invasions,  intestinal  worms;  (7)  reflex  disturbances 
associated  with  disease  of  the  ovaries,  uterus,  bladder,  kidneys,  etc. 

Intestinal  colic  usually  comes  on  suddenly  with  severe  pain  radiating 
in  different  directions  (though  it  may  remain  localized) ;  it  varies  much 
in  intensity  (from  moderately  severe  "griping"  to  extremely  severe 
pains),  remits  and  intermits,  and  varies  in  duration  from  a  few 
moments  to  several  hours.  Nausea,  vomiting,  flatulence,  and  faint- 
ness  are  not  uncommon;  if  the  pain  is  severe,  cold  perspiration 
usually  breaks  out;  and  exhaustion  and  collapse  may  supervene.  The 
attack  usually  subsides  with  the  removal  of  the  exciting  cause,  often  with 
the  discharge  of  feces  (stercoral  colic),  sometimes  with  the  evacuation 
of  gas  (flatulent  colic),  or  of  mucus  (mucous  colic). 

Intestinal  colic  may  simulate  hepatic  and  renal  colic  in  the  sudden 
onset  and  sudden  cessation,  as  well  as  severity,  of  the  pain,  but  in 
hepatic  colic  the  pain  is  usually  referred  to  the  right  hypochondrium, 
and  may  be  referred  to  the  right  shoulder;  it  is  not  so  likely  to  be  inter- 
mittent; jaundice  and  bile-stained  urine  may  occur;  there  may  be  a 
history  of  similar  attacks;  and  gallstones  may  be  found  in  the  feces. 
In  renal  colic  the  pain  is  usually  in  the  back,  loin,  or  groin,  and 
radiates  to  the  testicle,  which  may  be  retracted;  strangury  or  frequent 
micturition  is  common,  the  urine  may  become  bloody,  and  a  calculus 
may  be  found  in  the  urine. 

The  term  intestinal  neuralgia,  or  nervous  enteralgia,  may  be  applied 
to  attacks  of  abdominal  pain,  seen  in  nervous,  hysterical,  and  hypo- 
chondriacal women  (rarely  men),  which  come  on  suddenly,  spread 
usually  from  the  umbilicus  over  the  abdomen,  last  a  variable  time 
are  likely  to  recur,  and  seem  to  be   unusual  in  severity,  leading  fre- 


650  DISEASES  OF  THE  INTESTINE 

quently  to  collapse,  and  in  which  there  is  no  etiological  or  other  eN'idence 
of  true  intestinal  colic,  nor  of  inflammation  of  the  abdominal  viscera  or 
peritonemn.  Vomiting  is  absent,  the  stomach  and  intestines  perform 
their  functions  normally;  but  cutaneous  hj-peresthesia  and  other  evi- 
dence of  hysteria,  etc.,  are  present.  In  the  absence  of  better  knowledge, 
the  condition  is  described  as  a  neurosis — a  neuralgia  of  the  mesenteric 
plexus  and  the  splanchnic  nerves;  but  in  some  cases,  as  for  instance 
the  crises  and  other  perhaps  analogous  conditions,  the  pain  is  doubtless 
due  to  angiospasm. 

Diminished  sensihUity  (anesthesia)  of  the  intestine  attends  and 
may  be  the  cause  of  constipation.  It  is  found  especially  in  different 
diseases  of  the  brain  and  spinal  cord  associated  with  paralysis,  and  in 
fecal  accumulations.  If  the  motor  innervator  of  the  intestine  is  unim- 
paired, spontaneous  evacuations  occur,  but  with  defective  motility 
constipation,  often  extremely  obstinate,  occurs. 

Paresthesia  of  the  iniestine  is  rather  unusual,  though  it  may  be  com- 
plained of  by  the  hysterical  and  the  insane.  The  paresthetic  phenom- 
ena are  usually  (though  not  always)  referred  to  the  rectum. 

Treatment. — ^The  treatment  of  the  sensory  disorders  of  the  intestine 
is  determined  by  the  etiological  factor.  The  pain  may  be  relieved  by 
hot  applications  to  the  abdomen — ^poultices,  hot-water  bag,  mustard 
plaster,  spice  poultice,  turpentine  stupe,  and  by  the  internal  administra- 
tion of  spirit  of  ginger,  aromatic  spirit  of  ammonia,  compound  spirit  of 
ether,  camphor,  chloroform  water,  or  a  dry  Martini  cocktail  (the  one 
instance  in  which  it  subserves  a  very  useful  purpose).  Rarely  morphine 
or  other  preparations  of  opium  must  be  resorted  to.  The  bowel  should 
be  evacuated  immediately  by  rectal  enemas,  and  by  castor  oil  by  the 
mouth.  Subsequently  attention  must  be  directed  to  the  diet,  to  regu- 
larity in  the  movement  of  the  bowels,  and  to  the  underlying  general 
condition.  Tonics,  stimulants,  and  other  measures  mentioned  under 
constipation  (page  656)  are  sometimes  necessary  to  overcome  the  con- 
stipation due  to  diminished  sensibility;  in  some  cases  manual  removal 
of  the  feces  may  have  to  be  resorted  to. 

Secretory  Disorders. — ^The  intestinal  juice  under  the  influence  of 
the  nervous  system  is  subject  to  increase  and  decrease — depending 
upon  a  variety  of  factors.  Diminution  is  doubtless  a  factor  in  some 
cases  of  constipation;  increase  is  an  important  factor  in  so-called 
nervous  diarrhoea,  in  which  the  evacuated  fluid  is  largely  serous  in 
character;  but  the  only  disease  descril^ed  as  wholly  or  almost  wholly  a 
secretory  disorder  or  neurosis  is  so-called  mucous  colic  or  colitis. 

INTESTINAL  INDIGESTION." 

{Intestinal  Dyspepsia:  Di/strypsia.) 

In  health  the  entrance  of  the  chyme  into  the  duodenum,  by  activat- 
ing the  prosecretin  of  the  duodenal  mucosa  and  thus  forming  secretin, 
gives  rise  to  the  secretion  of  bile  and  of  pancreatic  juice  which  not  only 


INTESTINAL  INDIGESTION  651 

neutralize  the  acidity  of  the  chyme,  but  also  produce  that  alkalinity 
required  for  the  proper  digestive  activity  of  the  ferments  contained  in 
these  juices.  Intestinal  digestion  then  depends  not  only  upon  the  proper 
amount  of  bile  and  of  pancreatic  juice  of  good  quality,  as  well  as  of 
intestinal  juice,  but  also  upon  the  functional  integrity  of  the  stomach: 
since  defective  gastric  digestion  not  only  results  in  the  introduction  into 
the  duodenum  of  chyme  ill  adapted  to  the  intestinal  functions,  but  defi- 
cient or  increased  acidity  results  in  corresponding  derangement  of  the 
flow  of  bile  and  of  pancreatic  juice  into  the  intestine — though  doubtless 
minor  deviations  from  the  normal  can  be  compensated  for.  Intestinal 
indigestion — disorders  of  the  processes  of  digestion  occurring  in  the 
intestine — may  be  primary  or  secondary,  although  it  is  often  difficult, 
if  not  impossible  to  separate  the  one  from  the  other. 

Etiology. — Primary  intestinal  indigestion  results  from:  (1)  Disease  of 
the  small  intestine,  of  whatsoever  natm-e,  but  especially  chronic  catarrh, 
interfering  with  the  absorptive  power  of  the  mucous  membrane,  as  well 
as  with  the  formation  of  an  active  intestinal  juice.  (2)  Change  in  the 
quality  or  quantity  of  the  bile.  A  diminished  amount  of  bile  may  be 
due  to  sluggish  action  of  the  liver  or  to  obstruction  to  the  entrance  of 
bile  into  the  intestine  arising  from  any  cause  whatever.  Changes  in  the 
quality  of  the  bile  are  ill  understood,  though  it  seems  that  the  liver  has 
the  function  of  eliminating  by  way  of  he  bile  and  the  intestine  certain 
end  products  of  metabolism,  and  it  is  not  inconceivable  that  these  in 
excess  may  interfere  w^ith  the  action  of  the  bile  or  irritate  the  intestinal 
mucosa.  (3)  Changes  in  the  cjuantity  or  quality  of  the  pancreatic  juice. 
Secondary  intestinal  indigestion  may  arise  in  consequence  of  any  form 
of  gastric  indigestion — especially  gastric  hyperacidity,  but  also  subacidity, 
deficient  motor  power,  etc. 

Symptoms. — ^The  symptoms  of  intestinal  indigestion  usually  accompany 
and  sometimes  cannot  be  dissociated  from  those  of  gastric  indigestion. 
The  patient  usually  complains  of  loss  of  appetite,  acid  eructations,  flatu- 
lency, epigastric  distress  and  distention  (in  consequence  of  acid  fermen- 
tation of  carbohydrates,  putrefactive  decomposition  of  albuminous 
foodstuffs),  and  of  diarrhoea,  the  result  of  irritation  and  consequent 
increased  peristalsis  often  occasioned  by  abnormal  acidity  of  the  intes- 
tinal contents.  The  diarrhoea  is  often  and  characteristically  preceded 
by  pain,  which  may  be  colicky  in  nature.  The  stools  at  first  consist  of 
the  contents  of  the  lower  part  of  the  bowel,  but  soon  present  the  charac- 
teristics of  the  contents  of  the  jejunum,  being  semifluid,  gelatinous,  and 
tenacious — due  to  a  large  amount  of  mucus,  the  normal  contents  of  the 
jejunum,  and  not  the  result  of  catarrh  (as  shown  by  the  absence  of 
formed  elements,  epithelial  cells,  and  round  cells  so  common  in  catarrh). 
Furthermore,  the  stools,  often  yield  a  pronounced  reaction  for  bile 
(though  this,  of  course,  varies  with  the  amount  of  bile  present);  they 
are  sometimes  quite  greenish  in  color,  though  often  light  yellowish  and 
foamy,  and  yield  an  odor  of  butyric  acid. 

The  nature  of  the  disorder  in  protracted  cases  is  best  determined  by 


652  DISEASES  OF  THE  INTESTINE 

study  of  the  stools  after  the  use  for  three  days  or  more  of  Schmidt's  test  diet. 
This  consists  of:  In  the  morning,  500  c.c.  of  milk  and  50  grams  of  Zwie- 
back; in  the  forenoon,  500  c.c.  of  oatmeal  gruel  (made  up  of  40  grams  of 
oatmeal,  10  grams  of  butter,  200  grams  of  milk,  300  grams  of  water,  1 
egg,  and  some  salt);  at  noon,  125  grams  of  chopped  beef  broiled  rare, 
with  20  grams  of  butter,  and  250  grams  of  potato  puree  (190  grams  of 
potatoes,  100  grams  of  milk,  10  grams  of  butter,  and  a  little  salt);  in  the 
afternoon,  milk  and  Zwieback,  as  in  the  morning;  and  in  the  evening, 
oatmeal  gruel,  as  in  the  forenoon.  This  diet  furnishes  about  2250 
calories.  Special  attention  should  be  paid  to  the  presence  in  the  stool 
of  connective  tissue,  muscle  tissue,  potato  (or  starch)  granules,  fat 
(fatty  acids  and  soaps),  mucus,  and  bacteria.  Special  importance  at- 
taches to  the  presence  of  muscle  tissue,  starch  granules,  and  fatty  acids. 
Resort  may  also  be  had  to  Sahli's  dermoid  test,  etc. 

Persistence  of  the  attack  soon  leads  to  catarrh  of  the  intestine,  and  the 
usual  catarrhal  stools  (alkaline  reaction,  evidences  of  catarrhal  desqua- 
mation, etc.). 

Diagnosis. — The  cases  due  to  disorder  of  the  stomach  may  be  distin- 
guished by  symptoms  especially  referable  to  the  stomach,  the  results  of 
analyses  of  the  gastric  contents  after  a  Boas  or  Ewald  test  meal,  the 
presence  of  much  connective  tissue  in  the  stools  after  Schmidt's  test  diet, 
and  improvement  following  treatment  directed  to  the  stomach. 

Treatment. — ^The  treatment  consists  especially  in  regulating  the  diet, 
in  accordance  with  the  findings  of  a  gastric  analysis  and  a  study  of  the 
stools.  The  medicinal  measures  depend  upon  the  underlying  conditions 
and  the  digestive  capacities.  Gastric  hyperacidity  or  subacidity  calls  for 
appropriate  treatment.  Carminatives  and  so-called  intestinal  antiseptics, 
such  as  resorcin,  bismuth  salicylate,  naphthalene,  creosote,  carbolic  acid, 
aromatic  spirit  of  ammonia,  salicylic  acid,  etc.,  are  usually  indicated. 
Calomel  in  small  doses,  4V  to  2ir  grain  (0.0015  to  0.003  gram)  three  or 
four  times  a  day,  is  an  excellent  remedy  in  some  cases,  from  time  to 
time,  although,  if  it  stimulates  peristalsis,  the  dose  should  be  reduced. 


INTESTINAL  HEMORRHAGE. 

{Enter  orrhagia.) 

Etiology. — Blood  issuing  from  the  body  by  way  of  the  anus  may  be 
evidence  of  hemorrhage  from  any  part  of  the  gastrointestinal  tract,  and 
may  be  due  to  many  causes — local  and  general.  The  general  causes  are 
such  as  determine  hemorrhage  in  other  parts  of  the  body — purpura, 
scurvy,  malignant  (or  hemorrhagic)  forms  of  certain  specific  infections 
(smallpox,  yellow  fever,  cholera,  malaria,  measles,  scarlatina,  diphtheria, 
etc.),  septic  infections  (malignant  endocarditis,  etc.),  leukemia,  perni- 
cious anemia,  etc. ;  and  it  is  rarely  a  manifestation  of  vicarious  menstru- 
ation. The  local  causes  are :  (a)  Hyperemia  of  the  intestine,  common  in 
advanced  cirrhosis  of  the  liver,  and  in  heart  disease,  less  common  in  the 


INTESTINAL  HEMORRHAGE  653 

early  stages  of  acute  inflammations,  such  as  typhoid  fever,  (b)  Inflam- 
mation, erosion,  and  ulceration  of  the  intestine,  such  as  the  inflammation 
provoked  by  irritant  poisons  or  drastic  cathartics ;  peptic  or  other  ulcera- 
tion of  the  stomach  or  duodenum;  and  the  various  forms  of  ulceration 
(simple,  tuberculous,  syphilitic,  carcinomatous,  etc.)  of  other  portions 
of  the  intestine;  typhoid  fever;  dysentery;  etc.  In  some  cases  even  large 
hemorrhages  seem  to  have  resulted  from  mere  superficial  erosion  of  the 
mucous  membrane,  (c)  Embolism  and  thrombosis  of  the  mesentric 
vessels,  (d)  Changes  in  the  vessel  walls,  such  as  occur  in  amyloid 
disease,  nephritis,  etc.,  may  occasion  hemorrhage — in  some  cases  in 
consequence  of  the  formation  and  rupture  of  miliary  aneurysms,  (e) 
Zooparasitic  invasion  of  the  intestine,  as  by  Uncinaria  duodenalis, 
Schistosoma  haematobium,  etc.  (/)  Hemorrhoids,  internal  and  external, 
and  anal  fistula  or  fissure,  (g)  Trauma,  external  blows,  or  internal 
injuries  provoked  by  divers  kinds  of  foreign  bodies  (chicken  bones, 
oyster  shells,  enteroliths,  hard  feces,  etc.).  In  women,  blood  supposed 
to  issue  from  the  bowels  sometimes  comes  from  vaginal  sources.  In 
addition,  blood  issuing  from  the  anus  may  be  due  to  swallowing  of 
blood  coming  from  the  nose,  throat,  oesophagus,  or  lungs  (hemoptysis). 

Symptoms. — The  symptoms  of  intestinal  hemorrhage  vary  much 
with  the  cause  and  the  amount  of  the  hemorrhage.  When  slight,  the 
hemorrhage  often  passes  unnoticed,  or  may  be  merely  an  accidental 
finding  in  the  stool.  This  is  sometimes  the  case  in  latent  ulceration, 
carcinoma,  or  parasitic  invasion  of  the  intestines  (occult  blood),  and  may 
require  microscopic  or  chemical  tests  for  its  detection.  A^Tien  large  the 
symptoms  may  be  exceedingly  severe,  and  occasionally  lead  directly  to 
death,  although  as  much  as  two  or  three  quarts  may  be  lost  at  one  time, 
and  even  a  debilitated  patient  survive  (typhoid  fever).  Sudden  large 
hemorrhage  is  manifested  by  faintness,  dimness  of  vision,  and  vertigo, 
often  progressing  to  collapse,  pallor  of  the  skin  and  visible  mucous 
membranes,  profuse  perspiration,  and  fall  of  temperature  (often  5°  to  8° 
or  more).  Repeated  small  hemorrhages  lead  to  the  gradual  develop- 
ment of  marked  anemia  (see  chronic  secondary  anemia,  page  367). 

When  the  blood  comes  from  the  stomach  or  the  upper  part  of  the 
intestine  it  is  usually  altered  by  the  digestive  juices,  and  issues  from 
the  anus  as  black  tarry  fluid  or  masses  (melena).  Very  rarely  a  massive 
hemorrhage  coming  from  the  stomach  or  upper  part  of  the  duodenum 
and  issuing  soon  from  the  anus  may  be  but  little  altered.  Blood  coming 
from  the  lower  part  of  the  small  bowel,  or  from  the  colon  or  the  rectum, 
is  comparatively  unaltered  and  readily  recognized  as  blood.  Should  the 
hemorrhage  occur  from  the  stomach,  or  from  the  upper  part  of  the  intes- 
tine, and  the  blood  find  its  way  into  the  stomach,  hematemesis  may 
accompany  the  enterorrhagia.  But  very  hirge,  and  even  fatal  hemor- 
rhages may  occur  without  any  external  discharge  of  the  blood. 

Treatment. — ^The  treatment  of  intestinal  hemorrhage  is  to  be  based 
entirely  upon  its  source.  In  general  it  is  similar  to  that  of  hemorrhage 
occurring  in  typhoid  fever  (page  59). 


654  DISEASES  OF  THE  INTESTINE 

MUCOUS  COLIC. 

(Mucous  Colitis;  Pseudomembranous  Enteritis;  Tubular  Diarrhoea.) 

Mucous  colic  is  a  secretory  neurosis  of  the  colon  characterized  by  the 
formation  of  an  excessive  amount  of  tough,  tenacious  mucus. 

Etiology. — ^Mucous  colic  is  not  so  rare  a  disease  as  was  formerly  sup- 
posed, and  is  most  common  in  neurotic  and  hysterical  women  (80  per 
cent,  of  the  cases).  It  is  rare  in  children.  In  most  cases  it  is  an  inde-. 
pendent  disorder,  and  occurs  without  noteworthy  anatomical  lesions  in 
the  intestinal  mucosa.  In  some  cases,  however,  it  seems  to  become 
engrafted  upon  an  intestinal  catarrh;  that  is,  to  the  catarrhal  altera- 
tions are  added,  either  permanently  or  periodically,  the  manifestations 
of  the  neurosis  (hypersecretion  of  mucus).  Constipation  appears  to  be  a 
contributing  etiological  factor  in  some  cases. 

Symptoms. — ^The  disease  is  characterized  by  the  passage  from  the 
bowel  of  large  amounts  of  mucus.  This  occurs  usually  in  paroxysms, 
frequently  of  unknown  cause,  but  sometimes  induced  by  psychic  dis- 
turbances, dietetic  indiscretions,  and  divers  extraneous  causes.  The 
paroxysm  is  usually  attended  by  severe  abdominal  pain,  which  is  some- 
times so  severe  as  to  suggest  to  the  patient  impending  dissolution,  and 
to  engender  the  morphine  habit.  The  pain  is  most  commonly  along  the 
course  of  the  descending  colon,  and  is  frequently  accompanied  by 
tenderness.  The  pain  and  tenderness,  however,  may  be  on  the  right 
side,  and  being  sometimes  associated  with  palpable  tenderness  of  the 
appendix,  suggest  an  etiological  relationship,  which  seems  to  be  proved 
in  some  cases  by  recovery  after  removal  of  the  appendix.  Rarely  pain 
is  absent.  Tenesmus  is  a  distressing  feature  of  some  cases.  The  attack 
may  last  for  from  several  days  to  two  weeks  or  longer,  but  mucus  is  not 
passed  with  each  paroxysm  of  even  severe  pain.  The  mucus  occurs 
as  shreds,  flakes,  narrow  cylinders  (suggesting  certain  intestinal  worms), 
or  sometimes  as  tubes  forming  veritable  casts  of  the  bowel.  Usually  the 
stool  consists  exclusively  of  this  mucus,  and  a  very  large  amount  may  be 
passed  at  one  time.  As  a  rule,  the  mucus  is  opaque  and  grayish;  occa- 
sionally it  is  brownish  from  admixture  with  feces,  and  rarely  reddish, 
from  admixture  with  blood.  Occurring  in  masses  or  as  casts  the  mucus 
often  resembles  fibrinous  exudates,  but  microscopic  examination  (mucus 
cells,  cylindrical  epithelial)  and  chemical  examination  (mucin  reaction) 
reveals  it  to  be  composed  exclusively  of  dense,  tough,  altered  mucus. 

As  a  rule,  the  patients  present  the  ordinary  manifestations  of  hysteria, 
neurasthenia,  hypochondriasis,  etc.  Constipation  is  the  rule  between 
attacks.  The  condition  lasts  for  years,  and  in  many  cases,  ultimately 
leads  to  marked  anemia  and  emaciation. 

Treatment. — ^The  treatment  is  eminently  unsatisfactory.  During  the 
paroxysm  measures  should  be  taken  to  relieve  the  pain,  such  as  hot 
fomentations  to  the  abdomen,  and  to  get  rid  of  the  cause  of  the  pain  by  a 
thorough  evacuation  of  the  bowels — by  castor  oil  and  rectal  enemas. 


CONSTIPATION  655 

The  cure  of  the  disorder  comprises  attention  to  the  underlying  hysteria 
or  neurasthenia,  rather  than  measures  suggested  by  a  supposed  intes- 
tinal catarrh  (which  is  rarely  present).  Attention  to  the  common  con- 
stipation is  frequently  followed  by  marked  improvement  in  the  mucus 
colic.  A  right-sided  colotomy  with  maintenance  of  an  artificial  anus 
for  some  time,  and  consequent  rest  of  the  colon,  has  been  successful  in 
a  few  cases. 

CONSTIPATION. 

(Costiveness.) 

Constipation  is  a  condition  in  which  the  feces  are  retained  in  the 
intestinal  canal  an  unusually  long  time;  as  a  rule,  the  feces  when 
'passed  are  unduly  hard.  There  may  be  a  daily  movement,  in  which 
event  the  evacuation  is  insufficient. 

Etiology. — Constipation  may  be  due  to  many  causes — general  and 
local.  The  general  causes  comprise  family  or  individual  tendency, 
"bad  habits"  (non  response  to  the  calls  of  nature),  sedentary  life,  die- 
tetic errors  (too  little  food,  or  foods  that  leave  little  residue),  habitual 
use  of  purgatives,  certain  nervous  disorders  (such  as  hysteria  and  neuras- 
thenia, as  well  as  organic  disorders  interfering  with  the  evacuation  of  the 
bowel),  hepatic  disorders  associated  with  jaundice,  acute  infectious 
fever,  general  debility,  etc.  The  local  causes  are:  (1)  Diminished 
expulsive  power,  that  is,  defective  intestinal  peristalsis,  atony  of  the 
intestine  (itself  also  a  result  of  chronic  constipation),  or  weakness  of 
the  diaphragm  or  the  abdominal  muscles  (obesity,  distention  from 
repeated  pregnancies,  etc.);  and  (2)  increased  resistance  to  the  onward 
movement  of  the  feces,  which  may  be  due  to  (a)  hardness  and  dryness 
of  the  feces;  (b)  lessening  of  the  intestinal  lumen  from  any  cause 
(see  intestinal  obstruction) ;  (c)  inhibition  of  the  free  movement  of 
the  intestine  in  consequence  of  adhesions  or  abdominal  bands;  (d) 
displacement  of  the  intestine  (V-shaped  colon,  redundant  sigmoid); 
(e)  spasm  of  the  intestine,  usually  of  the  lower  colon  or  sigmoid  (with 
atony  and  dilatation  of  the  proximal  parts  of  the  intestine)— so-called 
spasmodic  constipation,  observed  especially  in  hysterical  and  neuras- 
thenic women,  particularly  the  subjects  of  ovarian  or  uterine  disease. 

Constipation  is  symptomatic  when  due  to  obvious  causes,  idiopathic 
when  no  cause  can  be  ascertained.  When  symptomatic,  it  is  usually 
more  or  less  temporary;  when  idiopathic,  it  is  not  infrequently  a  habit — '■ 
so-called-  habitual  constipation. 

Symptoms. — ^There  is  marked  diversity  in  the  reaction  to  constipation. 
Many  persons  are  habitually  constipated  and  otherwise  apparently  well ; 
others,  occasionally  constipated  for  greater  or  less  periods,  suffer  little 
discomfort;  whereas  in  others  the  failure  to  have  the  daily  evacuation 
produces  immediate  and  notal)le  discomfort,  and  protracted  consti- 
pation brings  a  long  train  of  symptoms  in  its  wake — copremia  (intes- 
tinal   auto-intoxication).     Most    extraordinary  cases   are^  occasionally 


656  DISEASES  OF  THE  INTESTINE 

observed — cases  in  which  no  evacuation  has  occurred  for  weeks  and 
even  months. 

Although,  in  many  cases,  constipation  is  the  only  complaint,  there  is 
often  a  feeling  of  discomfort  in  the  rectum.  Overloading  and  conse- 
quent distention  of  the  sigmoid  may  occasion  pain  from  pressure  on 
regional  nerves.  There  is  frequently  associated  flatulence,  borborygmi, 
occasional  attacks  of  colicky  pain,  and  diarrhoea  (which  should  not  be 
misinterpreted).  Hemorrhoids  are  common;  inflammation,  dilatation, 
ulceration,  and  even  perforation  of  the  intestine  may  result;  and  men- 
struation is  likely  to  be  painful.  The  retained  feces  usually  become 
hardened,  in  consequence  of  absorption  of  the  watery  constituents,  and 
form  scybalous  masses;  these  may  be  palpated  through  the  abdomen 
as  irregular,  sometimes  sausage-shaped  tumors,  in  the  course  of  the 
colon.  Occasionally  scybalous  masses  retained  in  sacculi  of  the  colon 
give  rise  to  the  development  of  enteroliths.  In  spasmodic  constipation 
the  fecal  discharges  may  be  narrow  and  ribbon-like,  or  resemble  the 
discharges  of  sheep. 

In  many  cases  the  appetite  is  lost  (or  lessened),  the  tongue  coated, 
and  the  breath  foul;  headache,  vertigo,  palpitation  of  the  heart,  are  not 
uncommon;  and  depression  of  spirits,  hypochondriasis,  etc.,  are  likely 
to  supervene. 

Constipation  in  infants  may  be  congenital,  or  due  to  dietetic  indis- 
cretions, or  to  local  causes  similar  to  those  causing  constipation  in  adults. 
Some  infants,  constipated  from  birth,  require  for  months  a  daily  enema 
or  aperient  to  secure  an  evacuation.  Certain  artificial  foods  seem  to 
engender  constipation  in  some  infants,  a  deficiency  of  fat  being  believed 
to  be  the  active  factor.  In  older  children  the  costive  habit  is  often 
favored  by  inattention  on  the  part  of  the  mother. 

Treatment. — ^The  cultivation  of  habits  of  regularity  is  of  the  utmost 
importance,  and  only  those  who  have  observed  know  the  good  effects 
that  may  be  thus  achieved.  The  patient  should  go  to  stool  at  the  same 
time  every  day,  whether  there  is  a  desire  to  evacuate  the  bowels  or  not, 
and  every  such  desire  should  be  immediately  gratified.  The  diet  should 
comprise  considerable  fruit  and  vegetables  (which  leave  a  residue).  A 
glassful  of  cold  water  before  breakfast,  an  orange  or  oatmeal  at  break- 
fast, and  stewed  fruits  and  salads  at  dinner  subserve  a  useful  purpose 
in  many  cases.  Persons  of  sedentary  habits  are  often  benefited  by  exer- 
cise; abdominal  massage  is  useful  in  some  cases;  and  an  abdominal 
binder  is  of  value  to  those  with  a  pendulous  flabby  abdomen  and 
visceroptosis. 

Drugs  should  be  dispensed  with  as  long  as  possible.  Even  in  long- 
standing cases  much  and  lasting  benefit  may  be  secured  by  dietetic  and 
hygienic  measures.  Medicinal  measures  when  necessary  vary  with  the 
nature  of  the  causal  factor,  which  must  be  diligently  searched  for.  At 
the  beginning  of  the  treatment  it  is  often  advisable  to  clear  the  in- 
testine thoroughly  with  castor  oil,  a  blue  mass  pill,  or  calomel,  followed 
by  a  saline  aperient.    In  many  cases,  the  best  results  are  obtained  by  a 


ACUTE  ENTERITIS  657 

daily  injection  of  tepid  water  with  or  without  soap;  in  other  cases 
injections  of  oil  are  much  better;  but  enemas  should  not  be  too  lono- 
continued.  Some  patients  are  much  benefited  by  a  saline  aperient 
water,  sodium  phosphate,  or  other  saline,  taken  a  half  hour  before 
breakfast.  Those  who  are  occasionally  constipated,  find  relief  in  a 
Seidlitz  powder,  compound  licorice  powder,  the  official  compound 
cathartic  pill,  or  a  glycerin  suppository.  Should  a  course  of  medicine 
be  necessary,  the  desired  results  may  usually  be  secured  by  the  use  of 
cascara  sagrada,  which  has  the  advantage  that,  having  been  continued 
for  some  time,  the  dose  necessary  to  secure  a  daily  evacuation  may  be 
gradually  reduced,  and  the  drug  ultimately  dispensed  with,  should  the 
patient  continue  habits  of  regularity.  The  pill  of  aloin  (^  grain,  0.008 
gram),  strychnine  (-^  grain,  0.0015  gram),  and  extract  of  belladonna  (jj 
grain,  0.006  gram),  though  much  abused,  is  very  useful  in  many  cases. 
The  following  pill  night  and  morning  is  also  useful : 

I^— Podophyllin To  *»  i  grain  0,006  to  0.012 

Strychnine ^L  grain  0'0015 

Ext.  physostigma i  grain  0  008 

Ext.  belladonna i  grain  0  01 

Instead  of  the  podophyllin,  aloin,  extract  of  cascara  sagrada,  or  com- 
pound extract  of  colocynth  may  be  substituted.  Phenolphthalein  (1  to 
2  grains,  0.06  to  0.12  gram)  at  night  is  often  attended  by  good  results. 
Rhubarb  and  sodium  bicarbonate  also  are  of  value  in  some  cases.  A  pill 
of  iron  (dried  sulphate  of  iron,  2  grains,  0.12  gram)  and  extract  of  aloes 
(1  grain,  0.06  gram),  with  or  without  rhubarb  (5  grains,  0.3  gram),  is 
often  efficacious  in  the  constipation  of  anemic  and  chlorotic  conditions. 
Agar-agar  (15  to  30  grains,  1  to  2  grams  or  more)  eaten  with  cream, 
twice  or  thrice  daily,  is  often  serviceable  when  the  feces  are  hard  and 
small  in  amount.  Similar  results  may  be  achieved  by  the  use  of  large 
amounts  of  fats,  olive  oil,  butter,  cream,  etc. 

In  children  the  best  results  follow  attention  to  the  diet,  the  giving 
of  cream,  barley  water,  oatmeal  water,  etc.  Rectal  injections  may  be 
required,  or  a  conical  piece  of  soap  may  be  introduced  within  the  anus. 
Among  medicines,  magnesia,  manna,  rhubarb  and  soda,  and  olive  oil  are 
probably  the  best,  but  if  possible  all  medicine  should  be  avoided. 


ACUTE  ENTERITIS. 

(Acute  Intcdinal  Cuiarrh;  Cholera  Morbus;  Cholera  Nostras.) 

s 

Acute  enteritis  is  an  acute  inflammation  of  the  intestinal  mucous 
membrane,  characterized  by  abdominal  pain  and  diarrhoea. 

Etiology. — ^The  affection  occurs  at  all  ages,  in  both  sexes,  and  is 
especially  prevalent  during  the  summer  months.  Its  causes  are:  (1) 
Bacterial  infection,  which  sometimes  causes  a  primary  infectious  enter- 
itis. An  enteritis  is  common  also  in  many  infectious  diseases,  such  as 
typhoid  fever,  cholera,  pneumonia,  dysentery,  etc.  (2)  Animal  para- 
42 


658  DISEASES  OF  THE  INTESTINE 

sitic  infections — ^^^orms,  etc.  (3)  Toxic  and  mechanical  irritants,  such 
as  improper  food  (tainted  meats,  overripe  or  underripe  fruit);  stomach 
contents  improperly  prepared  for  the  intestine;  intestinal  contents  that 
remain  too  long  in  the  intestine  (in  consequence  of  stenosis  or  imperfect 
action  of  the  intestinal  musculature) ;  drastic  cathartics ;  irritant  poisons ; 
certain  articles  of  diet  and  waters  to  which  the  individual  may  be  un- 
accustomed (personal  idiosyncrasy),  etc.  (4)  Certain  autogenic  poisons, 
such  as  occur  in  uremia,  and  which  irritate  the  intestinal  mucosa.  Second- 
ary enteritis  occurs  in  heart  disease  and  liver  disease  in  consequence  of 
passive  congestion;  in  amyloid  disease  (undue  permeability  of  the 
intestinal  bloodvessels),  etc. 

Pathology. — ^The  lesions  are  those  of  catarrhal  inflammation  in  general 
— swelling,  h}^eremia,  and  increase  of  mucous  secretion,  with  des- 
quamation of  the  surface  epithelium.  In  many  cases,  however,  at  the 
necropsy,  but  few  or  slight  changes  may  be  apparent.  Frequently,  in 
addition  to  swelling,  there  is  superficial  erosion  or  ulceration  of  the 
solitary  and  agminate  lymph  follicles  (catarrhal  and  follicular  ulcera- 
tion). In  severe  cases,  small  hemorrhages  in  the  mucosa  may  occur 
(hemorrhagic  enteritis).  The  lesions  may  extend  throughout  the  entire 
intestinal  tract,  but  are  often  more  marked  in  one  part  than  another. 

Symptoms. — Diarrhoea  may  be  the  only  symptom,  and  even  this  may 
be  inconspicuous  in  catarrh  of  the  upper  part  of  the  small  bowel.  The 
stools  vary  much  in  frequency — four  to  twenty  or  more  in  the  twenty- 
four  hours;  in  amount,  from  small  movements  to  great  losses  of  fluid 
(liters);  in  color,  from  dark  brownish  to  light  yellowish  or  grayish,  de- 
pending upon  the  amount  of  biliary  coloring  matter;  and  in  consistency, 
depending  upon  the  amount  of  watery  constituents  and  the  increased 
peristalsis  hurrying  on  the  fluid  intestinal  contents.  Diarrhoea  charac- 
terized by  the  evacuation  of  much  fluid  is  spoken  of  as  serous;  that 
in  which  there  is  much  fecal  matter,  as  stercoral;  that  in  which  the 
stools  contain  undigested  food,  as  lienteric;  and  the  profuse  serous 
discharges  occurring  in  and  adding  to  the  exhaustion  of  the  last  stages 
of  severe  diseases,  such  as  tuberculosis,  etc.,  as  colliquative  diarrhoea. 
Mucus  is  always  present  in  greater  or  less  amount,  and  microscopicly 
one  may  detect  mucus,  desquamated  epithelial  cells,  particles  of  food 
(muscle  fibers,  starch  granules,  etc.),  crystals  of  calcium  phosphate  and 
oxalate,  cholesterin,  and  different  microorganisms. 

In  most  cases  there  is  more  or  less  abdominal  distress,  which  often 
amounts  to  severe,  sometimes  colicky,  pain,  and  is  often  marked  just 
before  a  stool.  There  is  often  also  some  abdominal  distention,  tympanites, 
borborygmi,  and  tenderness,  and  in  case  the  lower  colon  be  involved, 
tenesmus.  The  appetite  is  lessened  or  lost,  the  tongue  is  coated,  thirst 
may  be  marked,  and  rarely  there  is  vomiting  (severe  cases).  The  urine 
is  lessened,  sometimes  greatly  lessened,  and  may  contain  a  little  albumin, 
and  indican  and  ethereal  sulphates  in  excess.  There  may  be,  though 
usually  there  is  not,  slight  fever. 

In  very  severe  cases  (primary  infective  enteritis)  the  pain  may  be 


CHRONIC  ENTERITIS  659 

marked,  vomiting  severe,  and  the  stools  many  and  copious  (resembling 
cholera:  cholera  nostras,  cholera  morbus);  cramp-like  pains  in  the  calf 
muscles  is  common;  and  collapse  attended  by  heart  failure,  cold  ex- 
tremities, somnolence,  and  delirium  may  supervene.  JMany  of  these 
are  undoubtedly  cases  of  ptomaine  or  other  food  poisoning. 

Diagnosis. — The  diagnosis  is  usually  easy,  though  several  days' 
observation  is  sometimes  necessary  to  exclude  certain  infectious  dis- 
eases— typhoid  fever,  dysentery,  etc.  Especial  involvement  of  the  small 
intestine  is  suggested  by  less  frequent  stools,  borborygmi,  colicky  pain 
about  the  umbilicus,  greenish  or  yellowish  stools  rather  intimatelv  mixed 
with  mucus  and  containing  particles  of  undigested  food  (lienteric  stools), 
and  the  fact  that  a  stool  is  often  induced  by  taking  food.  Involvement 
of  the  large  bowel  is  suggested  by  pain  along  the  course  of  the  colon, 
tenesmus,  frecjuent  fluid,  "soupy,"  grayish  stools,  containing  large 
flakes  of  mucus.  Duodenitis  is  suggested  by  the  development  of  jaun- 
dice (from  the  extension  of  the  catarrhal  inflammation  to  the  bile  duct). 

Prognosis. — ^The  prognosis  in  general  is  good,  the  ordinary  cases 
resulting  in  a  cure  in  from  three  to  five  days.  The  manifestations, 
however,  sometimes  become  chronic.  The  prognosis  is  often  very  serious 
in  the  infective  form,  as  well  as  in  debilitated  subjects  (tuberculous, 
cardiac,  hepatic,  and  nephritic  lesions).  Children  and  debilitated 
subjects  often  die. 

Treatment. — ^The  prime  indication  in  all  cases  is  to  rid  the  intestine 
of  all  irritating  substances — whence  an  initial  purgative  is  called  for  in 
almost  all  cases,  even  in  many  cases  in  which  the  evacuations  have  been 
numerous.  Mild  cases  respond  well  to  warm  applications  to  the  abdo- 
men, 1  ounce  (30  c.c.)  of  castor  oil  with  20  minims  (1.25  c.c.)  of  tincture 
of  opium,  or  calomel  in  repeated  small  doses,  and  restriction  of  the  diet 
(milk,  whey,  and  toast)  for  several  days.  It  is  well  to  give  in  addition 
intestinal  antiseptics  and  astringents,  such  as  the  bismuth,  salol,  and 
chalk  mixture  (page  148),  or  a  lead  and  opium  pill  (page  149). 
Resorcin,  creosote,  beta-naphthol,  bismuth,  and  similar  preparations 
are  also  useful.  Involvement  of  the  large  bowel  is  best  treated  by 
cleansing  enemas  (to  which  boric  or  salicylic  acid  may  be  added),  fol- 
lowed by  a  starch  enema  with  tincture  of  opium.  Depression  is  to  be 
treated  by  stimulants,  hot  tea  with  whiskey  or  cognac,  camphor,  etc. 
The  extreme  depression  that  sometimes  attends  many  serous  evacua- 
tions, as  well  as  the  evacuations  themselves,  are  often  promptly  con- 
trolled by  morphine,  I  grain  (0.015  gram).  Tonics  are  indicated  during 
convalescence,  and  the  diet  must  be  regulated. 


CHRONIC  ENTERITIS. 

Etiology. — Chronic  enteritis  is  due  to:  (1)  The  repeated  or  long- 
continued  action  of  the  factors  causing  acute  enteritis;  (2)  protozoan 
infection  (amoeba,  trichomonas,  cercomonas,  balantidium,  etc.);  and  (3) 


660  DISEASES  OF  THE  INTESTINE 

it  may  occur  secondarily  to  diseases  of  the  heart,  kings,  stomach,  liver, 
and  kidneys. 

Pathblogy. — ^The  lesions  are  similar  to  those  found  in  chronic  gastritis, 
and  are  most  frequent  and  marked  in  the  lower  part  of  the  ileum  and 
the  colon.  They  consist  of:  (1)  Hypertrophic  processes — thickening 
of  the  mucosa  (with  the  formation  of  much  mucus),  sometimes  going 
on  to  polypoid  masses,  swelling  of  the  solitary  lymph  nodes  and  plaques, 
follicular  ulceration;  and  (2)  atrophy — of  the  glandular  tissue,  with 
cicatrization,  and  consequent  thickening  of  the  intestinal  wall.  These 
two  processes  are  often  observied  side  by  side.  The  follicular  ulcera- 
tion sometimes  leads  to  phlegmonous  infiltration  of  the  intestinal  wall 
(in  consequence  of  secondary  infection);  and  in  consequence  of  healing 
and  cicatrization,  stenosis  sometimes  results. 

Symptoms. — Several  groups  of  cases  may  be  distinguished:  (a)  In  a 
minority  of  the  cases  the  s}Tnptoms  are  much  like  those  of  the  acute 
catarrh,  although  more  mild.  The  patient  has  several  diarrhoeic  stools 
daily,  attended  by  colicky  pains  and  borborygmi,  and  in  the  event  of 
involvement  of  the  large  intestine  (as  is  usual)  with  tenesmus.  The 
diarrhoea  is  extremely  obstinate,  especially  in  the  event  of  ulceration, 
though  even  without  it.  In  consequence  of  the  common  ulceration,  blood 
and  pus,  and  even  particles  of  the  necrotic  tissue,  may  be  found  in  the 
stools,  (b)  More  common  than  diarrhoea  is  constipation,  the  consequence 
of  atony  of  the  intestinal  musculature  and  comparative  insensibility  of  the 
nerves  of  the  mucosa,  (c)  In  perhaps  the  majority  of  cases,  periods  of 
diarrhoea  alternate  with  periods  of  constipation.  During  the  period  of 
constipation  a  thick  mucus  is  secreted,  feces  accumulate,  fermentative 
processes  go  on,  the  intestine  becomes  distended,  and  these  culminate  in 
such  irritative  processes  as  to  result  in  rather  marked  serous  evacuations. 
In  some  cases  considerable  mucus  is  secreted,  and,  becoming  coagulated, 
forms  masses  or  veritable  casts  of  the  intestines.  In  most  cases  well- 
marked  nervous  symptoms  develop — apathy,  headache,  palpitation  of 
the  heart,  somnolence,  hypochondriasis,  etc.  Cutaneous  manifestations 
(urticaria,  pruritus),  as  well  as  tetany,  attributable  to  auto-intoxication, 
are  rarely  observed.  The  patient  frequently  emaciates  considerably, 
and  a  high  grade  of  secondary  anemia  may  develop. 

Diagnosis. — It  is  desirable  to  exclude  specific  ulceration — tubercu- 
lous, s}^hilitic,  dysenteric,  carcinomatous;  as  well  as  certain  neuroses. 

Prognosis. — The  prognosis  is  doubtful  in  many  cases.  In  children  and 
in  the  aged  it  is  very  bad. 

Treatment. — ^The  treatment  in  general  is  similar  to  that  of  acute 
enteritis,  but  the  strictest  attention  must  be  paid  to  dietetic  and  hygienic 
measures.  In  cases  marked  by  alternate  diarrhoea  and  constipation, 
special  effort  must  be  made  to  cure  the  constipation,  since  this  is  always 
an  irritating  factor.  A  clue  to  the  correct  diet  may  often  be  obtained 
by  a  study  of  the  stools  after  the  use  of  the  Schmidt  test  diet  (page 
652).  In  some  cases  no  improvement  follows  until  the  patient  is  put 
upon  the  strictest  dietetic  regimen,  whence  the  good  results  often  attained 


DIARRHCEAL  DISORDERS  OF  CHILDREN  661 

at  ditt'erent  spas  and  health  resorts.  The  chronic  lesions  of  the  diseased 
mucosa  are  very  resistant  to  medicinal  measures,  but  certain  good  results 
seem  sometimes  to  follow  the  administration  of  silver  nitrate,  lead  acetate, 
zinc  sulphate,  bismuth  preparations,  naphthalene,  tannic  acid  and  drugs 
containing  tannic  acid.  In  involvement  of  the  large  bowel  irrigation  is 
useful,  good  results  attending  the  use  of  sodium  chloride  solution,  0.6  per 
cent,;  silver  nitrate,  0.02  to  0.05  per  cent.;  boric  acid, 0.5  per  cent.;  sali- 
cylic acid,  0.1  per  cent.;  tannin,  0.2  to  0.5  per  cent. 


DIARRHCEAL  DISORDERS  OF  CHILDREN. 

{Summer  Diarrhoea  of  Children;  Gastro-enteritis  of  Children;  Acute  Gastro-intestinal 

Catarrh;  Acute  Dyspeptic  Diarrhoea;  Gastro-intestinal  Intoxication;  Cholera 

Infantum;  Enterocolitis;  Ileocolitis;  Infantile  Dysentery.) 

Etiology. — Diarrhoeal  disorders  are  exceedingly  common  during  the 
summer  months  (June,  July,  and  August,  but  also  May  and  September) 
among  children,  from  the  sixth  to  the  eighteenth  month.  ^Miile  espe- 
cially common  among  children  of  the  poor,  occurring  frequently  in  tene- 
ment houses  and  asylums,  they  attack  also  those  reared  under  the  most 
favorable  auspices.  The  special  etiological  factors  are  associated  with 
diet,  atmospheric  temperature  (summer  heat),  bad  hygiene,  and  general 
inattention.  Predisposing  factors  comprise  feeble  constitution,  malnu- 
trition, marasmus,  rickets,  etc.  According  to  Holt,  only  3  per  cent,  of 
the  fatal  cases  occur  among  breast-fed  infants. 

The  mild  cases,  so-called,  acute  dyspeptic  diarrhoea,  result  from  over 
feeding,  too  frequent  feeding,  the  use  of  improper  food,  and  the  sudden 
change  of  food  (such  as  may  occur  in  weaning),  and  they  are  predisposed 
to  by  the  heat  and  humidity  of  summer,  fatigue,  acute  infections,  etc. 
The  feces  usually  contain  the  normal  intestinal  bacterial  flora,  no  abnormal 
types  being  found  with  sufficient  frequency  to  be  considered  of  etiological 
significance.  More  severe  cases,  designated  gastro-enteritis,  gastro-intes- 
tinal intoxication,  or  cholera  infantum,  also  result  from  the  aforementioned 
causes;  some  of  them  are  examples  of  acute  milk  poisoning,  the  bacteria, 
perhaps,  having  been  destroyed  by  heat,  but  their  toxins  or  ptomaines  per- 
sisting; others  are  due  to  Bacillus  dysenterise  (Shiga)  or  allied  organisms, 
Bacillus  acidi  lactici.  Bacillus  coli,  Bacillus  proteus,  streptococci,  staphy- 
lococci, etc.,  all  of  which,  gaining  access  to  milk,  find  therein  conditions 
suitable  for  their  growth.  No  one  bacterial  type  is  answerable  for  all 
cases,  but  any  milk  that  contains  a  large  number  of  any  of  these  organ- 
isms may  provoke  the  disorder.  The  type  of  disorder  known  as  acute 
enterocolitis  (ileocolitis)  may  result  also  from  the  aforementioned  causes, 
but  seems  to  be  due  in  most  cases  to  Bacillus  dysenteric,  although  other 
organisms,  such  as  the  streptococcus,  may  participate  in  some  of  the 
lesions.  This  type  of  afi^ection  may  occur  as  a  primary  disorder,  or  it  may 
follow  acute  dyspeptic  diarrhoea  or  gastro-entei-itis  (chohM-a  infantum); 
it  occurs  as  a  terminal  infection  in  measles,  pneumonia,  marasmus,  etc., 


662  ■  DISEASES  OF  THE  INTESTINE 

especially  in  institutions.  Bacillus  dysenterise  is  found  especially  in 
cases  associated  with  mucus  and  blood  in  the  stools,  and  its  number  is 
said  to  be  proportionate  to  the  severity  of  the  infection.  It  is  least 
common  in  purely  fecal  discharges,  but  may  be  isolated  from  the  intes- 
tinal mucosa  in  fatal  cases.  Streptococci  are  often  associated  with 
Bacillus  dysenterise.  The  mode  of  infection  is  not  known,  although  it  is 
attributed  to  the  milk  and  water.  There  is  some  evidence  of  the  con- 
tagious nature  of  some  cases.  The  blood  serum  may  give  a  positive 
agglutination  test  with  Bacillus  dysenterise. 

Pathology. — ^The  lesions  vary  considerably  in  different  cases,  but 
they  are  usually  confined  to  the  colon  and  the  lowermost  parts  of  the 
ileum.  In  mild  cases  there  is  catarrhal  inflammation  of  the  small  and  the 
large  intestine,  with  some  swelling  of  the  lymphoid  follicles;  in  some 
cases  the  swelling  of  the  lymphoid  follicles  forms  a  conspicuous  feature. 
Many  cases  show  necrosis  and  ulceration  of  the  mucosa,  sometimes 
limited  to  the  follicles,  sometimes  more  widespread.  In  severe  cases 
pseudomembranous  inflammation,  usually  limited  to  the  mucosa,  occurs, 
sometimes  irregularly  distributed,  sometimes  widespread — and  is  asso- 
ciated with  submucous  oedema  and  cellular  infiltration.  The  diversity 
of  the  pathological  lesions  found  associated  with  Bacillus  dysenterise,  as 
well  as  the  large  number  of  associated  bacteria,  renders  it  impossible  to 
differentiate  the  lesions  due  to  the  Shiga  bacillus  from  those  due  to  the 
other  intestinal  bacteria.  In  some  cases  a  hyperplastic,  followed  by  an 
atrophic,  condition  of  the  intestinal  mucosa  ensues  and  leads  to  general 
malnutrition.  The  mesenteric  lymph  nodes  are  swollen,  the  kidneys 
are  the  seat  of  cloudy  swelling,  and  hypostatic  congestion  of  the  lungs  and 
bronchopneumonia  occur  frequently. 

Symptoms. — Of  the  diarrhoeas  of  children,  three  types  may  be  distin- 
guished: (1)  Acute  dyspeptic  diarrhoea;  (2)  gastro-enteritis,  gastro- 
intestinal intoxication,  or  cholera  infantum;  and  (3)  acute  enterocolitis. 

Acute  dyspeptic  diarrhcea  may  commence  insidiously  or  acutely,  and 
may  be  seen  in  children  of  all  ages.  The  attacks  may  be  connected 
directly  with  the  taking  of  deleterious  food.  In  many  cases,  at  first, 
aside  from  general  restlessness  and  a  little  looseness  and  increased 
frequency  of  the  bowels,  the  child  presents  no  symptoms.  After  a  day 
or  two  the  stools  increase  in  frequency,  become  very  malodorous,  and 
contain  milk  curds  and  other  undigested  food  (if  such  has  been  taken). 
In  other  cases  the  onset  is  sudden,  sometimes  with  convulsions,  but 
usually  with  high  fever  (103°  to  104°  F.),  vomiting,  diarrhoea,  abdominal 
pain,  tenderness,  and  distention.  The  stools  vary  much  in  number,  and 
consist  of  malodorous  yellowish  or  greenish-yellow  feces,  containing  much 
gas,  milk  curds,  and  undigested  food.  Generally  the  attack  subsides 
within  three  or  four  days  (after  the  intestine  has  been  relieved  of  irri- 
tating contents),  but  relapses  are  common,  and  the  lesions  may  go  on 
to  a  severe  enterocolitis. 

Gastro-enteritis,  gastro-intestinal  intoxication,  or  cholera  infantum 
is   an   extremely  severe    though    uncommon    intoxication  (2  to  3  per 


DIARRHCEAL  DISORDERS  OF  CHILDREN  663 

cent,  of  the  cases  of  summer  cUaiTlioea,  Holt),  that  usually  develops 
suddenly  in  artificially  fed  children  who  have  been  subject  to  intes- 
tinal dyspepsia  and  diarrhoea.  The  disease  is  marked  by  sudden 
onset,  high  fever  (105°  to  10G°  F.),  protracted  vomiting,  frecjuent  serous 
intestinal  discharges,  marked  prostration,  frequent  small  pulse  (130  to 
180  per  minute),  early  collapse,  and  frequently  early  death.  If  there 
has  been  no  preceding  dyspeptic  diarrhoea,  the  stools,  are  at  first  copious 
and  frequent,  fecal  in  character,  brownish  or  yellowish  in  color,  and 
malodorous ;  soon  they  become  greenish  and  later  grayish,  serous,  watery, 
alkaline,  and  almost  devoid  of  odor,  or  musty.  There  may  be  as  many 
as  twenty  or  thirty  stools  in  the  twenty-four  hours.  The  vomiting  is 
often  uncontrollable  and  is  augmented  by  food  and  drink.  At  first  it 
consists  of  the  contents  of  the  stomach,  highly  acid  or  dense  curds; 
later  it  becomes  watery,  mucoid,  bile-stained,  and  less  acid  or  alkaline. 
The  general  evidences  of  intoxication  are  marked  from  the  beginning: 
prostration  is  extreme,  the  skin  is  ashen,  the  features  pinched,  the  eyes 
and  fontanelle  sunken,  the  muscles  flabby,  the  pulse  rapid  and  feeble, 
the  breathing  shallow  and  rapid,  the  sensorium,  at  first  excited,  later 
becomes  benumbed  and  the  child  listless;  thirst  is  marked,  the  urine 
lessened,  the  tongue,  at  first  coated  and  moist,  becomes  red  and  dry, 
and  the  abdomen  retracted.  Death  may  ensue  within  twenty-four 
hours  in  collapse  with  cold  extremities  though  frequently  high  internal 
temperature.  With  the  apathy  and  coma  that  precede  dissolution,  the 
vomiting  and  diarrhoea  may  cease  (but  should  not  be  incorrectly  inter- 
preted). In  other  cases  the  severe  symptoms  abate  temporarily  or 
permanently.  The  patient  may  remain  for  several  days  apathetic, 
semi-comatose;  now  and  then  there  may  be  a  convulsive  seizure,  the 
head  may  be  retracted,  and  the  respirations  irregular,  sometimes  of  the 
Cheyne-Stokes  type  (hydrencephaloid,  or  spurious  hydrocephalus). 
Death  may  result  at  the  end  of  three  or  four  days;  or  the  child  may  go 
into  a  speedy,  though  usually  slow,  convalescence — a  marantic  condi- 
tion (sclerema)  persisting  for  some  time;  or  convalescence  may  progress 
slowly  or  imperfectly  and  the  child  ultimately  die  of  marasmus  with 
irregularly  recurring  attacks  of  diarrhoea. 

Enterocolitis  (ileocolitis,  follicular  enteritis,  follicular  dysentery),  is 
the  form  of  summer  diarrhoea  of  children  commonly  associated  with 
Bacillus  dysenterise,  and  characterized  by  necrotic  and  ulcerative 
processes  in  the  ileum  and  the  colon.  It  may  follow  acute  dyspeptic 
•diarrhoea,  or  any  of  the  acute  infectious  diseases.  The  onset  is 
usually  gradual,  though  it  may  be  abrupt.  The  fever  increases 
and  usually  remains  high  (though  h}'perpyrexia  is  not  as  common 
as  in  cholera  infantum).  The  stools  become  very  frequent  (12  to  30 
in  twenty-four  hours),  small  in  amount,  acid  in  reaction,  malodorous, 
and  contain  mucus  and  streaks  of  blood.  Though  vomiting  may 
occur,  especially  at  the  onset,  it  is  rarely  a  conspicuous  feature  of  the 
disease.  The  abdomen  is  distended  and  tender  along  the  course  of  the 
ileum.    Colicky  pains  may  precede  the  stools,  or  the  stools  may  be  passed 


664  DISEASES  OF  THE  INTESTINE 

painlessly,  or  there  may  be  tenesmus  if  the  lower  colon  and  rectum  are 
involved.  In  most  cases  the  diarrhoea  gradually  subsides,  the  mucus 
and  blood  become  less,  the  fever  lessens,  and  the  child  may  be  convales- 
cent in  two  or  three  weeks.  In  other  cases  the  convalescence  is  pro- 
tracted, the  diarrhoea  lessens  but  does  not  altogether  disappear,  and  the 
general  nutrition  of  the  child  suffers,  though  health  may  eventually 
be  restored. 

In  some  cases  the  onset  is  abrupt  and  resembles  dysentery  in  the 
adult.  It  is  more  common  in  elder  children  (past  the  third  year),  and 
begins  with  high  fever,  vomiting,  severe  abdominal  pains,  colonic 
tenderness,  marked  diarrhoea  (frequent  small  stools  containing  much 
mucus  and  blood),  tenesmus,  marked  intoxication,  and  great  prostra- 
tion. Death  may  occur  within  forty-eight  hours.  Generally,  however, 
the  symptoms  abate  after  twenty-four  or  thirty-six  hours,  but  the  child 
may  continue  ill  for  a  week  and  finally  succumb  or  go  into  a  tedious 
convalescence. 

Under  the  designation  cceliac  disease  has  been  described,  especially 
by  Gee,  a  variety  of  intestinal  catarrh,  of  unknown  cause,  occurring,  in 
children  from  one  to  five  years  of  age,  and  characterized  by  copious, 
diarrhceic,  often  frothy,  and  extremely  malodorous  stools,  resembling 
oatmeal  gruel  (diarrhoea  alba  sive  chylosa).  The  disease  begins  in- 
sidiously, and  progresses  frequently  to  a  fatal  termination,  the  con- 
spicuous general  symptoms  being  asthenia,  anemia,  and  emaciation. 

Diagnosis. — ^Acute  dyspeptic  diarrhoea  is  readily  recognized  by  the 
fecal  character  of  the  stools,  which  contain  undigested  food  and  milk 
curds.  It  is  well  not  to  attribute  any  case  to  teething  and  similar 
factors,  but  to  treat  it  as  a  disease  from  the  beginning.  Cholera  infantum 
is  distinguished  by  the  high  fever,  incessant  vomiting,  serous  discharges, 
general  collapse,  and  other  evidences  of  severe  intoxication.  The 
presence  of  mucus  and  blood  in  the  discharges  distinguishes  entero- 
colitis. 

Prognosis. — The  diarrhoeas  of  children  are  always  serious,  and  the 
prognosis  depends  upon  the  previous  condition  of  the  child  and  the 
severity  of  the  infection.  Acute  dyspeptic  diarrhoea  in  a  healthy  child 
usually  responds  to  treatment,  but  may  prove  fatal  in  a  debilitated 
child.  High  fever,  incessant  vomiting,  and  extreme  prostration  are 
serious  signs  in  cholera  infantum. 

Treatment. — ^An  essential  part  of  the  treatment  is  prophylaxis.  Since 
most  of  the  cases  are  related  etiologically  to  the  diet,  that  is,  artificial 
diet,  it  is  important  to  see  that  the  milk  is  pure  and  fresh,  that  the  dairy 
whence  the  milk  is  derived  meets  all  modern  requirements,  that  the 
milk  is  kept  cool  in  transit,  delivered  fresh,  and  placed  again  on  ice 
in  the  household.  Pasteurization  of  fresh  milk  may  be  resorted  to  in 
hot  weather  as  an  additional  measure  of  safety,  and  all  bottles  should 
be  sterilized  before  being  used.  Additional  safeguards  consist  in  reduc- 
ing somewhat  the  diet  (but  not  pure  water)  during  the  summer,  and 
treating  even  the  slightest  symptom  of  intestinal  disorder  by  stopping 


DIARRHCEAL  DISORDERS  OF  CHILDREN  665 

all  milk  for  a  day  at  least,  and  immediately  cleansing  the  bowel  by 
castor  oil  or  small  doses  of  calomel  -^-jj  to  y^  grain  (0.003  to  0.006 
gram)  three  or  four  times  a  day. 

Hygienic  Treatment. — Hygienic  treatment  is  of  the  utmost  impor- 
tance, and  scarcely  anything  conduces  so  much  to  the  comfort  and  health 
and  recovery  of  the  child  as  removal  from  the  oppressive  air  of  an  over- 
crowded city  to  the  cooler  and  more  wholesome  breezes  of  the  country, 
mountains,  or  seaside.  Wlien  this  is  impossible,  the  city  child  should  be 
kept  out  of  doors  in  the  parks  or  on  the  river,  and  lightly  clad.  Freciuent 
bathing  (tepid  water)  is  an  excellent  measure,  and  should  be  resorted 
to,  especially  if  the  temperature  goes  above  102°  F. 

Dietetic  Treatment. — ^The  dietetic  treatment  is  of  paramount  im- 
portance. At  the  onset  of  the  attack  of  summer  diarrhoea,  milk  must 
be  absolutely  prohibited.  During  the  first  twelve  to  twenty-four  hours 
no  food  should  be  given,  but  pure  water  should  be  administered  in 
amount  equal  to  that  of  the  fluid  food  to  which  the  child  has  been  ac- 
customed. In  very  young  and  marantic  infants  (under  four  months) 
it  may  be  necessary  to  resort  to  food  at  the  end  of  the  first  day,  as  the 
lesser  of  two  evils,  and  pasteurized  whey  or  barley  water  may  be  given  in 
small  amounts.  In  ordinary  cases,  however,  it  is  advisable  to  discon- 
tinue milk  for  at  least  four  or  five  days,  and  to  substitute  barley  water 
(one  tablespoonful  of  barley  and  a  little  salt  to  a  pint  of  water  and  boil  for 
half  an  hour,  add  hot  water  to  make  up  for  loss  by  evaporation,  and 
strain);  or  rice  water;  or  albumen- water  (the  whites  of  two  or  three  eggs, 
1  pint  of  water,  1  dram  of  brandy,  and  a  little  salt) ;  or  beef  juice.  Older 
children  (three  or  four  years)  may  be  permitted  chicken  broth,  mutton 
broth,  or  beef  broth,  but  caution  in  the  use  of  broths  is  necessary,  since 
of  themselves  they  are  laxative.  In  some  cases  the  intolerant  stomach 
may  be  made  more  retentive  by  lavage  with  warm  saline  solution,  and 
in  the  event  of  insufficient  water  being  introduced  by  the  mouth,  recourse 
may  be  had  to  enteroclysis.  The  return  to  milk  diet  must  be  gradual, 
small  amounts  of  a  suitable  mixture,  well  diluted,  being  added  day  by 
day,  and  being  discontinued  upon  the  slightest  return  of  intestinal  de- 
rangement. In  the  majority  of  cases  satisfactory  milk  mixtures  may  be 
readily  prepared  by  diluting  whole  milk  one-fourtii,  one-half,  or  three- 
fourths  with  sterile  water  or  barley  water  and  adding  5  per  cent,  of  lime 
water  and  a  sufficiency  of  milk  sugar  to  bring  the  mixture  to  the  desired 
percentage.  Ordinary  whole  milk  contains :  fat,  4  per  cent. ;  sugar,  4.5  per 
cent. ;  and  proteins,  3.5  per  cent.  Twenty  ounces  is  a  convenient  amount 
of  the  mixture  to  make  at  one  time.  By  adding  5  ounces  of  whole  milk  to 
1  ounce  of  lime  water,  1  ounce  of  milk  sugar,  and  enough  water  to  make  20 
ounces,  a  mixture  is  obtained  that  approximates :  fat,  1  per  cent. ;  sugar, 
0  per  cent.;  and  proteins,  0.9  per  cent.  Ten  ounces  of  milk  and  the 
other  ingredients,  as  mentioned,  make  a  mixture  approximating:  fat,  2 
per  cent.;  sugar,  7  per  cent.;  and  proteins,  l.S  per  cent.  Fifteen  ounces 
of  milk,  the  lime  water  and  water  as  mentioned,  and  ^  ounce  of  milk 
sugar  make  a  mixture  approximating:  fat,  3  per  cent. ;  sugar,  5.5  per  cent. 


666  DISEASES  OF  THE  INTESTINE 

and  proteins,  2.7  per  cent.  In  most  cases  one  or  the  other  of  these  mix- 
tures usually  suffices.  One  should  begin  with  the  weaker  and  proceed 
to  the  stronger,  remembering  that  the  infants  usually  can  digest  fats 
more  easily  than  proteins.  In  intractable  cases  resort  should  be  had  to 
more  accurately  prepared  mixtures.  Whey  and  cream  mixtures  rather 
than  milk  may  be  found  advantageous  in  many  cases  for  a  time  at  least. 
A  wet-nurse  is  sometimes  advisable. 

Medicinal  Treatment. — Medicinal  treatment  is  in  many  cases 
subsidiary  to  the  foregoing.  Since,  however,  all  cases  are  due  to  infec- 
tion of  the  intestinal  contents,  and  later  to  infection  of  the  intestine 
itself,  the  bowel  should  be  immediately  cleared  by  castor  oil,  or  small 
and  repeated  doses  of  calomel  (especially  useful  in  the  event  of  vomiting), 
or  by  lavage  and  colonic  irrigation.  In  acute  dyspeptic  diarrhoea  these 
measures  with  regulation  of  the  diet  often  suffice,  though  bismuth  sub- 
nitrate  (or  subcarbonate,  subgallate,  salicylate,  or  beta-naphthol),  is 
useful  for  its  restraining  influence  on  the  bowel.  In  very  severe  cases, 
bismuth,  salol  (or  resorcin),  and  chalk  mixture  will  be  found  useful;  if 
diarrhoea  persists,  a  little  deodorized  tincture  of  opium  may  be  added, 
but  it  should  not  be  given  until  the  intestinal  tract  has  been  thoroughly 
cleansed.  Pain  until  then  may  be  relieved  by  a  spice  poultice,  or  spirit 
of  chloroform  or  camphor. 

In  cholera  infantum,  which  may  be  serious  and  even  alarming  from 
the  outset,  the  stomach  and  intestines  should  be  cleansed  with  saline 
solution,  or  in  the  event  of  very  high  fever,  ice  water  may  be  used  by 
the  bowel,  or  the  child  put  in  a  tepid  bath,  and  the  water  gradually 
reduced  by  the  addition  of  ice.  An  ice-bag  should  be  applied  to  the 
head.  Morphine,  y^  grain  (0.0006  gram),  and  atropine,  -g-^  grain 
(0.00008  gram),  to  a  child  one  year  old,  may  be  given  hypodermicly 
to  allay  irritation,  and  to  overcome  the  effects  of  the  toxemia  on  the 
nervous  system.  It  is  especially  valuable  if  the  vomiting  and  purging 
persist  and  the  child  collapses.  The  dose  may  be  repeated  in  an  hour 
if  no  improvement  has  resulted.  To  replace  the  lost  body  fluids,  as 
well  as  to  reduce  the  toxemia,  enteroclysis  or  hypodermoclysis  is  of 
great  service.  Small  amounts,  20  to  40  c.c,  repeated,  are  sometimes 
more  serviceable  than  a  single  large  dose  (250  c.c).  In  the  collapse  of 
some  cases  small  amounts  of  caffeine  (1  to  400),  or  of  adrenalin  chloride, 
added  to  the  saline  solution,  may  prove  useful.  Stimulants  are  indicated 
in  severe  cases;  sometimes  small  amounts  of  brandy,  cognac,  or  cham- 
pagne may  be  retained  when  all  else  is  rejected.  Strychnine  may  be 
given  hypodermicly.  When  the  vomiting  has  been  overcome,  bismuth  and 
the  remedies  previously  mentioned,  are  sometimes  efficacious,  or  starch 
water  and  laudanum  may  be  given  by  the  rectum.  Return  to  feeding 
must  be  done  gradually,  beginning  with  albumin  water  and  beef  juice; 
later  whey  and  cream,  peptonized  milk,  or  the  milk  mixtures  men- 
tioned may  be  given.  If  convalescence  is  protracted  and  diarrhoea  per- 
sists, or  is  easily  provoked,  the  diet  should  be  looked  to;  but  the  condition 
may  be  one  of  enterocolitis,  in  which  event  injections  of  saline  solution 


PHLEGMONOUS  ENTERITIS  667 

or  silver  nitrate  (1  to  10,000)  may  be  serviceable.  Iron,  arsenic,  cod-liver 
oil,  and  change  of  climate  are  of  marked  service  during  convalescence  in 
many  cases.  An  effective  serum  for  Bacillus  dysenterise  infections 
has  not  yet  been  produced. 


CROUPOUS  OR  DIPHTHERITIC  ENTERITIS. 

Croupous  or  diphtheritic  enteritis  is  an  inflammation  of  the  intestinal 
mucosa  attended  by  necrosis  and  the  formation  of  a  croupous  (or 
fibrinous)  exudate. 

Etiology. — Croupous  or  diphtheritic  enteritis  is  due  to:  (1)  Bacterial 
infection — whence  it  occurs  in  certain  infectious  diseases,  such  as 
pneumonia  (the  pneumococcus  may  be  isolated  from  the  exudate  in 
some  cases),  typhoid  fever,  scarlet  fever,  smallpox,  and  septic  processes, 
(2)  It  occurs  in  conditions  of  reduced  vitality,  such  as  occur  in  chronic 
diseases,  when  it  is  frequently  a  terminal  infection,  as  in  nephritis, 
cirrhosis  of  the  liver,  heart  disease,  carcinoma,  etc. — the  reduced  vitality 
permitting  of  secondary  bacterial  infection.  (3)  It  occurs  also  in  poison- 
ing by  mercury,  arsenic,  ammonia,  lead,  etc. 

Pathology. — ^The  lesions  vary  in  different  cases.  In  the  one  there  is 
necrosis  of  the  mucous  membrane,  varying  in  extent  and  depth,  but  often 
confined  to  the  tops  of  the  folds  of  mucous  membrane  and  rather  super- 
ficial. In  other  cases  the  necrosis  is  more  widespread  and  may  involve 
the  entire  thickness  of  the  mucosa.  The  false  membrane  is  grayish, 
grayish  yellow,  or  grayish  white  in  color,  and  is  surmounted  on  a  congested 
base.  The  lesions  are  more  common  in  the  colon  than  in  the  small 
intestine.  In  the  second  group  of  cases  the  solitary  lymph  nodes  are  the 
seat  of  swelling  and  superficial  or  deep  necrosis,  attended  by  the  formation 
of  a  membranous  exudate. 

Symptoms. — Often  there  are  no  symptoms.  When  present,  the  symp- 
toms are  those  of  enteritis  and  colitis.  The  exact  nature  of  the  disorder 
cannot  be  recognized  unless  some  of  the  exudate  is  discharged  witli  the 
stools. 

Treatment. — The  treatment  is  that  of  the  primary  affection  plus  that 
of  catarrhal  enteritis. 


PHLEGMONOUS  ENTERITIS. 

Phlegmonous  enteritis  is  a  rare  disease  characterized  by  suppurative 
inflammation  of  the  mucous  and  muscular  coats  of  the  intestine.  As  an 
idiopathic  affection  it  is  exceedingly  rare  (even  rarer  tlian  phlegmonous 
gastritis);  as  a  secondary  affection  it  sometimes  attends  pyococcic  pro- 
cesses, and  may  be  associated  with  intestinal  intussusception  or  strangu- 
lation or  strangulated  hernia.  Anatomically  the  purulent  collection  may 
be  circumscribed  (abscess)  or  diffuse  (phlegmon).     The  sijnipioms  are 


668  DISEASES  OF  THE  INTESTINE 

usually  those  of  peritonitis,  and  the  affection  is  scarcely  susceptible  of 
dift'erential  diagnosis.  The  treatment,  apart  from  operative  procedures 
in  association  with  intestinal  obstruction,  is  unavailing. 


APPENDICITIS. 

Etiology. — Inflammation  of  the  vermiform  appendix  is  an  extraordin- 
arily common  disorder :  the  commonest  intra-abdominal  disease.  It  is  mos't 
common  in  early  adult  life,  and  more  common  in  men  than  in  women.  It 
is  really  the  consequence  of  infection  occurring  in  an  organ  provided  with 
a  precarious  blood  supply  and  ill  adapted  to  drainage — both  of  which 
in  circumstances  permit  of  the  ready  operation  of  bacteria.  The  factors 
impeding  drainage  are  the  excessive  length  of  the  organ,  the  narrowness 
and  often  tortuosity  of  the  lumen,  Gerlach's  valve,  and  the  swelling 
of  the  mucosa  that  readily  occurs.  To  these  one  may,  perhaps,  add  the 
influence  of  appendicular  calculi — ^which  are  not  fecal  concretions  in  a 
true  sense,  but  the  result  of  appendicular  inflammation;  when  formed, 
they  tend  to  keep  up  the  inflammation,  and  by  pressure,  attrition,  and 
interfering  with  local  blood  supply  they  are  a  factor  in  determining  the 
site  of  ulceration.  Foreign  bodies  and  worms  are  rarely  found  in  the 
appendix,  but  when  occurring  may  be  of  etiological  significance.  The 
chief  infectious  cause  is  Bacillus  coli,  but  streptococci,  staphylococci, 
pneumococci.  Bacillus  influenzae.  Bacillus  typhosus,  Bacillus  dysenterise. 
Bacillus  tuberculosis,  Streptothrix  actinomyces,  and  other  organisms 
may  be  the  active  etiological  agent. 

Pathology. — ^Acute  and  chronic  cases  may  be  distinguished.  The 
lesions  of  the  acute  cases  comprise  the  ordinary  phenomena  of  inflam- 
mation, congestion,  oedema,  round-cell  infiltration,  etc.,  which  very 
rarely  may  be  lirnited  to  the  mucosa  (so-called  catarrhal  appendicitis). 
In  most  cases  the  lesions,  although  they  vary  much  in  many  cases, 
extend  more  or  less  throughout  the  wall  of  the  appendix.  Sometimes 
they  consist  only  of  the  aforementioned  inflammatory  phenomena,  with 
perhaps  only  a  little  superficial  erosion  of  the  lining  mucosa  (acute 
interstitial  appendicitis).  But  in  the  great  majority  of  cases  in  which 
the  lesions  are  widespread  or  severe  there  is  more  or  less  suppuration, 
necrosis,  and  loss  of  the  mucosa  (ulcerative  appendicitis);  the  lesions 
may  or  may  not  progress  to  perforation  of  the  organ.  In  other  cases,  in 
consequence  of  virulent  infection  or  defective  or  abolished  blood  supply, 
gangrene  supervenes.  The  chronic  lesions  also  are  rarely,  perhaps, 
confined  to  the  mucosa  (chronic  catarrhal  appendicitis).  In  the  great 
majority  of  cases,  however,  all  the  coats  of  the  organ  are  involved,  the 
conspicuous  changes  consisting  of  connective-tissue  hyperplasia  of  the 
submucosa  and  the  musculai-is,  round-cell  infiltration,  and  atrophy  of 
the  muscular  tissue.  In  some  cases,  the  mucosa  having  been  the  seat 
of  more  or  less  suppuration  and  necrosis,  is  finally  entirely  lost,  and 
the  opposed  ulcerating  surfaces  by  a  process  of  organization  may  become 


APPENDICITIS  669 

united  into  a  firm  fibrous  union  with  obliteration  of  the  himen  throughout 
more  or  less  of  the  length  of  the  organ  (chronic  obliterative  appendicitis). 
Most  of  the  chronic  cases  are  subject  to  acute  exacerbations — in  which 
to  the  chronic  hyperplastic  process  acute  manifestations  may  super- 
vene (recurring  or  relapsing  appendicitis).  In  many  of  these  cases  the 
appendicular  contents  become  and  remain  purulent  (clironic  empyema) ; 
and  at  any  time  any  of  the  severe  acute  lesions,  such  as  perforation  or 
gangrene,  may  supervene. 

The  chief  significance  of  appendicitis  attaches  to  the  peritonitis  it 
provokes.  In  mild  cases  this  may  be  strictly  localized  to  the  region 
about  the  appendix,  and  serous  or  serofibrinous  in  character.  In  many 
severe  cases,  usually  with,  but  often  without,  perforation,  the  peritoneal 
lesions  may  also  remain  localized,  but  they  become  purulent  in  char- 
acter— so-called  peri-appendicular  abscess.  Limiting  adhesions  may 
suffice  to  "wall-ofl^"  the  abscess  from  the  rest  of  the  peritoneal  cavity, 
but  in  many  cases  the  pus  finds  its  way  into  the  pelvis,  or  by  a  progressive 
breaking  down  of  adhesions  and  the  formation  of  new  adhesions  in 
advance  of  the  old  ones,  more  or  less  of  the  peritoneal  cavity  may  ulti- 
mately become  involved  (progressive  fibrinopurulent  peritonitis).  In 
some  cases  there  are  few",  if  any,  adhesions,  the  peritoneum  constituting 
a  veritable  pus  sac  (diffuse  or  generalized  suppurative  peritonitis).  Oc- 
casionally the  lesions  become  putrid.  Rarely  the  peritoneum  is  found 
quite  dry  and  lustreless — in  cases  of  very  severe  and  overwhelming 
intoxication  (toxic  peritonitis).  The  peri-appendicular  abscess  is  some- 
times situated  behind  the  peritoneum,  about  the  kidney,  near  the  liver. 
These  extraperitoneal  as  well  as  intraperitoneal  collections  of  pus  may 
burrow  in  various  directions — into  the  intestine,  into  the  pelvis  (and 
be  discharged  through  the  rectum  or  vagina),  behind  the  liver,  through 
the  diaphragm,  and  be  expectorated  through  a  bronchus,  etc.  Multiple 
abscesses  of  the  liver  (suppurative  pylephlebitis)  is  a  common  complica- 
tion in  neglected  cases;  general  septicopyemia  also  may  ensue.  Pri- 
mary carcinoma  is  not  uncommonly  found  in  appendices  removed  for 
appendicitis. 

In  chronic  appendicitis,  in  addition  to  the  lesions  already  mentioned, 
peritoneal  adhesions  are  usually  found.  These,  binding  the  appendix 
to  adjacent  organs,  are,  in  large  part,  the  cause  of  the  symptoms  of 
chronic  appendicitis,  and  may  lead  to  strangulation  or  kinking  of  the 
appendix  or  intestine  and  various  disturbance  of  the  organs  to  which 
they  may  be  attached. 

Symptoms.— In  acute  a'pfendicitis  the  onset  is  usually  sudden.  The 
chief  symptoms  consist  of  severe  abdominal  pain,  nausea  and  vomiting, 
tenderness  and  muscular  rigidity  in  the  region  of  the  appendix,  and  fever 
(101°  to  103°  F.).  The  pain  is  usually  sudden  in  onset  and  severe,  often 
colicky  in  character.  It  is  usually  at  first  epigastric  or  umbilical  insituation, 
or  may  be  diffuse;  but  it  soon  becomes  localized  to  the  right  lower  abdom- 
inal quadrant.  It  may  radiate  to  the  bladder,  to  the  testicle,  or  the  lumbar 
region;  and  may  be  aggravated  by  movement  of  the  right  thigh,  which  is 


670  DISEASES  OF   THE  INTESTINE 

often  flexed  to  relieve  the  pain.  Tenderness  also  may  be  more  or  less 
general  at  first,  but  it  soon  becomes  localized  to  the  region  of  the  appen- 
dix, and  is  usually  most  marked  at  McBurney's  point  (a  point  midway 
on  a  line  drawn  from  the  anterior  superior  spine  of  the  ilium  to  the 
umbilicus).  In  some  cases  depending  upon  the  direction  of  the  appen- 
dix, the  tenderness  may  be  most  marked  in  the  lumbar  region  (retro- 
peritoneal appendix  pointed  upward),  in  the  pelvis,  to  the  left  of  the 
median  line,  etc.  The  rigidity  of  the  muscles  in  the  right  lower  abdom- 
inal quadrant  may  be  very  marked.  At  the  onset,  accompanying  the 
fever,  the  pulse  is  usually  rapid,  and  a  polynuclear  leukocytosis  com- 
monly supervenes  (12,000  to  25,000).  The  bowels  are  usually  consti- 
pated, and  painful;  and  perhaps  frec}uent  micturition  may  occur  if  the 
appendix  reaches  into  the  pelvis  and  impinges  on  the  bladder. 

In  the  course  of  a  day  or  two  the  lesions  and  the  symptoms  may  sub- 
side and  the  patient  may  go  on  to  apparent  recovery.  Seeming  improve- 
ment, such  as  lessening  of  pain  and  of  the  fever,  however,  by  no  means 
indicates  subsidence  of  the  inflammatory  phenomena;  both  the  pain 
and  fever  may  lessen  in  cases  attended  by  perforation  and  suppuration. 
The  pulse  is  a  much  better  index  of  the  intra-abdominal  conditions 
than  is  the  pain  or  the  fever.  In  the  cases  that  do  subside  the  appendix, 
usually  does  not  return  to  its  previous  normal  condition,  and  recurrences 
and  relapses  are  likely  to  ensue. 

In  the  cases  that  do  not  improve,  more  or  less  severe  peritoneal 
lesions  develop — either  a  peri-appendicular  abscess  or  diffuse  peri- 
tonitis. The  peri-appendicular  abscess  may  be  recognized  by  a  more 
or  less  well-defined  mass  in  the  region  of  the  appendix;  it  is  usually 
doughy  to  the  touch  and  may  disclose  deep  oedema;  it  is  dull  on  percus- 
sion or  perhaps  tympanitic  from  overlying  and  distended  intestinal 
coils;  and  on  auscultation  it  reveals  no  peristaltic  sounds.  This  abscess 
may  follow  directly  upon  what  seemed  to  be  a  relatively  mild  appen- 
dicitis; that  is,  there  may  be  no  signs  whatever  suggesting  a  perforation 
or  other  serious  complication.  Occasionally  sudden  severe  pain  does 
occur,  and  may  be  interpreted  as  rupture  of  the  appendix.  Generalized 
peritonitis  is  disclosed  by  generalized  pain,  tenderness,  and  rigidity, 
vomiting,  rapid  feeble  pulse,  fever,  leukocytosis,  Hippocratic  counte- 
nance, and  other  evidences  of  marked  intoxication,  and  final  collapse. 
This  generalized  peritonitis  may  be  preceded  by  more  or  less  well-defined 
evidences  of  localized  abscess,  or  it  may  develop  directly  in  consequence 
of  rupture  or  gangrene  of  an  appendix  not  enclosed  within  adhesions. 

Chronic  apj}e»dicitis  is  characterized  clinically  by  various  gastro- 
intestinal and  neurasthenic  manifestations.  The  chief  symptoms  are 
comprised  within  the  term  indigestion  (!Moynihan's  appendix  dyspepsia); 
to  which  may  be  added  frequent  or  infrequent  attacks  of  more  or  less 
well-marked  or  frank  appendicitis.  The  dyspeptic  phenomena  simu- 
late and  are  readily  mistaken  for  disease  of  the  gall-bladder,  gastric 
ulcer  (exaggerated  activity  of  the  pylorus,  pylorospasm),  etc.,  and  often 
can  scarcely  be  distinguished   therefrom   aside  from   operative   inter- 


APPENDICITIS  671 

vention.  Well-marked  neurasthenia  is  quite  common  and  the  patient 
may  emaciate.  Mucous  colitis  also  may  be  a  manifestation  of  chronic 
appendicitis. 

Diagnosis. — Sudden  severe  abdominal  pain,  nausea  and  vomiting, 
tenderness  and  muscular  rigidity  in  the  region  of  the  appendix,  and 
fever,  usually  suffice  for  the  diagnosis  in  the  acute  cases.  However, 
in  some  cases  one  has  to  take  into  consideration  the  possibility  of 
the  many  acute  abdominal  conditions  that  may  cause  sudden  pain, 
nausea,  and  vomiting,  especially  perforated  gastric  or  duodenal  ulcer, 
gallstone  colic,  renal  colic,  intestinal  colic,  menstrual  pains,  acute 
pancreatitis,  Diehl's  crisis  in  floating  kidney,  intestinal  intussusception 
and  strangulation,  etc.;  but  these  and  other  abdominal  disorders  are 
in  themselves  well  characterized  symptomatically  and  scarcely  any  one 
of  them  is  likely  to  present  all  the  characteristic  symptoms  of  acute 
appendicitis.  Chronic  appendicitis  may  be  recognized  in  the  cases  that 
do  not  present  unequivocal  symptoms,  in  the  cases  in  which  dyspepsia 
is  the  obtrusive  feature,  by  bearing  in  mind  that  most  cases  of  intractable 
dyspepsia  have  an  anatomical  basis,  and  that  this  is  usually  gastric 
ulcer,  gastric  carcinoma,  perigastric  adhesions,  chronic  cholecystitis,  with 
or  without  gallstones,  chronic  pancreatitis,  or  chronic  appendicitis. 

Prognosis. — ^The  prognosis  in  acute  cases  is  extraordinarily  uncertain, 
since  no  one  can  foretell  in  the  early  stage  whether  the  disease  is  likely 
to  be  mild  or  severe;  the  symptoms  bear  no  constant  relationship  to  the 
severity  of  the  lesions  (the  most  grave  anatomical  lesions  may  be  present 
with  mild  or  slight  symptoms);  and  apparent  improvement  may  occur 
with  advancing  intra-abdominal  conditions.  In  the  event  of  recovery, 
relapses  and  recurrences  are  likely.  The  outlook  in  the  chronic  cases  as  to 
permanent  relief  is  bad  unless  recourse  is  had  to  surgical  intervention. 

Treatment. — ^The  treatment  of  appendicitis  is  surgical;  there  is  no 
really  dependable  effective  medical  treatment.  It  is  true  that  some 
patients  recover  under  medical  treatment,  and  it  is  also  true  that  many 
die  who  might  be  saved  by  timely  resort  to  surgical  measures.  Fur- 
thermore, it  is  true  that  some  patients  die  after  an  operation,  but  the 
great  majority  of  these  are  subjects  in  whom  the  operation  has  been 
unduly  delayed  or  they  are  the  subjects  of  fulminating  infections — doomed 
from  the  very  outset.  The  mortality  following  a  timely  operation  is 
much  less  than  under  any  other  form  of  treatment.  The  foregoing 
are  the  facts  that  should  guide  us  in  our  treatment,  and  operation 
should  not  be  delayed  until  the  patient  is  "sick  enough"  to  warrant  it. 

Pending  the  arrival  of  the  surgeon,  and  in  any  event  as  soon  as  the 
patient  is  seen,  all  food  and  water  should  be  stopped  (and  none  should 
be  given  until  the  patient  is  recovering);  the  stomach  should  be  washed 
out,  and  the  procedure  repeated  if  nausea  and  vomiting  continue;  and 
the  bowels  should  be  opened  by  an  enema.  If  the  patient  is  seen  early, 
before  the  development  of  peritonitis,  the  bowels  may  be  unloaded  by 
castor  oil,  but  if  peritonitis  (local  as  well  as  general)  has  supervened, 
no  cathartics  should  be  given  by  the  mouth.    An  ice  bag  may  be  applied 


672  DISEASES   OF  THE  INTESTINE 

to  the  abdomen  to  relieve  pain,  or  hot,  moist  compresses,  if  these  are 
more  grateful  to  the  patient.  Ochsner  recommends  hot  boric-acid  solu- 
tion and  alcohol.  Enteroclysis  by  the  drop,  or  the  Murphy,  method  may. 
be  used  to  relieve  thirst;  perhaps  it  has  also  some  good  effect  on  the 
developing  peritonitis.  If  deemed  necessary,  stimulants  and  liquid 
meat  extracts  (which,  however,  contain  more  alcohol  than  nutriment) 
may  be  added  to  the  physiological  saline  solution,  and  given  three  or 
four  times  a  day.  Opium  -should  be  entirely  withheld  if  possible;  it 
should  never  be  given  until  the  diagnosis  is  at  least  reasonably  certain, 
and  then  only  the  smallest  possible  amount,  sufficient  only  to  mitigate 
the  pain  and  not  obtund  the  sensibilities  and  mask  the  symptoms. 


SIGMOID  DIVERTICULITIS. 

(Perisigmoiditis.) 

Etiology. — Aside  from  congenital  diverticula  of  the  intestine,  of  which 
the  most  common  is  Meckel's  diverticulum,  acquired  diverticula  may 
occur  almost  anywhere  in  the  intestine,  sometimes  in  the  region  of  the 
appendix,  but  most  commonly  in  the  sigmoid  flexure  of  the  colon.  The 
cause  of  the  condition  is  not  well  understood.  They  are  common  in 
elderly  obese  subjects  who  have  been  constipated.  They  have  been 
attributed  to  localized  areas  of  muscular  weakness,  and  are  often  related 
to  the  absorption  of  the  fat  of  epiploic  appendages. 

Pathology. — In  the  sigmoid  these  diverticula  occur  either  in  two  parallel 
rows  along  the  sides  of  the  intestine  or  along  the  attachment  of  the 
mesentery;  they  may  be  confined  to  the  epiploic  appendages.  There 
may  be  several  or  many.  They  vary  in  size  from  1  to  2  mm.  in  diameter 
to  a  centimeter  or  more.  When  small  they  are  usually  spheroidal;  but 
when  elongated  they  are  likely  to  be  flask-shaped.  They  commonly 
communicate  with  the  lumen  of  the  gut  by  a  constricted  orifice.  They 
become  the  seat  of  more  or  less  well-marked  inflammation,  which  in 
acute  cases  may  be  catarrhal,  suppurative,  or  gangrenous ;  and  this  may 
give  rise  to  localized  peritonitis  with  abscess  formation  or  to  generalized 
peritonitis — in  all  of  which  respects  the  lesions  are  somewhat  analogous 
to  appendicitis.  More  or  less  inspissated  fecal  matter  and  even  enter- 
oliths may  be  found  within  the  pouches.  In  the  chronic  cases  there  is 
usually  much  connective-tissue  hyperplasia  and  consequent  thickening 
and  stenosis  of  the  bowel  (chronic  hyperplastic  sigmoiditis  and  peri- 
sigmoiditis). The  condition  much  resembles  and  has  been  mistaken  for 
carcinoma. 

Symptoms  .^ — ^The  acute  cases  most  simulate  acute  appendicitis,  the 
pain,  tenderness,  and  muscular  rigidity,  however,  being  on  the  left  side. 
(As  is  well  known,  this  may  occur  in  appendicitis,  when  the  appendix 
reaches  over  to  the  left  side  or  depends  into  the  pelvis.)  The  lesions 
may  go  on  to  abscess  formation  and  divers  suppurative  complications. 
In  the  chronic  cases  the  symptoms   consist  of  constipation,  gradually 


ULCERATION  OF  THE  INTESTINE  673 

increasing  colonic  obstruction,  and  a  tumor  mass  in  the  left  inguinal 
region.  These  occurring  in  an  elder  person  (usually  a  man),  simulate 
carcinoma.  Doubtless  some  supposed  carcinomas  of  the  sigmoid 
removed  at  operation  were  in  reality  cases  of  sigmoid  diverticulitis. 
This  sigmoiditis,  rather  than  carcinoma,  is  suggested  by  long-standing 
constipation,  gradually  increasing  intestinal  obstruction,  absence  of  blood 
in  the  feces,  and  slight  anemia  and  cachexia. 

Prognosis. — The  outlook  is  good  under  appropriate  treatment. 

Treatment. — ^The  treatment  is  wholly  surgical  and  consists  of  removing 
the  diseased  portion  of  the  sigmoid. 


ULCERATION  OF  THE  INTESTINE. 

Etiology. — ^The  following  forms  of  ulceration  of  the  intestine  are  de- 
scribed by  Nothnagel:  (1)  Ulceration  due  to  necrotic  processes — ^simple 
duodenal  ulcer,  ulcer  following  burns,  embolic  and  thrombotic  ulcers 
(including  those  seen  in  patients  with  multiple  neuritis),  and  amyloid 
ulcers.  (2)  Ulceration  due  to  inflammatory  processes — catarrhal  ulcer, 
follicular  ulcer,  and  stercoral  or  decubital  ulcer.  (3)  Ulceration  due  to 
acute  infectious  diseases — typhoid  fever,  dysentery,  diphtheria,  anthrax, 
sepsis,  erysipelas,  and  varioloid.  (4)  Ulceration  due  to  chronic  infectious 
diseases — tuberculosis,  syphilis,  leprosy,  and  pellagra.  (5)  Ulceration  due 
to  constitutional  disease — gout,  scurvy,  and  leukemia.  (6)  Ulceration 
due  to  intoxications — uremic  ulcer,  mercurial  ulcer. 

Symptoms. — Duodenal  ulceration,  as  well  as  typhoid,  dysenteric,  and 
diphtheric  ulceration,  are  discussed  elsewhere.  Diarrhoea  with  blood,  pus, 
mucus,  and  shreds  of  necrotic  tissue  in  the  stools  are  the  important 
symptoms  of  ulceration  of  the  intestine.  Although  diarrhoea  is  common, 
it  is  not  invariable  and  may  be  absent  in  the  presence  of  even  extensive 
ulceration.  Nothnagel  believes  that  the  presence  or  absence  of  diarrhoea 
is  determined  primarily  by  the  site  of  the  ulcerative  lesions,  stating  that 
if  the  ulcers  are  in  the  small  intestine,  cecum,  or  ascending  colon  they 
probably  never  produce  diarrhoea  unless  the  ulceration  is  complicated 
by  other  conditions,  such  as  intestinal  catarrh,  amyloid  disease,  special 
forms  of  infection,  or  other  factors  that  may  influence  directly  intes- 
tinal peristalsis.  If  the  ulcers  are  in  the  lower  portion  of  the  colon  and  the 
rectum,  diarrhoea  occurs  with  great  regularity,  but  it  may  be  absent 
if  the  ulcers  are  few  in  number  and  if  the  nervous  irritability  of  these 
portions  of  the  bowel  is  lowered  or  inhibited.  Blood  is  often  present, 
but  it  may  be  absent,  and  if  present  may  be  due  to  causes  other  than 
ulceration.  It  is  a  valuable  sign  when  it  occurs  in  circumstances  that 
render  likely  the  presence  of  ulceration.  Pus  is  usually  present  in  greater 
or  less  amount,  and  often  requires  careful  search  to  detect  it;  it  is  of 
greater  diagnostic  significance  than  the  presence  of  blood.  Large 
amounts  indicate  perforation  into  the  intestine  of  an  extra-intestinal 
abscess  (peri-appendicular,  peri-uterine,  etc.),  the  presence  of  a  suppurat- 
43 


674  DISEASES  OF  THE  INTESTINE 

ing  and  ulcerating  carcinoma,  or  a  croupous  inflammation  of  the  intestine. 
A  purulent  mucus  is  sometimes  present,  and  in  some  cases  one  may 
encounter  peculiar  sago-like  grains  of  mucus,  formerly  but  no  longer 
considered  diagnostic  of  follicular  ulceration.  Shi-eds  of  tissue  (mucosa, 
connective  tissue,  and  even  muscularis)  are  important  diagnostically, 
but  they  are  rather  rare.  Pain  may  or  may  not  be  present;  it  is  of  value 
only  when  present  continuously  at  the  one  place  and  intensified  by  press- 
ure. If  the  ulceration  is  slight  the  general  nutrition  is  not  much  impaired, 
but  extensive  ulceration  usually  leads  to  marked  deterioration  of  the 
general  health.  Secondary  infection  of  the  ulcer  may  cause  a  little  fever, 
but  usually  there  is  none.  Perforation  is  not  uncommon,  and  may  give 
rise  to  local  or  generalized  peritonitis,  or  to  a  retroperitoneal  abscess. 

Diagnosis. — ^The  diagnosis  of  the  nature  of  the  ulceration  may  some- 
times be  made  by  attention  to  the  attending  phenomena  and  examina- 
tion of  the  stools  for  tubercle  bacilli  and  other  specific  organisms,  as  well 
as  shreds  of  tissue.  Tubercle  bacilli  in  the  stools,  however,  may  have 
been  swallowed,  and  do  not  necessarily  mean  ulceration  of  the  intestine. 

Prognosis. — ^The  prognosis  varies  with  the  nature  of  the  etiological 
factors. 

Treatment. — ^The  treatment  in  many  cases  is  determined  by  the  nature 
of  the  primary  disorder;  the  treatment  of  the  primar}^  and  the  secondary 
conditions  is  not  separable — such  as  ulcers  occurring  in  infectious  dis- 
eases (typhoid  fever,  dysenter}- ,  tuberculosis,  s^-philis,  etc.),  in  constitu- 
tional diseases,  in  poisoning,  etc.  In  all  cases  regulation  of  the  diet  is 
of  the  utmost  importance,  a  suitable  diet  being  determined  upon  largely 
by  a  study  of  the  individual  patient.  Direct  treatment  of  the  ulcers,  by 
means  of  topical  applications  or  rectal  enemas,  is  scarcely  possible  unless 
the  ulcers  are  situated  in  the  rectum  or  the  lower  part  of  the  colon, 
though  in  some  cases  even  the  ascending  colon  may  be  reached  by 
enemas.  The  most  suitable  medicated  enemas  consist  of  boric  acid  or 
salicylic  acid  (0.3  to  0.5  per  cent.),  thjnnol  (0.1  per  cent.),  silver  nitrate 
(0.3  to  1  per  cent.),  or  tannic  acid  (0.3  to  1  per  cent.).  Recently  some 
good  results  have  been  achieved  by  the  operative  establishing  of  an  arti- 
ficial anus  through  the  medium  of  the  cecum  and  the  giving  of  complete 
rest  to  the  colon;  in  other  cases,  a  communication  has  been  established 
with  the  exterior  through  the  medium  of  the  cecum  or  the  appendix  and 
the  entire  colon  and  the  rectum  subsec{uently  periodically  irrigated  with 
medicated  enemas,  with  asserted  good  results.  Internally  few  prepara- 
tions are  of  much  service;  but  some  relief  maybe  afforded  the  patient 
by  the  symptomatic  treatment  of  diarrhoea,  pain,  hemorrhage,  etc. 


INTESTINAL  OBSTRUCTION. 

The  term  intestinal  obstruction  is  inclusive;  it  comprises  a  number  of 
somewhat  different  though  related  conditions,  to  which  several  names 
have  been  applied:  Occlusion  signifies  a  complete  closure  of  the  lumen 


INTESTINAL  OBSTRUCTION  675 

of  the  intestine  entirely  arresting  the  onward  passage  of  the  intestinal 
contents.  Stenosis  signifies  a  lessening  of  the  lumen  of  the  intestine, 
an  incomplete  occlusion,  arising  from  any  cause  whatsoever — a  con- 
dition in  which  the  onward  passage  of  the  intestinal  contents  is 
impeded,  but  not  arrested.  Stricture  signifies  a  lessening  of  the  lumen, 
the  result  of  disease  (usually  annular)  of  the  wall  of  the  intestine. 
Constriction  signifies  lessening  of  the  lumen  of  the  intestine  in  con- 
sequence of  pressure  (compression)  or  traction  from  without.  Obtura- 
tion signifies  obstruction  from  within  the  lumen  of  the  intestine,  as  by 
impacted  feces,  an  enterolith,  a  gallstone,  etc.  Incarceration  signifies 
an  imprisonment  of  the  intestine  in  a  part  or  cavity.  Strangulation 
signifies  a  form  of  constriction  in  which  the  compression  is  so  severe 
as  to  interfere  seriously  with  the  vascular  and  nervous  supply,  and 
hence  the  functional  activity  and  even  the  life  of  the  intestine.  The 
term  ileus  is  sometimes  inappropriately  applied  to  any  severe  intes- 
tinal obstruction  or  occlusion  attended  by  stercoraceous  vomiting; 
and  the  term  paralytic  ileus  is  sometimes  applied  to  the  paresis  or 
paralysis  which  may  follow  abdominal  operations,  the  relief  of  intes- 
tinal obstruction  (release  from  constricting  bands,  rectification  of  a 
volvulus,  etc.),  or  that  occm-s  in  peritonitis,  etc.,  and  sometimes  even 
without  anatomical  basis. 

Etiology. — Intestinal  obstruction  may  be  due  to: 

1.  Disease  Outside  the  Intestine:  (a)  Tumors  of  any  of  the  intra- 
abdominal organs,  especially  of  the  ovary,  uterus,  omentum,  or  kidney, 
which  give  rise  to  obstruction  by  compression,  the  obstruction  being 
usually  chronic,  though  the  sjanptoms  may  develop  acutely.  Analogous 
in  action  to  tumors  are  abscesses,  especially  pelvic  and  peri-appendicular, 
as  well  as  collections  of  fluid,  such  as  pancreatic  cysts  and  hydronephrosis. 
(b)  Conditions  causing  strangulation,  such  as  internal  hernia  (diaphrag- 
matic, subcecal,  duodenojejunal,  intersigmoid,  through  the  foramen  of 
Winslow);  post-inflammatory  adhesions  and  bands,  pedicles  of  tumors, 
remains  of  fecal  structures,  such  as  INIeckel's  diverticulum  (especially 
when  adherent  at  its  unattached  end),  fibrous  remains  of  foetal  vessels, 
etc.,  beneath  which  a  loop  of  intestine  may  slip  and  become  constricted, 
or  which  by  traction  may  occasion  kinking  of  the  intestine ;  omental  and 
mesenteric  slits  and  peritoneal  pouches,  which  may  engage  and  strangle  a 
portion  of  the  bowel;  etc.  Strangulation  is  the  most  common  cause  of 
acute  intestinal  obstruction  (34  per  cent,  of  the  cases,  Fitz).  Seventy 
per  cent,  of  the  cases  occur  in  men;  40  per  cent,  between  the  fifteenth  and 
thirtieth  years.  In  90  per  cent,  the  small  intestine  is  involved;  in  87 
per  cent,  the  strangulation  is  in  the  right  iliac  fossa;  and  in  83  per 
cent,  in  the  lower  half  of  the  abdomen  (Fitz). 

2.  Disease  of  the  Intestinal  Wall:  (a)  Intussusception  or  invagina- 
tion, the  infolding  of  the  intestine  into  itself,  is  a  common  cause  of 
acute  obstruction  (31  per  cent,  of  the  cases,  Fitz),  and  occasionally  causes 
chronic  obstruction.  It  is  twice  as  common  in  males  as  in  females;  more 
than  one-half  of  the  cases  occur  before  the  tenth  year,  and  many  occur  in 


676  DISEASES  OF  THE  INTESTINE 

the  first  year  of  life  when  the  intestine  is  relatively  long  and  irregular; 
peristalsis  (an  essential  cause  of  the  disorder)  is  very  common.  The 
invagination  is  always  a  descending  process,  the  upper  portion  of  the 
bowel  descending  into  the  lower — whence  several  varieties  are  recognized : 
the  iliac,  in  which  the  ileum  alone  is  involved;  the  ileocecal,  in  which 
the  ileocecal  valve  enters  the  colon  (75  per  cent,  of  the  cases) ;  the  ileocolic, 
in  which  the  lower  part  of  the  ileum  passes  through  the  ileocecal  valve; 
the  appendiceal,  in  which  the  vermiform  appendix  enters  the  cecum; 
the  colic,  in  which  the  colon  alone  is  involved;  and  the  colicorectal,  in 
which  the  colon  descends  into  the  rectum.  The  intussusception  forms 
an  irregular  tumor  varying  from  less  than  an  inch  to  a  foot  or  two  in 
length.  It  consists  of  three  layers — an  outermost  or  receiving  layer,  a 
middle  or  returning  layer,  and  an  innermost  or  entering  layer.  The 
intussuscepted  intestine  is  usually  red,  congested,  and  much  swollen,  and 
about  it  there  is  more  or  less  peritonitis.  The  compression  of  the  mesen- 
teric vessels,  especially  those  supplying  the  middle  and  the  innermost 
layers,  is  often  so  extreme  as  to  lead  to  rupture  and  hemorrhage  from 
the  mucous  lining  and  consequent  blood  in  the  stools — an  important 
diagnostic  feature.  Sloughing  of  the  invaginated  portion  of  intestine 
sometimes  results,  and  should  the  middle  and  the  outermost  layers 
have  become  adherent,  spontaneous  cure  may  ensue — of  which  some 
remarkable  instances,  with  the  discharge  by  the  rectum  of  large  portions 
of  the  bowel,  have  been  recorded. 

(b)  Volvulus  or  twist  is  a  fairly  common  cause  of  acute  intestinal 
obstruction  (about  15  per  cent,  of  the  cases).  It  occurs  twice  as  commonly 
in  males  as  in  females,  is  most  frequent  in  the  fourth  decade  of  life, 
involves  the  sigmoid  flexure  in  50  per  cent,  of  the  cases  (less  commonly 
the  cecum  and  the  small  intestine) ;  and  is  usually  axial  and  associated 
with  a  long,  non-fatty  mesentery.  The  twist  seems  sometimes  to  have 
been  provoked  by  a  trauma  or  severe  diarrhoea. 

(c)  Tumors  of  the  intestine  are  a  rather  common  cause  of  chronic 
obstruction.  Cylindrical  epithelioma  (carcinoma)  is  the  most  common. 
It  is  usually  annular  (rarely  circumscribed),  involves  most  commonly 
the  sigmoid  flexure  or  the  descending  colon,  and  gives  rise  to  a  gradual 
lessening  of  the  lumen  of  the  bowel,  until  in  some  cases  occlusion  is  almost 
if  not  quite  complete.  It  is  more  common  in  males  than  in  females,  and 
occurs  especially  beyond  the  middle  period  of  life  (except  carcinoma  of 
the  rectum,  which  is  remarkably  common  in  early  adult  life).  Sarcoma 
is  much  less  common  than  carcinoma.  Benign  growths,  such  as  polyps, 
adenomas,  and  fibromas,  have  been  reported. 

(d)  Cicatricial  strictures  sometimes  cause  chronic  obstruction.  The 
lesions  are  most  common  in  the  large  intestine,  and  follow  the  healing  of 
dysenteric  ulcers  (colon),  syphilitic  ulcers  (rectum),  follicular  ulcers, 
tuberculous  ulcers,  and  rarely  typhoid  ulcers.  Occasionally  the  stricture 
is  congenital. 

(e)  Peritonitis,  occasioning  paralytic  distention,  is  not  an  uncommon 
cause  of  acute  or  subacute  intestinal  obstruction. 


INTESTINAL  OBSTRUCTION  677 

3.  Abnormal  Intestinal  Contents:  (a)  Fecal  impaction  (coprostasis) 
is  a  rather  common  cause  of  chronic  intestinal  obstruction,  though  the 
symptoms  may  develop  acutely.  The  accumulation  usually  occurs  in  the 
cecum  or  the  sigmoid  flexure.  It  may  occur  at  any  age,  but  is  most 
common  in  children,  adult  women,  and  in  aged,  debilitated,  hysterical, 
hypochondriacal,  and  insane  subjects.  The  accumulation  is  sometimes 
enormous,  and  may  be  favored  by  congenital  dilatation  of  the  colon, 
though  habitual  inattention  to  the  bowels  also  may  result  in  atony, 
distention,  and  excessive  accumulation.  The  retained  fecal  masses 
become  very  hard,  but  often  permit  the  passage  by  them  of  fluid  feces 
(sometimes  interpreted  as  evidence  of  the  absence  of  accumulation). 
Occasionally  inflammation  and  ulceration  of  the  bowel  results,  (h) 
Gallstones  having  ulcerated  through  the  gall-bladder  into  the  small 
intestine  sometimes  cause  obstruction,  usually  at  the  ileocecal  region, 
but  sometimes  in  the  duodenum.  Obstruction  is  rare  if  they  ulcerate 
into  the  colon,  (c)  Enteroliths  formed  by  the  deposition  of  magnesium 
and  calcium  salts,  especially  phosphates,  about  divers  nuclei,  such  as 
hard  feces,  a  small  gallstone,  hair,  etc.,  may  cause  obstruction,  (d) 
Foreign  bodies,  such  as  fruit  seeds,  buttons,  coins,  etc.,  as  well  as  large 
collections  of  tangled  round  worms,  and  occasionally  large  amounts  of 
bismuth  or  magnesium  taken  medicinally,  have  been  known  to  cause 
obstruction. 

Pathology. — ^The  anatomical  results  of  acute  obstruction  consist  of 
dilatation  of  the  intestine  above  the  obstruction  together  with  the  accu- 
mulation of  feces  and  gas,  and  narrowing  of  the  lumen  or  collapse  of 
the  intestine  below  the  obstruction.  In  chronic  obstruction,  above  the 
obstruction  there  is  more  or  less  dilatation  of  the  intestine  and  h}'per- 
trophy  of  its  walls,  the  latter  developing  in  consequence  of  the  long- 
standing difficulty  to  the  onward  movement  of  the  feces.  The  intestinal 
wall,  especially  the  mucous  membrane,  is  often  inflamed  and  ulcerated, 
and  perforation  or  spontaneous  rupture  and  consequent  peritonitis  are  not 
unknown. 

Symptoms. — Clinically  intestinal  obstruction  may  be  acute  or  chronic. 
Acute  obstruction  results  from  strangulation,  intussusception,  volvulus, 
foreign  bodies,  and  peritonitis;  chronic  obstruction  results  from  tumors, 
cicatricial  strictures,  fecal  impaction,  and  sometimes  intussusception.  In 
many  cases,  however,  in  which  the  obstruction  is  chronic,  that  is,  in  which 
the  narrowing  of  the  lumen  develops  and  progresses  slowly,  symptoms 
may  for  a  long  time  be  absent,  and  ultimately  develop  suddenly,  that  is, 
clinically  the  obstruction  is  acute. 

Acute  intestinal  obstruction  is  characterized  by  abdominal  pain, 
tenderness,  nausea,  vomiting,  constipation,  tympanites,  and  occasionally 
a  palpable  abdominal  tumor.  Pain  is  usually  an  initial  symptom,  comes 
on  suddenly,  is  acute  and  colicky  in  nature,  though  after  the  obstruction 
is  complete  it  generally  becomes  continuous,  and  is  always  very  severe. 
In  the  early  hours  of  the  attack,  at  least,  it  is  commonly  associated  with 
active  (visible  and  audible)  peristalsis.     It  is  not  always  localized  to 


678  DISEASES  OF  THE  INTESTINE 

the  site  of  the  obstruction,  but  may  be  referred  or  diffuse;  and  it  is 
often  associated  with  abdominal  tenderness,  which  also  may  be  diffuse. 
Nausea  and  vomiting  follow  soon  upon  the  pain,  and  are  sometimes  the 
most  distressing  symptoms,  especially  when  associated  with  hiccough, 
which  is  not  uncommon.  The  vomit  consists  at  first  of  the  stomach 
contents  (usually  food),  then  (second  or  third  day)  of  greenish,  bile- 
stained  fluid,  and  ultimately  (third,  fourth,  or  fifth  day),  if  the  obstruction 
is  complete  and  the  patient  is  not  relieved,  of  brownish-black,  feculent 
or  stercoraceous  material — an  important  diagnostic  feature.  At  the 
onset  of  the  obstruction,  or  soon  thereafter,  the  bowels  may  be  opened — 
a  discharge  of  the  feces  below  the  obstruction;  but  otherwise,  in  a  great 
majority  of  cases,  constipation  is  absolute,  neither  feces  nor  gas  being 
discharged,  though  in  a  few  cases  the  incessant  tenesmus  may  result  in 
the  passage  of  a  little  mucus,  and  in  intussusception  there  may  be  both 
blood  and  mucus.  Tympanites  is  a  feature  of  almost  all  cases,  coming  on 
after  the  lapse  of  twenty-four  hours.  It  varies  much  in  degree  in  dif- 
ferent cases,  being  marked  in  obstruction  of  the  large  bowel,  but  often 
slight  if  the  small  bowel  high  up  is  involved.  Rarely  an  abdominal 
mass  may  be  palpable,  especially  in  intussusception  or  fecal  impaction, 
but  in  many  cases  the  exquisite  tenderness  and  pain  preclude  satisfactory 
examination.  The  examination,  however,  in  obscure  cases  may  be 
facilitated  by  anesthetization,  and  a  rectal  or  vaginal  exploration  may 
furnish  conclusive  evidence. 

The  constitutional  symptoms  are  always  severe.  The  expression  is 
anxious,  the  face  pallid  and  bathed  in  cold  sweat,  the  eyes  sunken,  the 
pulse  rapid  and  feeble,  and  soon  evidences  of  collapse  supervene.  The 
temperature  is  usually  subnormal,  unless  peritonitis  develops.  The  urine 
is  diminished,  sometimes  greatly  diminished,  and  may  contain  an  excess 
of  indican  (especially  in  obstruction  of  the  small  intestine),  and  later 
some  albumin.  Leukocytosis,  sometimes  of  high  degree,  is  usually 
present.  If  not  relieved,  the  patient  usually  dies,  soon  after  the  third 
day,  with  manifestations  of  peritonitis  and  auto-intoxication — delirium, 
coma,  muscular  twitchings,  fever,  etc. 

Chronic  intestinal  obstruction  varies  somewhat  symptomatically, 
depending  upon  the  cause  of  the  obstruction.  Cicatricial  or  cancerous 
obstruction  is  characterized  by  long-standing  and  increasing  constipation, 
alternating  sometimes  with  attacks  of  diarrhoea,  and  frequently  associated 
with  colicky  pains.  The  pains,  however,  often  occur  at  long  intei-vals  and 
are  usually  attributed  to  indigestion.  The  masses  of  formed  fecal  matter 
are  sometimes  observed  to  diminish  progressively  in  caliber,  but  one 
must  remember  that  fecal  masses  narrowed  by  passing  through  a  stric- 
ture may  acquire  ordinary  size  and  contour  in  the  rectum.  There  is  often 
a  sensation  of  fulness  in  the  abdomen,  tympanites  develops  and  is  not 
uncommonly  associated  with  active  peristalsis  (visible  and  audible), 
which  often  furnishes  remarkably  trustworthy  evidence  of  how  far  down 
the  bowel  is  patulous.  Vomiting  may  occur,  but  is  rather  unusual  and 
rarely  fecal  in  character.     Attacks  of  more  or  less  complete,  though 


INTESTINAL  OBSTRUCTION  679 

temporary,  obstruction,  due  to  accumulation  of  feces  above  the  con- 
striction, may  occur  from  time  to  time,  and  are  sometimes  attended  by 
fever,  due  doubtless  to  auto-intoxication.  Intestinal  hemorrhage  is 
occasionally  observed.  In  some  cases  a  more  or  less  definitely  de- 
limitable  mass  is  palpable — usually  in  the  region  of  the  cecum  or  the 
sigmoid,  but  sometimes  elsewhere.  The  patient,  as  a  rule,  fails  in 
general  health,  becomes  anemic  and  cachectic,  and  ultimately  dies  from 
asthenia  or,  not  infrequently,  from  the  consequences  of  acute  obstruction. 

In  obstruction  due  to  fecal  impaction  the  symptoms,  for  the  most 
part,  are  quite  similar  to  the  foregoing;  constipation  is  of  long  stand- 
ing, but  channelling  of  the  fecal  masses  may  permit  the  discharge  of 
mucus  or  watery  stools.  Subjective  symptoms  are  for  a  long  time,  in 
many  cases,  notoriously  slight,  despite  even  great  accumulation;  but  in 
some  cases,  abdominal  pain  and  distention  may  be  complained  of.  When 
the  obstruction  is  complete  the  pain  and  distention  are  more  marked,  and 
vomiting  may  supervene  and  even  become  feculent.  Rectal  examina- 
tion, as  well  as  examination  along  the  course  of  the  colon,  may  disclose 
scybalous  masses,  which  have  a  peculiar  putty-like  consistency  and 
may  be  somewhat  moved  about. 

Diagnosis. — ^The  diagnosis  is  concerned  with  (1)  the  seat  of  the 
obstruction,  (2)  the  nature  of  the  obstruction,  and  (3)  the  differentiation 
from  other  conditions  that  may  give  rise  to  similar  symptoms. 

The  seat  of  the  obstruction  is  sometimes  impossible  of  certain  deter- 
mination, but  it  may  be  surmised  by  attention  to  the  age  and  sex  of 
the  patient  (having  reference  to  what  has  already  been  said  in  this  con- 
nection), and  by  bearing  in  mind  the  slightly  less  frequency,  more  sudden 
onset,  more  acute  course,  more  severe  local  and  general  symptoms,  more 
common  feculent  and  protracted  vomiting,  more  likely  suppression  of 
urine,  excessive  indicanuria  (due  to  decomposition  of  the  intestinal  con- 
tents), and  the  early  development  of  peritonitis,  in  obstruction  of  the 
small  intestine.  Obstruction  of  the  small  intestine  is  also  suggested  by 
uniform  distention  of  the  central  portion  of  the  abdomen,  with  slight  or 
no  distention  of  the  lateral  portions  (situation  of  the  colon),  and  active, 
visible,  palpable,  and  audible  peristalsis  (transverse  or  oblique  ridges). 
In  obstruction  of  the  beginning  of  the  jejunum  the  distention  and  peri- 
stalsis may  be  slight  and  limited  to  the  upper  part  of  the  abdomen,  or 
may  be  altogether  absent;  but  vomiting,  gaseous  eructations,  and  hic- 
cough are  likely  to  be  marked,  and  collapse  comes  on  early.  In  obstruc- 
tion of  the  beginning  of  the  duodenum,  the  symptoms  are  sinailar  to 
those  of  stenosis  of  the  pylorus;  in  obstruction  of  the  duodenum  below 
the  diverticulum  of  Vater,  pancreatic  juice  may  be  present  in  the  vomit 
(but  it  may  be  absent  in  disease  of  the  pancreas,  such  as  carcinoma  of 
the  head,  which  itself  may  be  the  cause  of  the  obstruction).  Obstruction  of 
the  large  intestine,  if  due  to  strangulation,  may  quite  simulate  obstruc- 
tion of  the  small  intestine,  but  otherwise  it  is  suggested  by  slower  devel- 
opment of  the  symptoms  of  occlusion;  less  rapid  course;  later  develop- 
ment and  less  frequency  of  vomiting  which  is  less  likely  to  be  feculent; 


680  DISEASES  OF  THE  INTESTINE 

limitation  of  the  initial  distention  and  peristalsis  to  the  colon  (horse- 
shoe curve,  but  frequently  irregularly  developed);  palpable  tumor  or 
fecal  masses  along  the  course  of  the  colon;  more  tenesmus  with  discharge 
of  mucus  and  blood;  less  likelihood  of  anuria;  and  the  later  development 
of  peritonitis.  A  rectal  or  vaginal  examination  should  not  be  neglected. 
In  obstruction  of  the  small  intestine  high  up  empty  and  collapsed  intes- 
tines may  be  found  in  the  pelvis;  in  some  cases  of  volvulus  of  the  sigmoid 
the  rectum  may  be  distended  (paralytic  distention),  but  contain  no  feces; 
and  in  intussusception  the  descending  intestine  may  be  palpable  in  the  rec- 
tum. Some  observers  have  advocated  rectal  exploration  with  the  entire 
hand,  and  if  the  hand  be  lady-like  this  may  not  be  devoid  of  service. 
Indefinite  or  well-defined  masses  (tumors  or  fecal  masses)  may  be 
palpable  through  the  abdominal  wall  in  some  cases,  even  despite  con- 
siderable tympany,  but  is  much  facilitated  by  anesthetization.  Some- 
times assistance  is  obtained  by  inflating  the  rectum  and  the  colon  with 
air  or  distending  it  with  water,  the  point  where  the  inflation  ceases,  or 
the  amount  of  water  that  may  be  introduced,  suggesting  the  seat  of  the 
obstruction;  or  after  the  introduction  of  air  or  of  bismuth  paste  a  radio- 
graphic examination  may  disclose  the  seat  of  obstruction.  Sometimes, 
as  suggested  by  Treves,  auscultating  while  inflating  or  distending  the 
bowel  may  afford  evidence  of  the  seat  of  obstruction. 

The  nature  of  the  obstruction  sometimes  cannot  be  diagnosticated, 
but  help  may  be  obtained  by  attention  to  the  age  and  sex  of  the  patient, 
an  examination  of  the  palpable  openings  (for  hernia),  a  rectal  or  vaginal 
examination,  and  the  clinical  history  of  the  case — acute  or  sudden  onset; 
an  injury  to  the  abdominal  wall;  previous  peritonitis,  pelvic  or  otherwise, 
localized,  or  difl^use  (suggesting  bands  or  adhesions  causing  compression 
or  traction);  the  ingestion  of  a  foreign  body;  previous  gallstone  colic; 
chronic  constipation;  symptoms  of  stenosis  of  the  bowel;  general  failure 
of  health,  with  the  development  of  anemia,  emaciation,  and  cachexia 
(suggesting  carcinoma),  etc.  Intussusception  is  more  readily  recognized 
than  other  conditions :  it  occurs  especially  in  children,  is  of  sudden  onset 
(sometimes  following  diarrhoea),  is  attended  by  tenesmus  and  bloody  and 
mucous  discharges,  and  occasionally  through  the  abdominal  wall,  in  the 
course  of  the  colon  (especially  the  transverse),  a  peculiar,  usually  sausage- 
shaped  mass,  may  be  palpable,  and  may  even  become  hard  and  firm 
(contracted)  under  the  hand;  in  other  cases  it  may  be  felt  through  the 
rectum.  Volvulus  and  strangulation,  except  in  so  far  as  they  are  suggested 
by  adult  life,  can  rarely  be  recognized  with  certainty  before  operation. 
Fecal  impaction,  and  in  many  cases  malignant  stenosis,  should  readily 
be  distinguished. 

Conditions  resembling  symptomatically  intestinal  obstruction  are 
often  difficult  of  differentiation.  Internal  hernias  (obturator,  diaphrag- 
matic, internal  inguinal  ring,  etc.)  can  rarely  be  distinguished.  Other 
conditions  which  may  occasion  confusion  are  acute  appendicitis,  acute 
pancreatitis,  acute  peritonitis,  acute  enteritis  (especially  in  children), 
intestinal  colic,  gallstone  colic,  nephritic  colic,  torsion   of  the  pedicle 


INTESTINAL  OBSTRUCTION  681 

of  an  ovarian  or  uterine  tumor  or  of  a  floating  kidney,  a  phantom  tumor, 
etc.  In  many  cases  of  acute  obstruction  peritonitis  develops  so  promptly 
as  to  be  really  part  and  parcel  of  the  disease.  In  these,  as  well  as  in 
other  cases,  the  diagnosis  cannot  go  beyond  acute  obstruction. 

Prognosis. — ^The  prognosis  varies,  depending  upon  the  nature  of  the 
obstruction,  and  in  many  cases  upon  the  promptness  ol  appropriate 
treatment.  In  acute  obstruction  the  prognosis  is  always  grave,  a  fatal 
termination  occurring  usually  in  from  three  to  seven  days  unless  the  con- 
dition is  relieved.  In  chronic  obstruction  symptoms  are  often  present  for 
months,  until,  as  in  carcinoma,  the  patient  eventually  dies  of  asthenia,  or 
rather  suddenly  from  acute  obstruction.  When  due  to  fecal  impaction 
recovery  usually  follows  clearing  of  the  bowel.  In  the  event  of  certain 
complications,  such  as  gangrene,  perforation,  peritonitis,  etc.,  the  outlook 
is  practically  hopeless. 

Treatment. — A  knowledge  of  the  pathological  conditions  present  in 
intestinal  obstruction  suggests  the  futility  of  medicinal  treatment  in 
all  but  the  exceptional  case,  and  in  this  the  fortunate  outcome  is  often 
the  result  rather  of  good  luck  than  of  good  management.  Excepting  only 
fecal  impaction,  intestinal  obstruction  is  essentially  a  surgical  disease 
and  should  be  treated  on  surgical  principles.  Since  in  many  cases  it  is 
impossible  to  differentiate  between  the  different  forms  of  intestinal  ob- 
struction, and  since  delay  only  adds  to  the  danger,  operation  should  be 
undertaken  with  the  least  possible  delay. 

Pending  the  advent  of  the  surgeon,  the  stomach  should  be  washed  out 
repeatedly  with  warm  saline  solution — a  mode  of  treatment  warmly 
advocated  by  Kussmaul  and  others,  and  tending  to  relieve  not  only  the 
persistent  vomiting,  but  also  the  intestinal  distention  and  pressure  above 
the  obstruction,  and  thus  mitigate  the  violent  peristalsis  and  the  pain. 
Irrigation  of  the  rectum  and  colon  is  also  of  much  service  in  some  cases 
and  may  occasionally,  especially  in  intussusception  in  children,  result 
in  the  reduction  of  the  intussusception — though  it  is  not  wise  to  expect 
this  as  a  necessary  result  of  the  treatment.  The  amount  of  fluid  injected 
should  be  measured  with  a  view  to  determine  the  distance  of  the  obstruc- 
tion from  the  anus.  Under  no  circumstances  whatever  should  purgatives 
be  administered;  even  in  fecal  impaction  they  should  not  be  given  until, 
after  repeated  and  copious  oil  or  watery  enemas,  the  major  portion  of  the 
impacted  feces  has  been  discharged. 

The  question  of  the  use  of  opium  before  operation  has  been  much 
debated.  Personally,  I  prefer  not  to  use  it,  if  it  can  be  avoided.  In  some 
cases,  however,  the  pain  is  really  intolerable,  and  if  it  cannot  be  relieved 
by  hot  or  cold  applications  externally  and  atropine  internally,  morphine 
may  be  given  in  small  dose — the  smaller  the  better,  since  in  the  event  of 
operation  its  deleterious  effects  may  become  only  too  apparent.  Recently 
a  number  of  good  results  have  been  reported  from  the  use  of  atropine  in 
very  large  doses,  -ryj  to  yV  grain  (0.002  to  0.005  gram)  twice  or  thrice 
in  the  first  twenty-four  hours;  the  pain  has  been  relieved  and  spontaneous 
recovery  has  resulted.    The  treatment  merits  further  trial. 


682  DISEASES  OF  THE  INTESTINE 

That  some  patients  have  withstood  repeated  and  even  forcible  dis- 
tention of  the  rectum  and  colon,  drastic  cathartics,  violent  shakings, 
strenuous  kneading  of  the  abdomen,  etc.,  merely  illustrates  the  wonder- 
ful resources  of  the  human  economy;  and  that  some  patients  have  suc- 
cumbed to  this  treatment  (production  of  perforation,  etc.)  rather  than  to 
the  disease,  as  such,  cannot  well  be  doubted.  Personally,  I  should  prefer 
the  chances  of  operation,  in  what  is  admittedly  a  very  serious  disease, 
to  the  hazard  and  hope  of  medicinal  treatment. 


DILATATION  OF  THE  COLON. 

Dilatation  of  the  colon  may  be  due:  (1)  Gaseous  accumulation, 
which,  though  usually  transitory,  is  of  significance  from  the  fact  that  from 
pressure  upward  it  may  seriously  embarass  the  action  of  the  heart  and 
lungs,  particularly  if  these  organs  are  diseased.  (2)  Fecal  accumulations, 
with  which  gallstones,  enteroliths,  and  foreign  bodies  may  be  associated. 
(3)  Obstruction  of  the  colon,  usually  carcinomatous  or  a  volvulus; 
less  commonly  cicatricial  stricture,  sigmoid  diverticulitis,  etc.  (4) 
Idiopathic  dilatation  of  the  colon  (Hirschsprung's  disease;  Virchow's 
giant  growth  of  the  colon).  This  is  usually  congenital  and  is  seen  in 
children  in  more  than  three-fourths  of  the  cases.  There  may  be  stricture 
of  the  sigmoid,  but  usually  there  is  no  apparent  obstruction.  The 
colon  may  attain  really  a  giant  growth,  as  in  Formad's  case,  in  which 
it  measured  15  to  30  inches  in  circumference,  and  with  the  contained 
feces  weighed  47  pounds.  The  chief  symptoms  are  obstinate  and  pro- 
longed constipation,  alternating,  perhaps,  with  periods  of  diarrhea, 
markedly  protuberant  abdomen,  especially  in  the  course  of  the  colon, 
and  in  some  cases  visible  colonic  peristalsis.  The  disorder  is  intract- 
able, auto-intoxication,  emaciation,  in  some  cases  complete  intestinal 
obstruction,  peritonitis,  etc.,  eventually  ensuing.  Treatment  is  unsatis- 
factory.    Treves  has  successfully  removed  the  greater  part  of  the  colon. 


INFARCTION  OF  THE  MESENTERIC  VESSELS. 

Embolism  of  the  mesenteric  arteries  (most  commonly  the  superior 
mesenteric  artery)  may  occur  in  arteriosclerosis,  vegetative  endocarditis, 
aneurysm,  etc.  Thrombosis  of  the  mesenteric  veins  may  follow  directly 
on  infections,  especially  ulcerative  process  in  the  intestine  (appendicitis, 
intestinal  ulceration),  or  it  may  develop  secondarily  in  cirrhosis  of  the  liver, 
pylephlebitis,  and  anemic  and  cachectic  states;  and  it  usually  follows 
arterial  embolism.  Gangrene  of  the  supplied  part  of  the  intestine  follows; 
if  the  area  blocked  is  small,  an  efficient  collateral  circulation  may  be 
established,  but  if  the  superior  mesenteric  artery  (virtually  an  end-artery) 
is  involved,  death  is  inevitable.  The  symptoms  are  usually  abrupt  in 
onset,  and  consist  of  sudden  abdominal  pain,  nausea,  vomiting,  and 
bloody  diarrhoea.     Soon  peritonitis  sets   in,   and   the  patient  usually 


HEMORRHOIDS  683 

succumbs  within  two  or  three  days.  In  a  few  cases  the  onset  is  more 
insidious  and  the  symptoms  not  necessarily  obtrusively  intestinal.  The 
diagnosis  is  rarely  made  with  certainty.  It  may  be  suspected  in  the 
event  of  endocarditis  or  aneurysm,  which  may  furnish  the  obstructing 
embolus.  Usually  the  diagnosis  is  intestinal  obstruction.  Operation 
and  resection  of  the  gangrenous  bowel  is  occasionally  successful;  other- 
wise treatment  is  unavailing. 

INTESTINAL   SAND. 

Of  conditions  described  as  intestinal  sand  there  are  two — the  true  and 
the  false.  True  intestinal  sand  (intestinal  lithiasis)  consists  of  small, 
usually  dark-colored,  gritty  particles  formed  of  an  organic  base,  but 
made  up  largely  of  inorganic  salts  (often  75  per  cent,  or  more),  especially 
calcium  phosphate  and  carbonate.  It  is  more  frequent  in  women  (two- 
thirds  of  the  cases)  than  in  men,  especially  in  nervous  and  hypochondriacal 
subjects,  between  the  thirtieth  and  the  fortieth  year. 

Etiology. — ^The  process  of  the  formation  of  true  intestinal  sand  has  been 
likened  to  that  of  appendicular  calculi  and  gallstones.  Duckworth  and 
Garrod  believe  that  since  the  sand  contains  only  traces  of  unaltered  bile 
pigment  and  no  cholesterin  (distinction  from  gallstones)  and  is  rich  in 
urobilin,  it  must  be  formed  in  the  upper  part  of  the  colon,  where  the 
conversion  of  bile  pigment  into  urobilin  is  well  advanced,  and  which  is 
structurally  better  adapted  than  the  small  intestine  for  the  lengthy  sojourn 
necessary  for  the  deposition  of  earthy  salts.  False  intestinal  sand  is 
made  up  of  the  residue  of  certain  articles  of  food  and  occasionally  of 
medicines.  The  sclerenchymatous  particles  of  pears  (pear  sand),  par- 
ticles of  bananas,  seeds  of  fruits  (figs  and  different  berries),  fish  bones, 
grain  residues,  etc.,  have  been  observed  as  forming  so-called  intestinal 
sand.  Olive  oil,  in  consequence  of  partial  digestion,  has  been  known 
to  form  masses  resembling  gallstones  (whence  the  erroneous  opinion 
as  to  the  efficacy  of  the  olive  oil  treatment),  and  substances  like  salol 
may  also  give  rise  to  so-called  (false)  intestinal  sand. 

Symptoms. — Clinically  the  discharge  of  the  sand  is  usually  attended  by 
more  or  less,  sometimes  very  severe,  colicky  pain,  due  to  constipation  or 
to  mucous  colic  (with  which  it  is  often  associated).  Clinically,  as  a  rule,  no 
pain  attends  the  discharge  of  false  intestinal  sand,  any  pain  complained 
of  being  likely  due  to  constipation,  for  the  relief  of  which,  figs,  etc.,  may 
have  been  taken. 

Treatment. — ^The  treatment  is  that  of  the  associated  conditions,  such 
as  intestinal  colic,  constipation,  and  mucous  colic. 

HEMORRHOIDS. 

{Piles;  Hemorrlioidal  Phkbeciasis.) 

Etiology. — Hemorrhoids,  or  varicose  dilatations  of  the  inferior  hemor- 
rhoidal veins,  is  a  purely  local  disease,  due  to  mechanical  obstruction  of  the 


684  DISEASES  OF  THE  INTESTINE 

circulation,  and  is  caused  by:  (1)  Local  disease  of  or  about  the  rectum, 
such  as  fecal  accumulation,  rectal  inflammations,  strictures  and  tumors 
of  the  rectum  or  adjacent  structures  (uterus,  ovary,  bladder,  prostate,  etc.) ; 
(2)  obstruction  to  the  portal  circulation  due  to  cirrhosis  and  other  dis- 
orders of  the  liver  and  portal  system;  and  (3)  chronic  passive  congestion 
due  to  heart  disease.  Sedentary  occupations,  repeated  pregnancies, 
straining  at  stool,  etc.,  are  believed  to  act  as  contributing  factors. 

Pathology. — Hemorrhoids  may  be  external  or  internal,  or  both.  In- 
ternal hemorrhoids  are  in  close  relation  with  the  sphincter,  but  some- 
times they  extend  high  up  in  the  rectum,  and  even  into  the  sigmoid. 
External  hemorrhoids  may  consist  of  (a)  a  small  venous  tumor,  that 
develops  suddenly  (in  consequence  of  rupture  of  one  of  the  external 
hemorrhoidal  veins),  is  dark  purplish  in  color,  and  very  tender;  (b) 
small  tabs  of  skin  and  connective  tissue,  which  originally  contained  some 
more  or  less  dilated  and  tortuous  veins.  They  may  be  single  or  multiple, 
pedunculated  or  sessile,  and  not  infrequently  surround  the  anus.  They 
rarely  occasion  symptoms.  Internal  hemorrhoids  may  be  (a)  diffuse, 
that  is,  thickened,  dilated,  tortuous,  and  closely  aggregated  venous  cords 
and  capillaries  (sometimes  also  arterioles) ;  usually  granular  on  inspection, 
and  covered  with  a  very  thin  and  readily  torn  mucous  covering — ^whence 
the  frequent  bleeding  (bleeding  piles);  (b)  circumscribed  tumor  masses, 
single  or  multiple,  roundish  or  irregular  in  outline,  and  more  or  less 
encircling  the  bowel.  They  may  be  pedunculated  or  have  a  broad  base 
of  attachment;  they  are  bright  red  when  inflamed,  and  dark  reddish  or 
purplish  when  much  congested  or  filled  with  clot  (due  to  rupture  of  a 
vessel).  They  may  become  extruded,  and  in  consequence  partially  or  com- 
pletely strangulated  by  the  sphincter,  or  ulcerated,  and  give  rise  to  more 
or  less  hemorrhage. 

Symptoms. — Small  and  even  moderately  large  hemorrhoids  often  exist 
without  occasioning  any  symptoms,  though  examination  may  reveal  their 
presence.  Symptoms,  when  present,  vary  with  the  number,  size,  and 
condition  of  the  hemorrhoids.  Probably  the  commonest  complaints  are 
sensations  of  discomfort,  sometimes  a  more  or  less  constant  desire  to 
evacuate  the  bowel,  a  temporary  dissatisfied  sensation  following  defe- 
cation, and  anal  itching  and  burning.  Defecation  is  often  painful,  some- 
times so  painful  as  of  itself  to  engender  voluntary  constipation.  The 
final  evacuation  of  the  hardened  feces  only  induces  more  severe  pain,  and 
eroding  the  piles  provokes  more  or  less  abundant  hemorrhage.  AVlien 
the  piles  are  inflamed,  ulcerated,  or  strangulated,  blood  and  mucus  may 
pass  from  the  bowel  altogether  independently  of  the  stools.  Sometimes 
a  high  grade  of  secondary  anemia  is  induced;  hypochondriasis  and 
melancholia  are  by  no  means  uncommon. 

Diagnosis. — External  piles  are  readily  recognized  by  inspection ;  internal 
piles  necessitate  digital  exploration  or  protoscopic  examination  for  their 
recognition. 

Prognosis. — Since  the  causes  of  hemorrhoids  are  so  largely  chronic, 
their  course  is  usually  progressive.     In  themselves  they  are  not  fatal, 


VISCEROPTOSIS  685 

except  in  so  far  as  neglect  may  lead  to  serious  and  even  fatal  complica- 
tions, such  as  strangulation  and  gangrene. 

Treatment. — ^The  treatment  is  either  palliative  or  cm-ative.  The  curative 
treatment  is  surgical — ligation  or  excision — and  may  be  resorted  to  in  the 
great  majority  of  cases.  Many  patients,  however,  will  not  submit  to 
operation,  and  an  operation  may  be  ill  advised  in  subjects  with  advanced 
heart  or  liver  disease.  Marked  benefit  may  usually  be  secured  in  many 
cases  by  securing  a  daily  evacuation  of  the  bowels,  by  habits  of  regularity, 
attention  to  the  diet,  and  saline  aperients  if  necessary.  Local  cleansing 
is  of  the  utmost  importance.  Applications  of  ice  water  or  of  an  ice 
bag,  or  even  a  cold  sitz  bath  after  the  daily  evacuation,  is  of  benefit. 
Local  pain  and  itching  may  be  relieved  by  belladonna,  ichthyol,  or 
iodoform  (by  suppository),  by  the  fluid  extract  of  hamamelis,  or  by 
equal  parts  of  gall  and  belladonna  ointment.  Li  other  cases  excellent 
results  follow  the  use  of  iron  subsulphate,  2  to  3  grains  (0.13  to  0.20 
gram)  by  suppository,  or  a  10  to  15  per  cent,  ointment.  Intractable 
hemorrhage,  ulceration,  strangulation,  etc.,  call  for  surgical  intervention. 


VISCEROPTOSIS. 

{Splanchnoptosis;  Enteroptosis;  Gastroptosis ;  Coloptosis;  Hepatoptosis;  Nephroptosis; 
Splenoptosis;  Glenard's  Disease). 

Visceroptosis  is  an  inclusive  term  used  to  describe  the  condition  in 
which  the  abdominal  viscera  fall  from  their  normal  to  a  lower  position 
in  the  abdomen.  The  stomach,  intestine,  transverse  colon,  and  the 
kidneys  are  most  commonly  involved,  but  any  or  all  of  the  abdominal 
viscera  may  "drop"  in  the  individual  case. 

Etiology. — Two  causative  factors  are  operative — a  congenital  weak- 
ness or  laxity  of  the  mesentery  and  ligament  supporting  the  abdominal 
organs,  and  lack  of  the  normal  support  afi^orded  by  the  abdominal  wall. 
The  majority  of  cases  occur  in  women,  in  whom,  in  consequence  of 
repeated  pregnancies,  ill-fitting  and  tightly  laced  corsets,  etc.,  the  ab- 
dominal wall  becomes  lax  and  flaccid.  In  both  sexes  factors  like  trau- 
matism, excessive  muscular  strain,  such  as  may  be  associated  with 
chronic  constipation  and  severe  coughing,  emaciation,  recurring  ascites, 
etc.,  may  lead  to  the  disorder.  In  some^  especially  young  subjects,  there 
seems  to  be  undoubtedly  a  congenital  weakness  of  the  supporting  liga- 
ment and  mesentery,  since  there  is  often  no  undue  laxness  of  the  abdom- 
inal wall. 

Pathology. — ^Visceroptosis  in  itself  is,  perhaps,  not  to  be  looked  upon 
as  a  disease  sui  cjeneris;  aside  from  their  abnormal  position,  the  organs 
may  be  quite  normal. 

Symptoms. — Several  classes  of  cases  may  be  encountered.  In  the  one, 
even  considerable  grades  of  ptoses  may  exist  without  notable  syin})tonis. 
In  a  second  series  of  cases,  obviously  due  to  a  markedly  relaxed  abdomen 
(repeated  pregnancies),  there  may  be  more  or  less  marked  symptoms. 


686  DISEASES  OF  THE  INTESTINE 

In  a  third  series,  the  conspicuous  symptoms  are  neurasthenic  (nervous- 
ness, headache,  backache,  asthenia,  anemia,  emaciation,  etc.),  with  spe- 
cial complaints  directed  to  the  gastro-intestinal  tract.  These  comprise, 
as  a  rule,  the  more  common  manifestations  of  indigestion,  such  as  poor 
or  capricious  appetite,  epigastric  pain  and  distress,  gaseous  and  acid 
eructations,  flatulence,  nausea,  and  constipation;  in  some  cases  there 
is  hyperacidity,  in  others  motor  insufficiency.  Examination  reveals  the 
stomach  dropped,  in  toto,  the  lower  border  two  or  three  inches  or  more 
below  the  umbilicus,  and  the  uppet  border  correspondingly  ptosed:  a 
depression  in  the  epigastrium  and  a  fulness  about  the  umbilicus.  The 
stomach  is  usually  more  vertical  than  normally,  especially  in  women 
who  have  laced  tightly;  and  it  may  also  be  dilated.  Waves  of  peristalsis 
may  be  visible,  but  they  are  much  weaker  than  those  due  to  organic 
obstruction;  occasionally,  however,  considerable  pyloric  obstruction 
may  be  caused  by  malposition  of  the  pylorus,  perigastric  adhesions,  a 
displaced  right  kidney,  etc.  The  intestines,  also,  especially  the  colon, 
may  be  much  displaced.  The  transverse  colon  may  fall  as  low  as  the 
brim  of  the  pelvis,  occasioning  a  so-called  V-  or  M-shaped  colon;  and 
the  sigmoid  may  be  markedly  redundant:  in  both  cases  constipation  is 
usually  a  marked  symptom. 

Ptosis  of  one  or  both  kidneys,  usually  the  right,  is  often  associated  with 
gastro-enteroptosis,  but  it  may  occur  independently  thereof.  There  is 
usually  more  or  less  pain  in  the  lumbar  region,  or  a  sense  of  weight  and 
dragging;  it  may  be  so  severe  as  to  simulate  and  be  indistinguishable 
from  renal  colic;  or  it  may  be  a  part  of  Dietl's  crises:  severe  pain,  chills, 
fever,  nausea,  vomiting,  and  collapse;  the  urine  is  usually  lessened  in 
amount  and  may  contain  blood  and  pus,  and  the  kidney  may  be  en- 
larged and  tender.  The  cause  of  these  crises  is  not  well  understood; 
they  have  been  attributed  to  twists  or  kinks  of  the  renal  vessels  or  ureters, 
obstruction  of  the  bowels,  etc.  On  examination,  the  kidney,  when 
ptosed,  may  be  just  palpable  on  deep  inspiration,  which  is  quite  common, 
especially  in  women  and  on  the  right  side,  and  is  not  of  much  conse- 
quence; it  may  be  so  movable  that  on  deep  inspiration  it  descends  to 
about  the  level  of  the  umbilicus,  and  may  be  retained  there  by  the  pal- 
pating hand  during  expiration;  or  it  may  be  floating,  quite  low,  and 
readily  pushed  about  to  or  beyond  the  median  line,  in  the  iliac  fossa,  etc. 

Ptosis  of  the  liver  and  spleen  is  much  less  common,  and  may  be  readily 
recognized  by  physical  exploration. 

Diagnosis, — The  diagnosis  is  readily  made  upon  physical  examination. 
The  most  trustworthy  results  follow  radiographic  examination,  in  the 
case  of  the  stomach  and  intestine,  after  inflation  with  air  or  bismuth 
paste.  Some  diagnostic  importance  has  been  ascribed  by  Stiller  to  a 
floating  tenth  rib,  which  he  believes  the  most  common  stigma  of  the  basic 
congenital  asthenic  condition;  but  a  floating  tenth  rib  occurs  under  other 
circumstances. 

Prognosis. — The  outlook  as  regards  relief  of  symptoms  and  improve- 
ment in  the  general  health  is  good.     One  must  remember  that  even  con- 


DISEASES  OF  THE  LIVER  687 

siderable  degrees  of  ptosis  may  be  present  without  notable  symptoms. 
So  long  as  the  motor  power  of  the  stomach,  for  instance,  is  efficient, 
symptoms  may  be  entirely  in  abeyance. 

Treatment. — ^The  underlying  neurasthenic  condition  demands  the 
most  careful  attention — ^hydrotherapy,  regulated  feeding,  general  tonics 
(especially  nux  vomica),  change  of  scene  and  air,  etc.  Gastric  hyper- 
acidity or  subacidity,  flatulence,  and  constipation  must  be  treated,  as 
mentioned  under  these  headings.  Much  relief  may  be  afforded  by  a 
properly  made,  fitted,  and  applied  bandage  or  abdominal  supporter;  in 
fact,  the  bandage  in  itself  may  lead  to  symptomatic  cure.  Occasionally 
resort  may  be  had  to  operative  measures — to  elevate  a  markedly  dis- 
placed stomach  or  colon,  to  resect  a  redundant  sigmoid,  etc. 


DISEASES  OF  THE  LIVER. 

Pathological  Physiology. — The  functions  of  the  liver  are:  To  detoxify 
poisons  that  enter  the  body  by  way  of,  or  are  elaborated  within,  the 
gastro-intestinal  tract,  or  are  perhaps  produced  elsewhere;  to  secrete  bile; 
to  warehouse  some  of  the  excess  of  fat  taken  as  food  and  to  release  it 
when  the  supply  from  without  becomes  deficient;  to  warehouse  gly- 
cogen derived  from  the  carbohydrates  taken  as  food,  or  from  the  non- 
nitrogenous  part  of  the  proteins  when  the  supply  of  carbohydrates  is 
deficient,  and  to  convert  the  glycogen  into  glucose  and  liberate  it  as  it 
is  required  by  the  system;  and  to  assist  in  the  metabolism  of  the  pro- 
teins, to  the  extent,  at  least,  of  forming  urea  from  ammonia  compounds. 
There  are  other  functions,  such  as  erythrocytolysis,  etc.,  that  are  of 
minor  interest  in  the  present  connection. 

Disorder  of  the  functions  of  the  liver  may  be  primary  or  secondary; 
and  it  may  be  partial,  involving  perhaps  only  one  function,  or  it  may  be 
total,  involving  presumably  all  the  functions.  The  belief  in  a  primary 
general  disorder  of  function  is  well  exemplified  in  the  terms  torpid  liver, 
biliousness,  bilious  headache,  litheemia,  etc.  Present-day  opinions  tend, 
perhaps  unwisely,  to  minimize  the  influence  of  the  liver  in  these  disorders; 
but  this  seems  an  almost  inevitable  result  of  the  knowledge  that  phe- 
nomena commonly  attributed  to  a  supposed  torpid  liver  and  the  other 
affections  mentioned  may  result  from  factors  that  do  not  involve  the 
liver  primarily,  if  at  all,  and  that  uric  acid  (lithemia),  by  no  means  the 
important  factor  in  disease  it  was  once  thought,  is  not  formed  exclusively 
in  the  liver.  The  dyspeptic  symptoms  of  a  supposed  torpid  liver  are 
usually  due  to  a  gastro-intestinal  catarrh  set  up  by  dietetic  indiscretions, 
excessive  eating  (especially  of  proteins  and  carbohydrates),  the  con- 
sumption of  too  much  alcohol,  etc.;  the  spread  of  this  catarrh  to  the 
diverticulum  of  Vater  and  the  common  bile  duct,  or  perhaps  rarely  a 
toxic  descending  radicular  cholangitis,  is  answerable  for  the  subicteric 
tint  of  the  conjunctiva  and  skin  common  in  these  subjects;  and  the  head- 
ache and  other  nervous  symptoms  result  from  the  absorption  and  circu- 


688  DISEASES  OF  THE  LIVER 

lation  in  the  blood  stream  of  enterogenic  toxins.  The  liver  usually 
participates  in  the  process  onlj  secondarily;  perhaps  the  enterogenic 
toxins  are  produced  in  such  amounts  that  the  liver  is  incapable  of  neu- 
tralizing them  and  they  pass  over  into  the  circulation,  or  they  are  so 
virulent  that  they  impair  the  functional  activity  of  or  set  up  congestive 
and  other  alterations  in  the  liver.  In  either  event  the  symptoms  are 
gastro-intestinal  rather  than  hepatic  in  origin,  and  the  liver,  responding 
to  excessive  demands  and  being  in  consecjuence  actively  congested,  is 
often,  for  a  time  at  least,  of  increased  rather  than  of  decreased  func- 
tional activity.  The  bearing  of  these  facts  on  treatment  is  obvious  and 
material. 

There  is,  however,  another  series  of  cases,  such  as  the  passive  con- 
gestion of  chronic  cardiac  and  pulmonary  disease,  in  which  there  is  reason 
to  believe  that  the  functional  activity  of  the  liver  is  reduced.  It  is  not 
unlikely  that  the  headache  and  other  nervous  svmptoms,  digestive  dis- 
turbances, and  loss  of  flesh  and  strength  that  occur  in  these  cases  are 
due,  in  part  at  least,  to  the  disordered  functions  of  the  liver.  This  is 
perhaps  due  directly  to  the  influence  of  enterogenic  poisons  which,  being 
carried  to  the  liver  by  the  portal  circulation,  encounter  an  organ  reduced 
in  vitality  by  the  long-continued  passive  congestion,  and  incapable  of 
exerting  as  it  should  its  detoxifying  function;  the  toxins,  in  consequence, 
pass  over  into  the  general  circulation  and  cause  at  least  some  of  the 
symptoms. 

In  another  series  of  cases,  moi'e  or  less  complete  functional  failure  of 
the  liver  ensues.  These  are  cases  of  severe  intoxication  or  infection,  in 
which  widespread  destruction  or  disorganization  of  the  hepatic  paren- 
chyma occurs.  The  striking  clinical  phenomena,  which  may  develop 
suddenly,  although  they  are  sometimes  preceded  by  minor  sjmiptoms, 
are  for  the  most  part  nervous;  they  are  variously  designated  hepatarffia, 
acholia,  cholemia,  hepatic  auto-intoxication,  etc.  Headache  is  a  con- 
spicuous symptom,  and  is  soon  followed  by  mental  excitement,  delirium 
(which  may  be  very  active  or  maniacal),  muscular  twitchings,  and  con- 
vulsions; or  mental  hebetude  progressing  to  deep  coma  may  ensue. 
]\Iost  of  these  cases  are  associated  with  varying  grades  of  jaundice  and 
other  phenomena  that  will  be  more  fully  discussed  under  jaundice  and 
acute  yellow  atrophy  of  the  liver. 

Disturbances  in  the  detoxifying  function  of  the  liver  is  believed  by 
some  observers  to  be  the  basis  of  the  eclamptic  manifestations  of  uremia, 
pregnancy,  etc.  Disorder  of  the  fat  metabolism  often  leads  to  acidosis 
and  acid  intoxication,  due  to  the  presence  of  acetone,  diacetic  acid,  and 
/?-oxybutyric  acid  in  the  blood.  These  substances  are  formed  princi- 
pally in  the  liver  and  the  muscles,  but  probably  also  in  other  tissues. 
They  result  from  imperfect  oxidation  and  are  directly  related  to  deficient 
glycogen  in  the  liver  and  muscles — which  may  be  the  consequence 
of  insufficient  intake  (as  in  starvation),  or  of  excessive  output  (as  in 
diabetes). 

Aliimentary  levulosuria  has  been  suggested  as  a  test  of  the  functional 


J  A  UN  DICE  689 

capacity  of  the  liver,  and  is  perhaps  of  some  diagnostic  significance  in 
cirrhosis.  The  test  should  be  performed  as  follows:  Food  should  be 
withheld  after  the  evening  meal  until  the  test  has  been  completed.  In 
the  morning  the  patient  should  void  his  urine,  and  then  (upon  an  empty 
stomach)  he  should  take  100  grams  of  levulose  dissolved  in  500  c.c.  of 
water.  Weak  tea  without  cream  may  be  substituted  for  the  water  if  pre- 
ferred by  the  patient.  At  the  end  of  an  hour,  and  hourly  thereafter  for 
four  hours,  the  patient  should  void  his  urine.  The  specimens  should  be 
examined  separately  for  levulose,  preferably  by  the  polariscope,  or  by  the 
Seliwanoff  method,  which  is  as  follows:  Equal  parts  of  the  urine  and 
of  a  half-and-half  solution  of  concentrated  hydrochloric  acid  and  water 
should  be  mixed  in  a  test-tube,  and  a  few  grains  of  resorcin  added.  The 
mixture  should  then  be  boiled,  whereupon,  if  levulose  is  present,  a  beau- 
tiful red  color  appears ;  this  deepens  on  standing  and  a  dark-red  deposit 
settles  in  the  test-tube.  If  the  disorder  of  the  liver  be  of  moderate 
severity,  the  levulose  will  be  found  in  the  third  or  fourth  specimen  of 
urine,  perhaps  in  the  fourth  only;  if  there  be  profound  alteration  of  the 
hepatic  structure,  the  levulose  may  be  found  in  the  first  specimen  of 
urine,  as  well  as  in  the  subsequent  specimens,  and  it  may  persist  for 
several  additional  hours. 

JAUNDICE. 

Jaundice  is  a  term  applied  to  staining  of  the  tissues  with  bile  pigments 
— bilirubin  and  biliverdin.  It  is  merely  a  symptom,  and  is  recognized 
clinically  by  a  yellowish  or  yellowish-green  discoloration  of  the  skin  and 
visible  mucous  membranes  and  by  the  presence  of  bile  pigment  in  the 
urine. 

Types  of  Jaundice. — Jaundice  can  result  only  from :  (1)  An  obstruction 
somewhere  in  the  course  of  the  biliary  tract,  in  consequence  of  which  the 
free  flow  of  the  bile  being  impeded,  it  becomes  absorbed  by  the  lymphatics 
or  bloodvessels — jaundice  from  stasis  of  bile;  or  (2)  disturbances  in  the 
functions  of  the  liver  cells,  whereby  the  bile  is  diverted  from  the  biliary 
capillaries  to  the  lymphatics  or  the  blood  channels — ^jaundice  from  para- 
pedesis  of  bile.  In  the  one  case  the  disorder  involves  the  bile  after  it 
has  been  formed  and  entered  the  biliary  channels;  in  the  other  it  involves 
the  bile  pigments  while  they  are  still  within  the  hepatic  cells. 

Obstructive  or  Mechanical  Jaundice. — ^In  the  event  of  obstruc- 
tion to  the  extrahepatic  or  intrahepatic  biliary  ducts  the  outflow  of  bile  is 
hindered,  while  the  hepatic  cells  still  continue  to  secrete  bile,  so  that  the 
biliary  ducts,  even  to  the  finest  biliary  radicles  (capillaries),  become 
often  enormously  dilated.  Finally,  the  biliary  capillaries  rupture  into  the 
lymph  spaces  between  the  hepatic  cells  and  the  bloodvessels;  thence  by 
way  of  the  lymphatic  vessels  and  the  thoracic  duct  the  biliary  constituents 
reach  the  blood  stream  and  the  tissues  of  the  body.  This  type  of  jaun- 
dice may  be  found  in  cases  of:  (1)  Obstruction  within  the  common  bile 
duct  or  the  hepatic  duct;  such  as  gallstones,  parasites,  foreign  bodies, 
44 


690  DISEASES  OF  THE  LIVER 

etc.;  (2)  inflammatory,  cicatricial,  or  neoplastic  stenosis  of  the  ducts; 
(3)  compression  of  the  ducts  from  without  by  tumors  of  the  pancreas, 
stomach,  intestine,  gall-bladder,  regional  lymph  nodes,  kidney,  retro- 
peritoneum,  mesentery,  etc.,  inflammatory  adhesions,  swollen  lymph 
nodes,  fecal  accumulations,  aneurysm  of  the  aorta  or  of  the  hepatic  or 
mesenteric  artery,  etc.;  (4)  kinking  or  torsion  of  the  ducts  the  conse- 
quence of  gastroptosis,  hepatoptosis,  nephroptosis,  the  pregnant  uterus, 
tumors  of  the  abdominal  or  pelvic  organs,  etc;  and  (5)  diseases  of  the 
liver  unattended  by  gross  obstruction  of  the  extrahepatic  biliary  ducts, 
such  as  localized  inflammatory  processes  (abscesses),  tubercles,  gummas, 
hydatid  cysts,  primary  and  secondary  newgrowths  within  the  substance 
of  the  liver,  etc. 

Hemolytic,  Toxic,  Infectious,  Hemohepatogenous  Jaundice. — 
Cases  of  jaundice  in  which  no  obstruction  of  the  biliary  ducts  can  be 
found  were  formerly  described  as  non-obstructive  or  hematogenous, 
in  contradistinction  to  the  obstructive  or  hepatogenous  cases.  But 
Naunyn,  Minkowski,  Stadelmann,  and  others  definitely  proved  that 
all  jaundice  is  hepatogenous — in  the  sense  that  bile  pigments  are 
formed  only  in  the  liver.  Since,  however,  in  many  cases  increased 
destruction  of  erythrocytes  provides  the  material  (hemoglobin)  from 
which  the  bile  pigments  are  formed  in  excess  (polychromia),  these  cases 
are  sometimes  spoken  of  as  hemohepatogenous  jaundice;  and  since  they 
occur  in  toxic,  infectious,  and  other  conditions  associated  with  increased 
hemolysis,  they  are  spoken  of  as  hemolytic,  toxic,  or  infectious  jaundice. 

The  mechanism  of  this  type  of  jaundice  is  not  well  understood. 
Frerichs  believed  that  the  bile  found  its  way  directly  into  the  blood- 
vessels, in  consequence  of  changes  in  the  tension  of  the  contents  of  the 
hepatic  cells  and  of  the  bloodvessels — either  an  increase  in  the  inter- 
cellular pressure  or  a  decrease  in  the  portal  pressure.  Liebermeister 
believed  that  the  disordered  liver  cells  lost  their  ability  to  retain  or  fix  the 
bile,  and  that  in  consequence  it  became  diffused  into  the  bloodvessels  or 
lymphatics — so-called  diffusion  or  akathektic  jaundice.  Minkowski 
assumed  a  disturbance  in  the  normal  currents  within  the  liver  cells,  so 
that  the  bile  became  diverted  from  the  biliary  capillaries  to  the  blood- 
vessels or  lymphatics — ^jaundice  from  parapedisis  (paracholia  of  Pick). 
It  is  probable  that  the  toxic  and  infectious  causes  of  this  form  of  jaundice 
seriously  compromise  the  functional  integrity  of  the  liver  cells;  but  it 
has  also  been  demonstrated  that  they  provoke  also  a  radicular  cholan- 
gitis— which  obstructs  the  free  flow  of  bile.  Eppinger  states  that  in 
these  cases  thrombi  made  up  of  coagulated  bile  occur  in  and  obstruct  the 
biliary  capillaries;  in  consequence  thereof,  mechanical  stasis  of  the  bile 
develops  in  the  finest  biliary  capillaries,  and,  as  in  cases  of  gross  obstruc- 
tion of  the  larger  extrahepatic  ducts,  the  biliary  canaliculi  dilate  and 
ultimately  rupture  into  the  pericellular  lymph  spaces.  In  these  cases 
there  is  at  first  an  increased  formation  and  excretion  of  bile  (polycholia) 
and  of  bile  pigments  (polychromia,  pleiochromia) ;  soon,  however,  the 
excretion  of  bile  lessens,  the  bile  that  is  excreted  becomes  viscid,  and 


J  A  UN  DICE  691 

finally  excretion  may  cease — which  may  be  attributed  to  a  radicular  cho- 
langitis or  the  biliary  thrombi,  or  both.  Thus,  although  this  form  of 
jaundice  is  properly  called  toxic,  infectious,  or  hemolytic,  it  is  at  the  same 
time  hepatogenous  and  obstructive. 

This  hemolytic  jaundice  occurs  in  many  infections,  such  as  the  different 
types  of  so-called  infectious  jaundice,  syphilis,  yellow  fever,  septico- 
pyemia, malaria,  pneumonia,  typhoid  fever,  etc.;  in  intoxications,  such 
as  poisoning  with  ptomaines,  phosphorus,  arseniuretted  hydrogen,  chlo- 
roform, mushrooms,  toluylenediamin,  pyrogallol,  snake  venom,  coal-tar 
products,  etc.;  in  acute  yellow  atrophy  of  the  liver;  occasionally  in  cir- 
rhosis and  other  diffuse  diseases  of  the  liver;  in  progressive  pernicious 
anemia  and  hemoglobinemia;  in  disturbances  of  the  circulation,  such  as 
passive  congestion;  in  certain  nervous  perturbations  (so-called  emo- 
tional jaundice,  menstrual  jaundice,  both  of  more  than  doubtful  occur- 
rence); in  the  newborn;  and  as  a  chronic  family  or  hereditary  disorder. 

In  a  number  of  cases,  in  addition  to  the  jaundice,  there  are  phenomena 
of  general  infection,  such  as  fever,  neuromuscular  pains,  enlargement  of 
the  spleen  and  liver,  gastro-intestinal  disorders,  such  as  vomiting  and 
diarrhoea,  nervous  manifestations,  such  as  headache,  stupor,  etc.,  often 
leukocytosis,  albuminuria,  tube  casts,  etc.;  to  these  cases  the  term  in- 
fectious jaundice  (Weil's  disease)  has  been  applied.  The  not  uncom- 
mon epidemic  occurrence  of  such  cases  warrants  the  use  of  the  term 
epidemic  jaundice.  In  other  cases  the  clinical  phenomena  are  more 
severe,  symptoms  attributable  to  hepatic  insufficiency  (hepatargia),  to 
poisoning  by  bile  acids  (cholemia),  or  to  hepatic  auto-intoxication  (acid- 
osis), supervene,  and  a  fatal  issue  usually  ensues;  the  condition  is  spoken 
of  as  grave  jaundice  (icterus  gravis).  When,  in  addition,  considerable 
destruction  of  the  liver  cells  occurs,  the  term  acute  yellow  atrophy  of  the 
liver  is  employed.  No  sharp  line  of  distinction  can  be  drawn  between 
these  cases;  cases  mild  in  the  beginning  may  progress  to  the  most  severe 
and  fatal  (acute  yellow  atrophy);  and  the  degree  of  jaundice  bears  no 
constant  relationship  to  the  demonstrable  changes  in  the  liver,  nor  to 
the  severity  of  the  other  clinical  phenomena. 

Icterus  neonatorum  is  a  peculiar  form  of  jaundice  that  develops  in  from 
two-thirds  to  three-fourths  of  newborn  infants  on  the  second  or  third  day 
of  life,  and  usually  fades  within  a  week  or  ten  days.  The  cutaneous  dis- 
coloration is  slight,  and  is  commonly  unattended  by  other  symptoms.  The 
urine  is  often  of  normal  color,  and  usually  does  not  contain  soluble  bile 
pigments,  but  may  reveal  biliary  granules  or  crystals  in  desquamated  renal 
epithelium.  The  nature  of  this  form  of  jaundice  is  not  well  understood. 
It  has  been  attributed  to  compression  of  the  biliary  capillaries  by  dis- 
tended portal  radicles;  to  catarrhal  cholangitis  (Virchow);  and  to  biliary 
stasis  in  consequence  of  the  diminutive  size  of  the  bile  ducts  and  conse- 
quent obstruction  (Kehrer  and  Cohnheim).  Frank  attributed  it  to 
absorption  of  bilirul)in  from  the  meconium;  and  Quincke  has  suggested 
that  this  bilirubin,  which  is  not  converted  into  urobilin  on  account  of 
the  absence  of  intestinal  fermentation  in  the  newborn,  being  absorbed, 


692  DISEASES  OF  THE  LIVER 

reaches  the  general  circulation  by  way  of  the  ductus  venosus  without 
traversing  the  liver.  Most  likely  it  is  really  due  to  the  erythrocytolysis 
of  the  early  days  of  life;  that  is,  it  is  hemolytic  in  nature.  This  benign 
form  of  jaundice  must  be  distinguished  from  a  more  severe  and  fatal  form 
that  may  also  occur  in  the  early  days  of  life  in  consequence  of  congenital 
syphilis,  septicopyemia,  Winckel's  disease,  congenital  obliteration  of  the 
bile  ducts,  etc. 

Chronic  family  jaundice  (hereditary  jaundice,  congenital  hemolytic 
jaundice,  acholuric  jaundice,  splenomegalic  jaundice,  hemolytic  ictero- 
aiiemia)  is  a  form  of  chronic  non-obstructive  jaundice  (first  accurately 
described  by  Minkowski)  that  is  usually  hereditary  or  occurs  in  several 
members  of  the  same  family,  although  some  cases  are  "acquired."  It 
may  date  from  birth  or  develop  during  adolescence;  and  it  usually  lasts 
for  years  without  notable  impairment  of  the  general  health.  Its  chief 
characteristics  are  slight  or  moderate  jaundice,  enlargement  of  the 
spleen,  well-colored  stools,  the  presence  of  urobilin  and  urobilinogen 
in  the  urine  (but  no  bile  pigments),  moderate  anemia,  and  occasional 
attacks  of  fever,  of  biliousness  (following  dietetic  indiscretions),  and  of 
epigastric  pain,  etc.  (due  to  complicating  gallstones).  Itching,  slow 
pulse,  multiple  hemorrhages,  xanthelasma,  and  other  usual  accompani- 
ments of  jaundice  are  commonly  absent.  The  disease  is  due  to  increased 
fragility  of  the  erythrocytes,  or  their  decreased  resistance  to  hemolyzing 
agents  (Chauffard).  In  the  differential  diagnosis  one  has  sometimes  to 
take  into  consideration  all  the  aforementioned  types  of  jaundice  occurring 
soon  after  birth,  as  well  as  (in  older  subjects)  Hanot's  biliary  cirrhosis — 
which  occasionally  occurs  in  several  members  of  the  same  family. 

Effects  of  Jaundice. — All  of  the  tissues  and  organs,  with  the  exception 
of  the  nervous,  are  stained  with  biliary  pigments;  and  in  some  severe 
cases  of  toxic  or  infectious  jaundice  the  nervous  system  also  may  be 
stained.  The  staining  is  due,  in  part,  to  the  deposition  of  biliary  pig- 
ments in  the  tissues,  in  part  to  the  circulation  of  blood  and  lymph  con- 
taining undeposited  pigments.  It  is  most  marked  in  the  skin,  mucous 
membranes,  serous  membranes  (endocardium,  intima  of  vessels,  etc.), 
the  liver,  kidneys,  heart,  sweat,  serous  transudates,  exudates,  etc.  The 
saliva,  tears,  mucus,  and  milk  are  not  stained  unless  an  inflammatory 
exudate  be  added  to  them. 

Jaundice  is  manifested  first  by  a  yellowish  discoloration  of  the  con- 
junctivae; in  mild  cases  the  discoloration  is  demonstrable  there  only. 
The  skin  becomes  of  a  characteristic  lemon-yellow,  orange-yellow, 
greenish-yellow,  olive,  or  olive-bronze  color.  The  discoloration  is  light 
in  many  cases  of  toxic  or  hemolytic  jaundice,  in  which  it  is  rarely  more 
than  moderate  in  grade;  it  is  light  also  in  mild  cases  of  catarrhal  cho- 
langitis; it  is  darkest  incases  of  permanent  and  complete  obstruction  of 
the  common  bile  duct,  and  it  may  become  so  dark — olive  bronze  or 
greenish  black — as  to  warrant  the  designation  black  jaundice  (melan- 
icterus,  icterus  melas).  The  intensity  of  the  jaundice  in  these  cases  is 
proportionate  to  the  completeness  of  the  obstruction  of  the  common 


JAUNDICE  693 

duct,  or,  in  case  the  obstruction  involve  one  of  the  larger  intrahepatic 
ducts,  to  the  size  of  the  duct  implicated.  Pruritus  is  common  and  dis- 
tressing; rarely  it  precedes  the  discoloration  of  the  skin.  Urticaria  and 
considerable  sweating  (often  localized  to  the  palms)  are  sometimes  ob- 
served. Local  infections,  such  as  boils,  occasionally  occur.  In  chronic 
cases,  local  telangiectases  of  the  skin  (sometimes  also  of  the  oral  and 
other  mucous  membranes)  tend  to  develop,  and  flat  or  nodular  yellowish, 
chamois-leather-colored  patches  (xanthelasma,  xanthoma,  vitiligoidea) 
may  appear  on  the  skin  or  mucous  membranes. 

Bradycardia  is  a  characteristic  feature,  especially  of  acute  cases  and 
those  of  short  duration.  The  pulse  rate  may  fall  to  60,  to  40,  even  to 
21  (Frerichs)  a  minute,  and  it  is  subject  to  sudden  fluctuations  upon 
slight  provocation.  This  has  been  attributed  to  a  local  inhibitory  action 
of  the  bile  acids  on  the  cardiac  muscle  or  ganglia;  but  recent  investiga- 
tions suggest  that  perhaps  the  action  is  on  the  central  nervous  system. 

Bile  pigments  are  present  in  excess  in  the  circulating  blood,  but  whether 
they  exert  any  deleterious  effect  on  the  blood  itself  has  not  been  satis- 
factorily determined.  The  clotting  time  of  the  blood  is  much  increased 
— from  the  normal  three  to  four  minutes  to  ten  to  twelve  minutes — a  fact 
of  much  importance  when  surgical  operations  in  jaundiced  patients  are 
under  consideration.  In  protracted  and  severe  cases  there  is  a  marked 
tendency  to  subcutaneous,  submucous,  and  subserous  hemorrhages. 

In  jaundice  a  considerable  portion  of  the  biliary  derivatives  is  excreted 
in  the  urine,  which,  in  consequence,  is  discolored  yellowish,  yellowish 
red,  greenish,  or  greenish-brown,  depending  upon  the  relative  amounts 
of  bilirubin,  biliverdin  (its  oxidation  product),  or  urobilin  (its  reduction 
product).  These  bile  pigments  may  be  found  in  the  urine  several  hours, 
sometimes  even  several  days,  before  there  is  any  obvious  discoloration 
of  the  skin  or  visible  mucous  membranes;  they  constitute,  thus,  the 
first  clinical  manifestation  of  jaundice.  In  addition,  the  urine  often 
contains  a  number  of  hyaline,  sometimes  bile-stained,  casts — attributable 
to  irritation  of  the  convoluted  and  Henle's  tubules  provoked  by  excreting 
the  bile  pigments  (which  are  not  excreted  by  the  glomeruli).  In  other 
and  particularly  long-standing  cases,  in  addition  to  casts,  the  urine  is 
diminished  in  amount,  of  increased  specific  gravity,  and  contains  more  or 
less  albumin — an  expression  of  nephritis  due  probably  to  associated  toxic 
conditions  rather  than  to  the  jaundice  per  se.  Urobilin  and  urobilinogen 
are  commonly  found  in  the  urine.  They  are  formed  in  the  intestine  by 
the  action  of  bacteria  on  bilirubin;  they  are  absorbed  and  carried  to  tlie 
liver  by  the  portal  circulation.  Some  diagnostic  significance  has  been 
attached  to  their  presence,  as  well  as  that  of  phenol,  in  the  urine  in  disease 
of  the  liver.  The  occurrence  of  urobilinuria  in  cases  of  jaundice,  how- 
ever, does  not  justify  the  designation  "urobilin  jaundice,"  since  the 
cutaneous  pigmentation  is  due  to  bilirubin  and  biliverdin. 

The  functions  of  the  liver,  in  addition  to  the  formation  of  bile,  may  be 
disturbed — reduction  in  the  glycogen  content  and  lessening  of  the  detoxi- 
fying function.     The  liver  cells  are  sometimes  much  degenerated,  not 


694  DISEASES  OF  THE  LIVER 

always,  however,  directly  in  consequence  of  the  jaundice,  Eppinger  has 
shown  that  in  these  cases  marked  regenerative  changes  occur  to  replace 
cells  destroyed.  In  advanced  cases  of  obstructive  jaundice  pericho- 
langitic  fibrosis  sometimes  occurs,  and  has  been  described  as  a  form  of 
biliary  cirrhosis.  The  absence  of  bile  from  the  intestinal  tract  results  in 
the  passage  of  large,  pale,  grayish,  slate-colored  or  clay-colored,  pasty, 
fetid  acid  stools.  The  pale  color  is  due,  in  part  only,  to  the  absence  of 
bile;  in  part  it  is  due  to  the  large  amount  of  imperfectly  digested  fats, 
which  may  be  increased  from  the  normal  7  to  10  per  cent,  to  as  much  as 
80  per  cent.  Microscopically  and  chemically  the  fats  are  found  to  con- 
sist of  free  fatty-acid  crystals  and  soaps  (calcium  and  magnesium)  of  the 
higher  fatty  acids;  neutral  fats  are  present  in  very  small  amounts. 
Rarely  pale  or  decolorized  stools  contain  biliary  derivatives  in  consider- 
able amounts — -determinable  by  chemical  examination;  this  occurs  espe- 
cially in  disease  of  the  pancreas  attended  by  obstruction  to  the  outflow 
of  the  pancreatic  juice,  but  unassociated  with  jaundice.  The  pale  color 
of  the  feces  in  these  cases  is  due  to  the  large  amount  of  fat,  and  to  the 
reduction  of  bilirubin  to  leukourobilin.  Constipation  is  the  rule,  but 
sometimes  the  bowel  movements  are  frequent,  perhaps  diarrhoeic,  which 
may  be  due  to  large  fecal  masses  resulting  from  imperfect  digestion  of 
fat  and  to  the  laxative  action  of  the  free  fatty  acids. 

Grave  disturbances  of  the  nervous  system  occur  in  many  cases  of 
jaundice;  on  the  one  hand,  there  are  manifestations  of  depression,  such 
as  general  neuromuscular  weakness,  asthenia,  headache,  vertigo,  mental 
depression  (that  may  progress  to  melancholia),  insomnia,  etc.;  on  the 
other  hand,  there  are  manifestations  of  irritation,  such  as  severe  head- 
ache, active  delirium,  coma,  convulsions,  etc.  These  manifestations  are 
more  common  in  cases  of  acute  toxic  or  infectious  jaundice  (associated 
with  fever)  than  in  the  more  protracted  cases  of  obstructive  jaundice; 
but  they  may  supervene  in  any  case  of  jaundice  and  not  uncommonly 
lead  to  the  fatal  issue.  They  are  commonly  described  under  the  name 
cholemia,  but  it  is  difficult  to  separate  from  one  another  the  symptoms 
due  to  bile  acidemia,  to  interference  with  the  detoxifying  function  of  the 
liver,  and  to  the  initiating  toxic  or  infectious  process.  The  condition 
is  not  cholemia  in  a  restricted  sense — that  is,  it  is  not  due  to  bile  acidemia, 
since  the  symptoms  may  occur  when  bile  acids  are  not  in  excess  in  the 
blood,  as  well  as  in  cases  of  disease  of  the  liver  (such  as  cirrhosis)  unas- 
sociated with  jaundice.  The  condition  is  most  likely  an  acid  intoxication, 
due  to  disturbances  of  the  detoxifying  function  of  the  liver,  which  may  be 
brought  about  by  disorganization  of  the  hepatic  parenchyma.  Xan- 
thopsia and  hemeralopia  also  are  probably  due  to  a  toxic  disturbance  of 
the  retina,  rather  than  to  the  sometimes  assumed  discoloration  of  the 
media  of  the  eye. 

Man  is  able  to  withstand  the  effects  of  jaundice  for  a  long  time.  The 
fatalities  that  ensue  in  the  acute,  as  well  as  in  the  chronic,  cases  are  due  not 
so  much  to  the  jaundice  per  se  as  to  other  causes — the  underlying  cause 
of  the  jaundice,  acid  intoxication,  etc.     In  long-standing  cases,  however, 


ANOMALIES  OF  FORM  AND  POSITION  695 

more  or  less  disturbance  of  the  general  nutrition  gradually  ensues — due 
largely  to  imperfect  fat  absorption.  To  supply  sufficient  calories  to  pre- 
vent breaking  down  of  the  body  tissues,  there  must  be  considerable 
increase  in  the  protein  intake;  this  results  in  loss  of  appetite,  disordered 
digestion,  perhaps  diarrhoea,  etc.,  so  that,  the  intake  being  reduced,  the 
patient  must  utilize  his  own  fat  or  protein  tissue  to  cover  the  continued 
loss,  and,  having  no  means  of  restoring  the  deficit,  a  very  dangerous 
inanition  results. 


ANOMALIES  OF  FORM  AND  POSITION. 

Congenital  Anomalies  of  Form. — ^The  liver,  in  consequence  of 
defects  of  development,  is  occasionally  found  in  the  thoracic  cavity  or  pro- 
jecting beneath  the  skin  near  the  umbilicus  (hepatomphalos) ;  in  mon- 
sters the  organ  may  be  entirely  absent.  In  partial  and  complete  transpo- 
sition of  the  viscera  the  liver  may  be  as  much  in  the  left  half  of  the  body 
as  normally  it  is  in  the  right;  in  this  event  the  left  lobe  is  the  larger. 

Acquired  Anomalies  of  Form  (Deformities). — ^The  important 
acquired  anomalies  of  form  consist  of  (1)  the  so-called  corset  or  constricted 
liver;  and  (2)  linguiform  lobulation.  The  corset  or  constricted  liver  is  the 
consequence  of  tight  lacing,  and  is  therefore  almost  wholly  confined  to  the 
female  sex  (as  much  as  25  per  cent,  of  female  cadavers  in  some  series); 
but  an  analogous  condition  is  sometimes  encountered  in  men,  the  result 
of  the  constricting  influence  of  a  tight  belt  or  strap.  The  basis  of  the 
deformity  is  a  pressure  atrophy  of  the  liver  parenchyma  followed  by 
fibrosis.  Sometimes  there  is  only  a  deep  circumferential  furrow;  usually 
the  liver  is  considerably  elongated  and  markedly  thinned  at  the  point  of 
greatest  constriction  (most  marked  atrophy),  which  often  corresponds 
with  the  plane  of  the  upper  pole  of  the  right  kidney.  Various  grades  of 
this  condition  are  encountered,  and  it  gradually  merges  into  that  spoken 
of  as  linguiform  (or  RiedeVs)  lobe  (partial  hepatoptosis).  This  also  is 
common  in  female  subjects,  but  it  is  intimately  related  to  cholelithiasis 
and  cholecystitis,  enlargement  of  the  gall-bladder  being  found  in  60  per 
cent,  of  the  cases.  These  linguiform  lobes  are  often  long  and  much 
attenuated;  frequently  they  are  attached  to  the  main  portion  of  the  liver 
by  a  thin  fibrous  band;  and  they  are  often  extremely  mobile  (partial 
hepatoptosis).  The  corset  liver  and  a  linguiform  lobe  may  be  entirely 
symptomless.  In  some  cases  there  are  symptoms  of  indigestion,  as  likely 
due  to  the  tight  lacing  per  se  as  to  the  changes  in  the  liver.  A  lingual 
lobe  is  sometimes  painful  and  tender,  due  to  congestion  or  associated 
cholecystitis  and  cholelithiasis;  occasionally  nausea  and  vomiting  ensue, 
and  have  been  attributed  to  interference  with  the  functions  of  the  pylorus 
and  duodenum;  occasionally  pains  of  biliary  colic  occur.  In  other  cases 
the  abnormality  of  the  right  lobe  is  detected  accidentally,  and  may  be 
mistaken  for  an  abdominal  tumor. 

Treatment. — ^The  corset  liver  is  better  prevented  than  cured.  The 
symptoms  attributable  to  a  linguiform  lobe  are  most  amenable  to  the 


696  DISEASES  OF  THE  LIVER 

surgical  measures  appropriate  to  the  cure  of  cholecystitis  and  cholelithi- 
asis, to  which  they  are  largely  due. 

Acquired  Anomalies  of  Position. — ^The  liver  may  be  displaced 
upward,  downward,  or  laterally,  or  it  may  be  rotated  on  its  antero- 
posterior axis  (anteverted  or  retroverted),  usually  the  result  of  disease 
of  adjacent  thoracic  or  abdominal  organs. 

The  important  acquired  anomaly  of  position  is  that  variously  spoken  of 
as  hepatoptosis,  wandering  liver,  movable  liver,  etc.,  a  condition  in  which 
the  liver  is  abnormally  movable  and  presents  variously  in  the  abdominal 
cavity.     It  is  mentioned  in  connection  with  visceroptosis  (page  685). 


DISEASES  OF  THE  BLOODVESSELS  OF  THE  LIVER. 

Hepatic  Artery. — Dilatation  is  observed  in  cirrhosis  and  other  condi- 
tions when  the  portal  vein  is  obstructed.  Thrombosis  is  very  rare.  Em- 
bolism occasionally  occurs;  it  may  be  mechanical,  infectious  (provoking 
multiple  abscesses),  or  sarcomatous  (usually  melanotic  from  the  eye). 
Aneurysvi  is  rare  (40  cases).  The  chief  symptoms  are  pain,  jaundice, 
and  hemorrhage  into  the  alimentary  tract. 

Hepatic  Veins. — Dilatation  occurs  in  chronic  heart  disease  attended 
by  failure  of  the  right  ventricle.  Thrombosis  is  rare,  but  may  occur  in 
various  sorts  of  disease  in  and  about  the  vein.  The  lesions  are  analogous 
to  those  of  chronic  passive  congestion.  It  may  be  suspected  in  cases  of 
aggravated  passive  hyperemia  upon  the  sudden  onset  of  ascites.  Em- 
bolism (retrograde  embolism)  occasionally  occurs  from  reversal  of  the 
blood  current,  due  to  vigorous  contraction  of  the  right  ventricle,  cough- 
ing, sneezing,  and  other  violent  expiratory  efforts,  and  the  forces  of 
gravity.  The  lesions  vary  with  the  nature  of  the  embolus  (mechanical, 
infectious,  neoplastic).  Suppurative  phlebitis  may  occur  in  pyogenic 
infections  of  the  liver.  Chronic  obliterating  hepatic  endophlebitis  is  rare. 
The  condition  resembles  and  is  usually  mistaken  for  cirrhosis. 

Portal  Vein. — Dilatation  is  part  of  portal  cirrhosis,  and  is  attributable 
to  increased  blood  pressure.  Thrombosis  (pylethrombosis,  pylephle- 
bitis adhesiva)  is  rather  common  in  cirrhosis  of  the  liver  and  in  intra- 
abdominal newgrowths,  but  it  may  occur  also  in  inflammatory  disorders 
of  the  abdominal  viscera.  The  thrombosis  may  begin  in  the  portal 
radicles  within  the  liver,  in  the  main  trunk  of  the  vein,  or  in  the  peripheral 
radicles  anywhere  within  the  area  of  collection  of  the  vein;  and  subse- 
quently, by  extension,  the  process  may  become  widespread.  In  some 
cases  the  disorder  seems  to  be  due  to  a  low-grade  infection.  The  portal 
vein  may  become  converted  into  a  fibrous  cord  (pylephlebitis  adhesiva), 
and  a  collateral  circulation  may  become  established.  The  diagnosis  is 
rarely  possible,  but  is  suggested  by  sudden  onset  of  ascites  of  high  grade, 
gastro-intestinal  hemorrhage,  enlargement  of  the  spleen,  abdominal  pain, 
and  symptoms  of  intestinal  obstruction.  Death  may  occur  soon;  at  all 
events,  usually  within  two  years.     The  treatment  is  palliative;  the  ascites 


FATTY  LIVER  697 

may  require  repeated  tapping.  Embolism  of  the  intrahepatic  branches  of 
the  portal  vein  is  a  common  sequence  of  inflammatory,  suppurative,  ulcer- 
ative, and  neoplastic  processes  in  the  organs  within  the  area  of  collection 
of  the  portal  vein.  SuiJ'purative  pylephlebitis  is  common,  especially  in 
early  adult  life,  and,  like  adhesive  pylephlebitis,  may  begin  in  the  portal 
radicles  within  the  liver,  in  the  main  trunk  of  the  vein,  or  in  the  peripheral 
radicles  anjw'here  within  the  area  of  collection  of  the  vein;  and  subse- 
quently, by  extension,  the  process  may  become  more  or  less  widespread. 
Usually  the  disorder  is  secondary  to  ulcerative  or  suppurative  processes  of 
the  gastro-intestinal  tract,  especially  appendicitis,  dysenteric  and  other 
ulcerations  of  the  intestine,  etc.  The  infecting  microorganisms  are 
staphylococci,  streptococci.  Bacillus  coli,  Bacillus  dysenterise,  etc.  The 
symptoms  consist  of  those  of  the  antecedent  disorder,  to  which  are  grad- 
ually added  (if  they  have  not  already  existed)  irregular  chills,  fever, 
sweats,  polynuclear  leukocytosis,  and  prostration;  as  well  as  extension  of 
abdominal  pain  beyond  the  seat  of  original  disease,  enlargement  and 
tenderness  of  the  liver,  perhaps  also  of  the  spleen,  and  sometimes  vomit- 
ing, hematemesis,  and  diarrhoea.  Usually  the  patient  soon  passes  into 
a  typhoid  state  and  dies.  Chronic  portal  endophlebitis  rarely  occurs:  as 
a  primary  disease  (syphilis,  splenic  anemia  with  sequential  Banti's  dis- 
ease, etc.),  or  as  a  secondary  process  (chronic  passive  congestion  and 
cirrhosis  of  the  liver).     Partial  or  complete  thrombosis  may  follow. 

FATTY  LIVER. 

Fatty  liver  is  a  comprehensive  term  applicable  to  the  different  con- 
ditions characterized  by  an  excess  of  fat  in  the  liver.  It  includes  fatty 
infiltration,  in  which  there  is  an  excessive  deposit  of  fat  in  otherwise  unal- 
tered or  slightly  altered  liver  cells;  and  fatty  degeneration,  in  which,  in 
addition  to  the  fat,  there  are  greater  or  less  degenerative  changes  in  the 
hepatic  parenchyma,  perhaps  the  direct  conversion  of  the  liver  cells  into 
fat.  Formerly  the  two  conditions  were  differentiated;  doubtless  there 
are  extreme  cases  of  fatty  infiltration  and  of  fatty  degeneration,  but  many 
cases  partake  of  the  nature  of  both  processes,  and,  contrary  to  former 
opinions,  there  is  now  considerable  trustworthy  evidence  to  suggest  at 
least  that  the  fat  in  the  liver  under  all  circumstances  is  derived  mainly 
from  adipose  tissue  elsewhere  in  the  body. 

Etiology. — ^The  causes  of  fatty  liver  are:  (1)  Dietetic  indiscretions  and 
the  disorders  of  metabolism  that  tend  to  produce  obesity,  of  which  fatty 
liver  (mostly  infiltration)  is  a  conspicuous  feature;  (2)  anemic  and  ca- 
chectic conditions,  such  as  occur  in  the  late  stages  of  tuberculosis,  amyloid 
disease,  carcinoma,  etc.;  (3)  passive  congestion;  (4)  poisons,  such  as 
alcoholism,  phosphorus,  arsenic,  antimony,  chloroform,  etc;  (5)  certain 
local  infections  of  the  intestinal  tract,  such  as  the  gastro-intestinal  catarrh 
of  children,  dysentery,  etc.;  (6)  certain  general  infections,  notably  strej)- 
tococcic,  staphylococcic,  and  other  pyococcic  infections  of  long  dura- 
tion (prolonged  suppuration),  tuberculosis,  etc. 


698  DISEASES  OF  THE  LIVER 

Pathology. — ^Usually  the  liver  is  enlarged,  and  may  weigh  3000  to  4000 
grams;  it  is  of  lessened  specific  gravity  (sometimes  floating  in  water), 
and  of  lessened  resistance;  it  is  normal  in  conformation,  and  has  a  smooth 
surface  and  rounded  edges,  and  is  pale  yellowish  in  color.  Histologically, 
fatty  infiltration  and  degeneration  may  be  combined  in  varying  propor- 
tions. 

Symptoms. — The  symptoms  of  fatty  liver  are  ill  defined.  In  general, 
the  symptoms  are  those  of  the  primary  disorder-obesity,  tuberculosis, 
alcoholism,  toxemic  conditions,  etc.  In  perhaps  the  majority  of  cases 
there  are  no  symptoms  referable  directly  to  the  liver;  occasionally  sensa- 
tions of  weight  may  be  due  to  the  mere  weight  of  the  liver,  and  ill-defined 
dyspeptic  symptoms  may  be  attributed  to  functional  inactivity  of  the 
liver,  although  they  are  more  likely  to  be  due  to  associated  disorders  of 
the  stomach  and  intestines,  improper  eating  and  drinking,  etc.  The 
liver  is  enlarged  and  commonly  palpable  two  or  three  fingers'  breadth 
below  the  costal  margin. 

In  phosphorus  poisoning  the  early  symptoms  are  those  of  gastro- 
intestinal irritation  (epigastric  distress,  nausea,  and  vomiting).  If  the 
patient  does  not  die  soon,  there  is  commonly  a  period  of  quiescence,  that 
to  the  unwary  suggests  recovery  and  speedy  cure.  At  the  end  of  two  or 
three  days,  however,  vomiting  and  epigastric  distress  return,  jaundice 
supervenes,  the  pulse  becomes  weak  and  accelerated,  the  heart  dilated, 
subcutaneous,  submucous,  and  subserous  hemorrhage  develop,  and  the 
patient  usually  dies  within  a  week.  In  most  cases  the  liver  is  enlarged 
throughout,  smooth  and  tender;  in  some  cases  it  decreases  in  size  before 
death. 

Diagnosis.— Minor  grades  of  fatty  liver  cannot  be  recognized  with  cer- 
tainty; the  more  marked  grades  must  be  differentiated  from  other  causes 
of  enlargement,  such  as  the  fatty  cirrhotic  liver,  amyloid  liver,  leukemic 
infiltration,  passive  congestion,  displaced  liver,  etc. 

Prognosis. — The  prognosis  depends  upon  the  primary  cause. 

Treatment. — -The  treatment  is  altogether  that  of  the  primary  disorder. 


ACUTE  YELLOW  ATROPHY  OF  THE  LIVER. 

Acute  yellow  atrophy  of  the  liver  is  an  acute,  widespread  autolytic 
necrosis  of  the  liver  cells,  characterized  clinically  by  jaundice,  reduction 
in  the  size  of  the  liver,  and  toxic  disturbances  of  cerebration,  proceeding  to 
a  fatal  issue. 

Etiology. — ^Acute  yellow  atrophy  of  the  liver  is  especially  frequent  be- 
tween the  twentieth  and  thirtieth  year  (50  per  cent,  of  the  cases),  and  in 
women  (two-thirds  of  the  cases).  Both  of  these  facts  are  explainable 
largely  by  the  frequent  occurrence  of  the  disease  during  pregnancy; 
almost  if  not  quite  one-half  of  the  cases  in  women  occur  about  the  middle 
or  during  the  latter  half  of  pregnancy.  The  causative  influence  of  preg- 
nancy is  akin  to  that  exerted  by  the  toxemia  of  pregnancy,  in  which  the 


ACUTE  YELLOW  ATROPHY  OF  THE  LIVER  699 

liver  frequently  shows  degenerative  changes,  and  in  the  production  of 
which  it  plays  an  important,  if  not  the  important,  part.  Various  known 
infections  exert  some  etiological  influence;  thus  10  per  cent,  of  the 
cases  occur  during  secondary  syphilis  (in  which  slight  jaundice  is  not  very 
rare);  pyogenic  infections  (septicopyemia,  osteomyelitis,  erysipelas,  etc.), 
typhoid  fever,  malaria,  diphtheria,  etc.,  may  antedate  the  liver  disorder. 
Etiological  significance  is  also  attributed  to  certain  non-bacterial  poisons, 
such  as  alcohol,  ptomaines,  chloroform,  phosphorus,  etc.  Chloroform  is 
of  undoubted  significance,  being  responsible  for  the  cases  of  so-called 
delayed  chloroform  poisoning.  Phosphorus  gives  rise  to  a  somewhat 
analogous  condition,  but  the  lesions  in  the  liver  are  not  alike  in  the  two 
disorders.  Similar  phenomena  may  develop  in  the  course  of  other  dis- 
eases of  the  liver,  such  as  advanced  passive  congestion,  cirrhosis,  cholan- 
gitis, etc.  All  of  the  foregoing  leads  to  the  conclusion  that  the  designa- 
tion acute  yellow  atrophy,  as  well  as  icterus  gravis,  comprises  a  series  of 
diverse  disorders  that  exhibit  more  or  less  superficial  resemblance.  We 
are  now  able  to  separate  some  of  the  cases  from  the  main  group,  such  as 
those  due  to  syphilis,  septicopyemia,  puerperal  eclampsia,  phosphorus 
poisoning,  delayed  chloroform  poisoning,  etc.,  but  the  definite  etiological 
factor  of  the  major  group  is  still  unknown. 

Pathology. — The  liver  is  much  reduced  in  size  and  weight,  being  often 
one-half  or  one-third  that  of  the  normal  (800  to  500  grams  or  less).  The 
organ  is  flaccid  and  has  so  lost  its  normal  elasticity  and  resistance  that 
it  may  be  folded  or  bent  upon  itself.  On  sectioning  the  liver  it  is  found 
to  be  dense  and  resistant;  the  section  surface  is  mottled — ^yellowish  or 
yellowish-red  areas  of  varying  size  and  configuration  alternating  and 
more  or  less  gradually  merging  the  one  into  the  other.  The  yellowish 
coloration  is  due  chiefly,  if  not  entirely,  to  bilirubin  rather  than  to  fatty 
alterations  (the  fat  content  is  usually  not  increased,  and  may  be  dimin- 
ished) ;  the  reddish  areas  seem  to  be  an  advanced  stage  of  the  yellow,  and 
to  be  more  numerous  or  larger  the  longer  the  patient  lives.  Examination 
of  the  fresh  liver  tissue  (scrapings  of  the  section  surface)  reveals  necrotic 
liver  cells,  erythrocytes,  leukocytes,  leucin,  tyrosin,  and  xanthin.  Histo- 
logically there  is  intense  and  widespread  (not  focal)  destruction  of  the 
liver  cells.  Ultimately  the  cells  disappear,  apparently  in  consequence 
of  autolysis,  and  leave  behind  the  supporting  framework  of  the  liver, 
granular  debris,  and  endothelium  of  the  capillaries  (the  reddish  areas  on 
macroscopic  inspection).  The  small  bile  ducts  become  obstructed  in 
consequence  of  desquamation  of  their  lining  epithelium  and  participate 
in  the  production  of  the  jaundice.  In  some,  especially  protracted,  cases 
there  are  conspicuous  evidences  of  attempts  at  regeneration  (compen- 
satory hyperplasia)  of  the  liver  cells;  pseudobiliary  canaliculi  derived 
from  the  liver  cells  as  well  as  the  smaller  bile  ducts  also  are  often  con- 
spicuous. All  the  organs  are  more  or  less  bile-stained.  The  spleen  is 
soft,  and  is  slightly  or  moderately  enlarged  in  about  two-thirds  of  the 
cases.  The  kidneys  are  enlarged,  softened,  pale,  o])aque,  and  often 
reveal  small  foci  of  hemorrhage,  cloudy  swelling,  and   fatty  changes. 


700  DISEASES  OF  THE  LIVER 

Small  hemorrhages  are  found  beneath  the  skin  and  the  various  serous 
membranes  (pleura,  pericardium,  peritoneum,  meninges)  and  mucous 
membranes  (gastro-intestinal,  respiratory,  and  genito-urinary  tract),  and 
are  doubtless  attributable  to  toxic  changes  in  the  blood  and  blood- 
vessels. 

F.  W.  White  supports  the  view,  originally  advanced  by  Flexner,  that  the 
process  is  autolytic  in  nature,  and  that  it  is  brought  about  by  some  poison 
having  a  specific  action  on  the  liver  cells  whose  life  it  destroys  without 
injuring  the  proteolytic  ferments  they  contain,  whence  autodigestion 
ensues.  The  leucin  and  tyrosin  result  partly  from  autolysis  of  the  liver, 
and  partly  from  non-conversion  into  urea  of  leucin  and  tyrosin  formed 
elsewhere.  Other  evidence  of  this  autolysis  is  found  in  the  albuminose 
(decomposing  protein)  and  purin  bodies  (destruction  of  nuclein)  some- 
times encountered  in  the  urine.  The  reduction  in  the  excretion  of  urea 
and  the  increased  excretion  of  ammonia  are  interpretable  as  efforts  on 
the  part  of  nature  to  neutralize  increased  acidosis,  whence  the  process 
may  be  looked  upon  as  an  acid  intoxication.  T\Tiite  believes  that  the 
chief  symptoms  of  the  severe  intoxication  are  due  largely  to  the  damage 
done  to  the  functions  of  the  liver,  and  that  the  special  poisonous  sub- 
stances are  probably:  (1)  Nitrogenous  antecedents  of  urea;  (2)  certain 
products  of  decomposition  in  the  bowel  which  are  normally  deprived  of 
their  toxic  power  in  passing  through  the  liver;  and  (3)  decomposition 
products  of  the  destroyed  liver  tissue;  and,  further,  that  this  view  is  borne 
out  by  observation  of  other  severe  diseases  of  the  liver  in  which  little 
or  no  jaundice  occurs. 

Symptoms. — The  initial  symptoms  are  those  of  gastro-intestinal  catarrh, 
soon  (one  to  four  days)  followed  by  jaundice;  these  may  last  a  variable 
period,  usually  five  to  seven  days,  but  sometimes  several  weeks.  During 
this  period  the  disorder  is  usually  looked  upon  as  ordinary  catarrhal 
jaundice  (cholangitis),  and  as  a  matter  of  fact  there  is  little  if  anything  to 
suggest  the  more  serious  disorder.  The  patient  complains  of  malaise, 
perhaps  fugitive  neuromuscular  pains,  poor  appetite,  coated  tongue,  occa- 
sional vomiting,  constipation,  etc. ;  there  is  usually  moderate  jaundice  and 
bile  pigment  in  the  urine.  Soon,  however,  the  graver  symptoms  super- 
vene. The  jaundice  deepens,  becoming  dark  yellowish  or  bronze-like, 
slightly  greenish  (in  rare,  extremely  rapid  cases  jaundice  may  be  absent); 
severe  nausea  and  vomiting  set  in  and  are  often  associated  with  hema- 
temesis;  diarrhoea  may  supervene;  and  grave  nervous  symptoms  ensue 
— ^headache,  mental  confusion,  hebetude,  and  restlessness,  soon  followed 
by  a  noisy  delirium,  and  later  coma  and  perhaps  convulsions.  Hemor- 
rhages (disordered  nutrition  of  the  vessel  walls  and  hemolytic  action  of  bile 
salts  on  the  erythrocytes)  occur  beneath  the  skin  and  into  and  from  divers 
mucous  membranes  (intestines,  urinary  tract,  respiratory  tract,  genital 
tract,  retina,  and  most  commonly  the  stomach);  abortion  may  occur  in 
pregnant  women.  Soon  the  patient  passes  into  a  profound  typhoid 
state.  There  may  be  slight  fever  (pyococcic  infection),  but  usually  the 
temperature  is  below  normal  (until  shortly  before  death,  when  there  may 


ACUTE   YELLOW  ATROPHY  OF  THE  LIVER  701 

be  an  agonal  rise);  the  pulse  becomes  rapid,  feeble,  and  of  low  tension; 
the  respirations  become  accelerated  and  irregular;  the  pupils  dilate  (said 
to  be  important,  diagnostically) ;  the  tongue  becomes  dry,  furred,  and 
tremulous;  sordes  collect  on  the  teeth  and  gums;  and  there  are  fibrillary 
twitchings  of  the  muscles,  etc. 

The  liver  in  some  cases  is  found  slightly  or  moderately  enlarged  in  the 
early  days  of  the  disorder;  this  may  be  due  to  preexisting  disease  (as  cir- 
rhosis), but  rarely  it  seems  to  be  a  part  of  the  acute  yellow  atrophy  itself. 
Soon,  however,  the  liver  dulness  diminishes  rapidly  in  extent,  until  it  may 
be  entirely  absent  or  constitute  a  small  area  in  the  axillary  region.  Slight 
or  moderate  enlargement  of  the  spleen  may  be  made  out  in  about  two- 
thirds  of  the  cases. 

The  feces,  as  a  rule,  are  dark  and  offensive.  The  dark  color  in  the 
early  stages  is  that  of  normal  feces;  that  of  the  feces  late  in  the  disease  is 
probably  due,  in  part  at  least,  to  contained  blood,  which  obscures  the 
paucity  of  the  bile,  since  very  little  if  any  bile  probably  enters  the  intestine 
in  the  advanced  stages  of  most  cases.  The  stools  may  be  light  colored, 
especially  if  there  be  diarrhoea. 

The  urine,  as  a  rule,  is  lessened  in  amount,  of  increased  specific  gravity, 
of  increased  acidity,  and  high  colored  (bile  pigment  and  excess  of  uro- 
bilin); it  usually  contains  a  small  amount  of  albumin,  and  hyaline, 
granular,  fatty,  and  epithelial  tube  casts.  The  highly  significant  changes 
consist  in  the  presence  of  leucin,  tyrosin,  and  the  other  amino-acids 
(largely  the  result  of  autodigestion  of  the  liver);  sarcolactic,  diacetic,  and 
other  fatty  acids  (lactic,  acetic,  butyric,  and  succinic);  marked  reduction 
in  the  amount  of  urea  with  an  associated  increase  in  the  amount  of  am- 
monia and  other  nitrogenous  substances.  A  moderate  leukocytosis  (up 
to  16,000)  may  be  present.     Occasionally  there  may  be  ascites. 

Diagnosis. — Careful  studies  of  the  urine,  especially  in  pregnant  women, 
and  in  cases  of  mild  jaundice,  and  the  detection  of  significant  urinary 
changes,  especially  evidences  of  an  acid  intoxication,  should  enable  us 
to  recognize  the  antecedent  conditions  and  perhaps  ward  off  the  more 
serious  later  stages.  The  development  of  nervous  symptoms  in  any  case 
of  jaundice  should  always  awaken  suspicion.  When  fully  developed, 
jaundice,  vomiting,  delirium  (and  other  cerebral  symptoms),  lessening  in 
the  size  of  the  liver,  and  the  presence  of  leucin  and  tyrosin  in  the  urine 
are  unmistakable  (although  leucin  and  tyrosin  may  be  found  in  other 
conditions). 

Phosphorus  poisoning  may  be  excluded  by  the  alisence  of  a  history  of 
the  ingestion  of  phosphorus  (not  always  trustworthy),  the  latter  develop- 
ment of  jaundice  (which  in  phosphorus  poisoning  usually  supervenes 
after  a  day  or  two  of  symptoms  referal)le  to  disordered  stomach),  decrease 
in  the  size  of  the  liver  (which  usually  remains  enlarged  in  ])]iosphorus 
poisoning),  the  more  severe  nervous  symptoms,  and  the  constant  occur- 
rence and  larger  amounts  of  leucin  and  tyrosin.  The  liver  of  phosphorus 
poisoning  may  contain  30  per  cent,  of  fat,  as  contrasted  with  5  per  cent, 
in  acute  atrophy. 


702  DISEASES  OF  THE  LIVER 

Prognosis. — The  disease  is  almost  invariably  fatal,  A  few  cases  of 
recovery  have  been  reported. 

Treatment. — ^In  the  early  stages  the  patient  should  be  confined  to  bed. 
Milk  is  the  best  food,  and  should  be  diluted  with  some  alkaline  mineral 
water;  cereals  and  other  carbohydrates  may  be  given  in  considerable 
amounts,  since  they  are  likely  to  prevent  or  limit  the  acid  intoxication. 
The  bowels  should  be  opened  freely  and  repeatedly,  with  a  view  to 
remove  all  noxious  matters  from  the  intestine,  as  well  as  material  from 
which  toxic  substances  may  be  formed;  calomel  and  the  saline  cathartics 
seem  the  best.  Insistence  should  be  laid  upon  the  drinking  of  large 
amounts  of  an  alkaline  water.  Alkaline  diuretics  and  other  alkalies 
(sodium  bicarbonate)  and  enteroclysis  and  hypodermoclysis  may  be 
resorted  to.  Intestinal  antiseptics  are  indicated  theoretically.  Stimu- 
lants, such  as  alcohol,  strychnine,  and  digitalis,  are  useful  for  the  general 
vital  depression  and  collapse;  an  ice-cap  to  the  head,  the  bromides  inter- 
nally, and  a  warm  bath  or  sponge,  or  a  small  amount  of  morphine  (^  to 
^ig-  grain,  9.002  to  0.006  gram)  or  of  cocaine  (^  grain,0.008  gram)  hypo- 
dermically,  may  control  the  restlessness  and  delirium;  warm  applications 
to  the  abdomen,  and  cocaine,  dilute  hydrocyanic  acid,  bismuth,  and  car- 
bolic acid,  or  small  amounts  of  champagne,  etc.,  may  control  the  vomiting. 

ACTIVE  CONGESTION  OF  THE  LIVER. 

Etiology. — Active  congestion  of  the  liver,  usually  toxic  in  nature  and 
gastro-intestinal  in  origin,  may  result  from:  (1)  The  processes  of  diges- 
tion, when  it  is  a  normal  condition;  (2)  endogenous  and  exogenous 
poisons  that  may  be  carried  by  the  portal  vein  (alcohol,  overeating, 
ptomaines,  bacterial  toxins,  etc.);  (3)  bacterial  toxins  that  may  reach  the 
liver  by  way  of  the  general  circulation  (typhoid  fever,  malaria,  pyococcic 
infections,  etc.);  (4)  "cold,"  "a  chill  upon  the  liver,"  the  "tropical 
liver;"  and  (5)  perhaps  vasomotor  disturbances  (menstruation,  etc.). 
Most  of  these  factors  are  the  causes  also  of  inflammation  and  degener- 
ative changes  in  the  liver;  it  is  difficult,  if  not  impossible,  to  separate  the 
one  set  of  conditions  from  the  other;  they  are  often  combined. 

Symptoms. — The  cases  associated  with  dietetic  indiscretions  are 
manifest  by  so-called  indigestion,  or  the  complex  popularly  designated 
"biliousness"  (poor  appetite,  coated  tongue,  epigastric  distress,  nausea, 
occasionally  vomiting,  constipation,  headache,  etc.).  Perhaps  there 
is  a  sub  icteric  hue  to  the  sclerse  and  the  skin;  the  liver  may  be  found 
slightly  enlarged  and  tender.  In  the  cases  met  in  infections,  such  as 
dysentery,  malaria,  etc.,  the  constitutional  symptoms  are  more  marked; 
slight  or  moderate  fever  is  usually  present  (progression  to  acute  hepa- 
titis); and  the  local  gastro-intestinal  symptoms  may  be  more  or  less  in 
abeyance,  although  they  may  become  aggravated  during  digestion.  The 
liver  becomes  enlarged  and  tender. 

Diagnosis. — ^Phe  diagnosis  is  usually  apparent  from  the  etiological 
factors,  the  general  disturbances  of  the  gastro-intestinal  tract,  the  slight 


PASSIVE  CONGESTION  OF  THE  LIVER  703 

jaundice,  and  enlargement  and  tenderness  of  the  liver;  by  no  means 
of  minor  diagnostic  importance  is  recurrence  of  attacks  in  a  person  of 
known  ill-chosen  habits  of  eating  and  drinking.  The  diagnostic  diffi- 
culties consist  in  determining  whether  or  not  to  the  congestion  permanent 
damage  to  the  liver  tissue  has  been  added.  With  recurrence  of  attacks, 
their  increasing  duration,  and  lessening  intervals,  this  becomes  the  more 
likely.  In  the  more  acute  cases  encountered  in  infections,  aggravation 
of  the  constitutional  symptoms,  together  with  enlargement  and  tender- 
ness of  the  liver,  usually  suffice  for  diagnosis.  In  these  cases  there  are 
usually  parenchymatous  changes  in  addition  to  the  congestion. 

Prognosis. — The  disorder  rarely  lasts  more  than  three  or  four  days; 
sometimes  a  week.  It  is  not  dangerous  in  itself,  but  acquires  its  impor- 
tance because  of  its  etiological  factors  (especially  alcohol)  and  its  fre- 
quent recurrence  in  the  indiscrete:  in  those  that  persist  in  the  use  of 
alcohol,  in  whom  it  is  likely  to  eventuate  in  cirrhosis;  and  in  those  con- 
tinuously exposed  to  other  etiological  factors,  such  as  malaria,  dysentery, 
etc.,  in  the  tropics,  in  whom  freedom  from  recurrences  can  only  be 
obtained  by  removal  to  temperate  zones  (freedom  from  etiological 
causes). 

Treatment. — ^The  treatment  is  that  of  acute  non-suppurative  hepatitis. 


PASSIVE  CONGESTION  OF  THE  LIVER. 

Etiology. — ^Passive  congestion  of  the  liver,  largely  mechanical  in  nature 
and  cardiac  in  origin  (whence,  cardiac  liver),  occurs:  (1)  In  acute  and 
chronic  failure  of  the  heart,  the  ultimate  condition  in  myocardial,  peri- 
cardial, and  chronic  valvular  disease;  (2)  in  advanced  stages  of  such 
diseases  of  the  lungs  as  cause  increased  work  of  the  right  side  of  the  heart 
and  finally  lead  to  its  failure  (chronic  bronchitis,  emphysema,  chronic 
adhesive  pleuritis,  etc.);  and  (3)  from  local  factors  that  obstruct  the  cir- 
culation about  the  junction  of  the  hepatic  veins  and  the  inferior  vena  cava 
(kyphosis,  inflammatory  adhesions,  angulation  by  a  displaced  heart, 
pleural  effusion,  etc.). 

Pathology. — ^Three  stages  of  passive  congestion  of  the  liver  may  be 
distinguished:  (1)  The  merely  congested  or  engorged  ' liver,  found  in 
cases  of  acute  or  recent  heart  failure  (common  in  infections,  such  as 
pneumonia,  typhoid  fever,  etc.),  and  in  chronic  valvular  disease,  with 
well-maintained  compensation,  in  which  death  has  occurred  suddenly 
or  after  a  few  days'  illness  only;  (2)  the  congested  nutmeg  liver,  found  in 
cases  of  long-standing  heart  disease,  with  dilatation  of  the  right  heart 
and  tricuspid  insufficiency,  in  which  compensation,  although  precari- 
ously maintained,  has  been  on  the  whole  fairly  satisfactory,  and  in  which 
no  serious  or  prolonged  failure  has  occurred  until  that  which  leads  to 
death;  and  (3)  the  fibrotic  nutmeg  liver  (red  atropliy  of  the  liver),  found 
also  in  cases  of  long-standing  heart  disease  with  dilatation  of  the  right 
heart  and  tricuspid  insufficiency,  in  which  one  or  more  severe  and  pro- 


704  DISEASES  OF  THE  LIVER 

longed  attacks  of  failure  of  compensation  have  occurred,  during  which 
likely  the  auricle  has  suffered  especially,  and,  being  perhaps  totally  inca- 
pacitated, has  permitted  the  full  force  of  the  ventricle  to  be  transmitted 
to  the  hepatic  lobules  with  consequent  rupture  of  the  venules  and  capil- 
laries, laceration  and  destruction  of  hepatic  parenchyma,  and  its  repair 
by  newgrown  connective  tissue  (scar  tissue).  It  is  likely  that  congestion 
of  the  liver  in  the  early  stages  of  cardiac  failure  (whether  due  to  endo- 
cardial, myocardial,  pericardial,  or  pulmonary  disorder)  is  a  compen- 
satory process;  that  this  is  especially  active  in  acute  failure,  such  as 
occurs  in  many  infections  and  in  the  early  stage  of  chronic  valvular  disease; 
that  not  until  the  liver  has  been  distended  to  and  beyond  its  capacity 
does  oedema  ensue ;  and  that  with  the  progress  of  th  valvular  defect  and 
the  gradual  loss  of  the  safety-valve  action  of  the  liver  oedema  appears 
more  and  more  easily. 

Symptoms. — The  symptoms  consist  of  those  due  to  the  primary  cardiac 
or  pulmonary  disease,  especially  dyspnoea,  cyanosis,  and  oedema,  and 
those  due  more  directly  to  the  disorder  of  the  liver  itself.  These  com- 
prise especially  pain  and  distress  or  a  sense  of  weight  and  heaviness 
in  the  right  hypochondrium,  and  gastro-intestinal  phenomena,  such 
as  poor  appetite,  epigastric  distress  especially  after  eating,  flatulence, 
nausea,  and  constipation.  These  are  due  in  part  to  general  venous  en- 
gorgement, in  part  to  portal  congestion  transmitted  from  the  congested 
hepatic  veins.  Slight  or  moderate  jaundice  is  common;  the  admixture 
of  the  jaundice  and  more  or  less  cyanosis  gives  to  the  patient  a  very  char- 
acteristic bluish  or  purplish,  green  or  yellow  discoloration.  (Edema, 
followed  by  ascites,  is  often  present,  being  part  of  the  cardiac  decom- 
pensation. Occasionally  the  ascites  is  disproportionately  large  in 
amount  and  may  require  repeated  tappings;  in  this  event  it  is  associated 
with  the  fibrotic  congested  liver  or  with  chronic  adhesive  peritonitis 
(perihepatitis).  The  liver  is  enlarged,  perhaps  reaching  to  or  below  the 
transumbilical  line;  it  is  tender,  and  it  may  reveal  an  expansile  ven- 
tricular systolic  pulsation. 

Diagnosis. — The  diagnosis  is  usually  evident  from  a  knowledge  of  the 
primary  disorder,  an  enlarged  and  tender  liver,  and  other  evidences  of 
failing  cardiac  compensation. 

Prognosis. — The  prognosis  is  altogether  that  of  the  primary  disorder. 

Treatment. — ^The  treatment  is  that  of  the  primary  cardiac  or  pul- 
monary disorder;  virtually  it  is  that  of  failing  cardiac  compensation. 

PERIHEPATITIS. 

Acute  Perihepatitis. — ^Acute  perihepatitis  is  almost  if  not  always  a 
secondary  disorder,  due  to  antecedent  disease  of  the  liver  or  adjacent 
viscera.  The  lesions  may  be  localized  or  diffuse,  and  fibrinous,  sero- 
fibrinous, or  purulent  in  character.  The  fibrinous  exudation  may 
undergo  organization  and  lead  to  filamentous  or  dense  adhesions;  the 
suppurative  lesions  may  be  part  of  one  form  of  subphrenic  abscess. 


ACUTE  HEPATITIS  705 

The  important  symptoms  consist  of  local  pain  and  audible  and  palpable 
frictions.  There  may  be  a  short,  hacking  cough  (perhaps  set  up  by- 
manipulation  of  the  liver),  hiccough  (suggesting  involvement  of  the 
diaphragm),  and  nausea  and  vomiting.  The  diagnosis  is  often  obscured 
by  the  predominance  of  the  symptoms  of  the  primary  disorder.  The 
treatment  is  that  of  the  primary  disease  and  local  measures  (strapping, 
counterirritation,  etc.)  to  relieve  the  pain.  Operation  is  required  in  the 
suppurative  cases. 

Local  Chronic  Perihepatitis. — ^I^ocal  chronic  perihepatitis  usually 
follows  and  is  therefore  due  to  the  same  causes  as  the  acute  process.  The 
lesions  are  usually  quite  firm  adhesions  that  serve  to  bind  the  neighboring 
organs  variously  to  one  another.  The  symptoms  are  scarcely,  if  ever, 
definite,  but  local  pain,  tenderness,  and  rigidity  may  suggest  the  disorder. 

General  chronic  perihepatitis  will  be  discussed  under  diseases  of  the 
peritoneum  (multiple  serositis,  page  750). 

ACUTE  HEPATITIS. 

Acute  Non-suppurative  Hepatitis. — ^The  term  acute  non-suppu- 
rative  or  parenchymatous  hepatitis  is  employed  to  include  a  series  of 
most  diverse  disorders  that  exhibit  all  stages  of  progression  from  acute 
congestion  to  the  inflammatory  focal  necroses  of  many  infections,  and 
the  more  widespread  process  manifested  clinically  as  the  different  forms 
of  icterus  gravis  and  acute  yellow  atrophy  of  the  liver.  Manifestly  the 
term  is  not  strictly  applicable  to  all  of  these. 

Etiology. — The  causes  of  acute  congestion  of  the  liver  already  men- 
tioned may  cause  acute  non-suppurative  hepatitis;  the  difference  be- 
tween these  disorders  is  one  of  degree  only.  As  a  matter  of  fact,  acute 
hepatitis  is  uncommon  in  temperate  climates.  In  the  tropics,  however, 
a  disorder  described  by  those  of  experience  as  acute  parenchymatous 
hepatitis  (tropical  liver)  is  of  frequent  occurrence;  it  is  most  commonly 
provoked  by  malaria,  but  also  by  dysentery  and  perhaps  other  infections. 
It  occurs  especially  in  young  adult  Europeans,  and  not  uncommonly  soon 
(during  the  first  year)  after  their  arrival  in  the  tropics.  Undoubtedly 
factors  other  than  malaria  and  dysentery  are  active  in  the  etiology,  al- 
though these  may  be  the  exciting  causes  acting  upon  a  liver  reduced  in 
vitality.  The  influence  of  immoderate  eating  (especially  of  animal  food), 
of  drinking  (especially  alcohol),  and  of  exposure  to  cold  and  fatigue  may 
not  be  overlooked.  These  induce  an  active  congestion  of  the  liver,  and 
on  account  of  the  consequent  increased  functional  demands  reduce  its 
vitality,  and  perhaps  in  this  way  render  the  liver  especially  vulnerable  to 
the  deleterious  influence  of  the  causes  of  malaria,  dysentery,  etc. 

Pathology. — ^Fhe  lesions  are  most  diverse;  they  include  combinations 
of  congestion,  cloudy  swelling,  focal  necroses,  and  the  vascular  and 
other  phenomena  of  inflammation.  The  lesions  vary  from  small  focal 
necroses  to  more  widespread,  if  not  general,  involvement  of  the  liver.  In 
slight  or  moderate  cases  the  appearances  of  the  liver  are  those  of  active 
45 


706  DISEASES  OF  THE  LIVER 

congestion  and  cloudy  swelling;  in  the  more  severe  cases  they  vary  [in 
grade  up  to  those  of  acute  yellow  atrophy.  In  some  (protracted)  cases, 
looked  upon  by  many  authors  as  a  subacute  form  of  acute  yellow  atrophy, 
there  is  more  or  less  compensatory  hyperplasia  of  the  liver  cells. 

Symptoms. — ^The  symptoms  virtually  are  those  of  active  congestion  of 
the  liver,  of  which  acute  hepatitis  is  only  an  advanced  stage.  Perhaps, 
although  not  necessarily,  the  symptoms  are  more  aggravated  in  the 
inflammatory  than  in  the  merely  congestive  disorder :  the  liver  pain  and 
tenderness  are  likely  to  be  more  marked;  nausea  and  vomiting  are  more 
common  and  usually  more  severe;  the  vomited  matter  partakes  of  the 
so-called  bilious  character  (greenish,  watery),  and  not  infrequently  con- 
tains blood — due  usually  to  violent  and  distressing  retching  that  provokes 
marked  thirst  and  ultimately  may  induce  marked  prostration  or  collapse; 
the  bowels  are  likely  to  be  constipated,  but  the  constipation  may  alternate 
with  a  foul,  ill-smelling  diarrhoea;  and  the  nervous  symptoms,  such  as 
headache,  restlessness,  irritability,  mental  depression,  disturbed  sleep, 
etc.,  are  usually  more  marked;  slight  jaundice  may  develop.  The 
liver  becomes  enlarged — sometimes  notably  enlarged.  In  malarial  cases 
the  spleen  also  becomes  enlarged.  Fever  (101°  to  103°  F.)  supervenes 
and  serves  to  distinguish  the  inflammatory  from  the  merely  congestive 
disorder. 

Diagnosis. — The  diagnosis  is  usually  apparent  from  the  etiological  fac- 
tors and  the  general  symptoms.  The  diagnostic  difficulties  pertain  to 
excluding  other  disorders,  such  as  the  different  forms  of  suppurative 
hepatitis,  and  in  the  presence  of  jaundice,  the  different  forms  of  toxic 
jaundice  and  acute  yellow  atrophy.  In  the  early  stages  it  is  frequently 
quite  impossible  to  differentiate  between  suppurative  and  non-suppu- 
rative  hepatitis;  in  some  cases  time  alone  will  bring  the  diagnosis.  In 
some  cases  the  one  is  a  later  stage  of  the  other,  and  the  suppuration  may 
not  be  susceptible  of  recognition  until  the  development  of  the  general 
phenomena  of  the  condition — irregular  chills,  fever,  sweats,  etc.  In 
acute  yellow  atrophy  the  constitutional  and  nervous  symptoms  are  more 
severe,  the  liver,  at  first  enlarged,  becomes  small,  the  duration  is  less,  and 
the  outcome  is  usually  death. 

Prognosis. — The  first  attack  of  acute  non-suppurative  hepatitis,  espe- 
cially as  observed  in  the  tropics,  usually  lasts  about  a  week  or  ten  days, 
and  results  in  recovery;  in  some  cases,  however,  suppuration  ensues. 
The  one  attack,  however,  predisposes  to  subsequent  attacks,  and  with 
each  recurrence  the  course  and  termination  are  less  favorable. 

Treatment.— The  treatment  of  acute  non-suppurative  hepatitis  (as 
well  as  of  its  antecedent  stage — active  congestion)  comprises  the  avoid- 
ance of  all  factors  likely  to  produce  it:  therefore,  wisdom  and  moderation 
in  eating  and  drinking;  in  the  tropics,  prophylaxis  of  the  infections 
known  to  involve  the  liver  (malaria,  dysentery,  etc.).  When  the  attack 
has  developed,  the  patient  should  go  to  bed  and  be  kept  there  until 
convalescence  is  complete.  The  guiding  principle  should  be  to  reduce 
the  functional  demands  upon  the  liver,  to  eliminate  all  factors  that 


SUPPURATIVE  HEPATITIS  707 

might  provoke  or  add  to  its  congestion,  and  to  reduce  any  existing  intes- 
tinal catarrh.  These  objects  are  best  achieved  by  dietary  regulations. 
The  diet  should  be  minimal  in  amount  and  absolutely  unirritating;  in 
general  it  should  consist  exclusively  of  milk,  which  should  be  given  at 
stated  (rather  long)  intervals,  and  well  diluted  with  lime  water,  Vichy, 
or  other  alkaline  water.  Wliey,  junket,  albumen-water,  strained  broths 
(without  seasoning),  barley  water,  calf's  foot  jelly,  etc.,  may  be  given 
later.  The  bowels  should  be  thoroughly  evacuated,  preferably  by  saline 
cathartics;  later,  by  calomel  or  blue  mass.  Ammonium  chloride  (60 
grains,  4  grams,  daily)  is  extensively  used  by  physicians  in  the  tropics, 
and  is  believed  to  control  the  congestion  and  prevent  inflammation  of 
the  liver,  to  relieve  the  intestinal  catarrh,  and  to  promote  the  elimination 
(by  diuresis)  of  retained  waste  products  (urea,  uric  acid,  etc.).  It  may 
be  given  in  the  early  stages,  when  it  should  be  combined  with  the  alkalies 
(alkaline  waters,  sodium  bicarbonate,  etc.),  or  later,  when  it  may  be  com- 
bined with  nitrohydrochloric  acid  (highly  extolled  in  hepatic  torpidity), 
nux  vomica,  or  strychnine,  and  a  bitter  tonic  (gentian,  columba,  quassia, 
etc.).  The  distressing  gastric  irritability  of  the  early  stage  of  some  cases 
may  be  controlled  by  sodium  bicarbonate,  bismuth  subnitrate,  and  car- 
bolic acid  or  creosote.  Intestinal  antiseptics  maybe  useful:  /5-naphthol, 
bismuth,  resorcin,  salol,  etc.  These  subject  to  exacerbations  or  recur- 
rences of  acute  congestion  of  the  liver  are  much  benefited  by  treatment 
at  such  spas  as  Carlsbad,  Marienbad,  Vichy,  Ems,  Saratoga,  etc. 

Suppurative  Hepatitis. — Suppurative  hepatitis  (abscess  of  the  liver) 
occurs  under  a  variety  of  circumstances  and  in  several  forms.  There  is 
some  justification  for  the  common  division  into  two  classes — the  large, 
single,  so-called  tropical  abscess,  and  the  small,  multiple,  non-tropical 
abscesses;  but  the  processes  are  not  altogether  different,  since  the  tropical 
abscess  may  be  double  instead  of  single,  and  even  when  single,  by  in- 
fecting adjacent  liver  tissue,  may  give  rise  to  the  development  of  many 
secondary  abscesses,  and  a  number  of  small  abscesses  by  peripheral 
extension  may  eventually  coalesce  and  give  rise  to  a  large  single  abscess. 

Etiology. — ^Abscess  of  the  liver  is  always  the  consequence  of  micro- 
organismal  infection;  the  microorganisms  are  various,  and  they  reach  the 
liver  by  one  of  several  pathways.  The  common  causative  microorganisms 
are  the  ordinary  staphylococci  and  streptococci.  Amoeba  coli  (Entamoeba 
dysenterise),  Bacillus  coli  communis.  Bacillus  pyogenes  foetidus,  Bacillus 
typhosus,  Bacillus  dysenterise.  Bacillus  pyocyaneus,  Diplococcus  pneu- 
moniae, Proteus  vulgaris,  Actinomyces  bovis,  etc.  The  infecting  agent 
or  agents  may  reach  the  liver  directly,  as  when,  in  consequence  of  trau- 
matism, bacteria  are  introduced  direcUy  into  the  liver,  or  when  they 
reach  the  liver  by  extension  of  disease  of  adjacent  organs;  or  the  infection 
may  be  carried  from  afar  by  the  blood  stream,  that  is,  by  the  portal  vein 
(dysentery,  and  other  causes  of  suppurative  pylephlebitis);  by  the 
hepatic  artery  (general  septicopyemic  processes);  by  the  hepatic  veins 
(retrograde  embolism);  by  the  biliary  ducts  (suppurative  cholangitis  and 
pericholangitis);  or  by  the  lymphatics. 


708  DISEASES  OF  THE  LIVER 

Pathology. — The  liver  is  enlarged,  swollen,  and  opaque,  and  presents 
the  ordinary  evidences  of  parenchymatous  degeneration  or  cloudy  swell- 
ing. In  addition,  in  the  cases  of  so-called  multiple  pyemic  abscesses,  it 
exhibits  a  number  of  variously  sized  abscesses — usually  small,  but  often 
coalescing  to  form  larger,  sometimes  many-chambered  cavities,  with  puru- 
lent contents.  The  so-called  single,  tropical,  or  amoebic  abscess  of  the 
liver  is  described  by  Manson  as  consisting  at  first  of  one  or  more  grayish, 
ill-defined,  anemic,  circular  patches,  half  to  one  inch  or  thereabouts  in 
diameter,  in  which  the  lobular  structure  of  the  liver  cannot  be  made  out. 
A  drop  or  two  of  reddish,  gummy  pus  may  be  expressed  from  the  necrotic 
patches.  Later,  the  centre  of  these  patches  liquefy,  and  distinct  but 
ragged  abscess  cavities  are  formed.  An  abscess  thus  commenced  ex- 
tends partly  by  molecular  breaking  down;  partly  by  more  massive 
necrosis  of  portions  of  its  wall;  partly  by  the  formation  of  additional 
foci  of  softening  in  the  neighborhood  and  subsequent  breaking  down  of 
the  intervening  septa.  These  may  involve  almost  if  not  an  entire  lobe, 
usually  the  right.  The  pus  is  usually  thick,  viscid,  chocolate-colored,  and 
streaked  with  blood,  and  often  contains  large  pieces  of  necrotic  liver 
tissue.  Entamoeba  dysenterise  may  be  found  in  more  than  one-half  of 
the  cases  (in  some  of  the  other  cases  in  the  wall  of  the  abscess").  The 
ordinary  pyogenic  organisms  are  rarely  encountered.  A  large  abscess 
may  consist  of  a  suppurating  hydatid  cyst. 

Symptoms. — Multiple  septicopyemic  abscesses,  whether  due  to  portal- 
vein,  hepatic-artery,  hepatic-vein,  or  biliary-duct  infection,  are  often  not 
recognized,  since  the  symptoms  of  the  primary  disorder  overshadow 
those  due  to  the  infection  of  the  liver.  In  some  cases,  however,  the 
spread  of  the  infection  to  the  liver  is  suggested  by  aggravation  of  the 
general  symptoms,  especially  chills  (or  chilliness),  fever,  sweats,  and  poly- 
nuclear  leukocytosis,  and  the  development  of  local  symptoms  referable 
to  the  liver.  These  consist  of  pain  in  the  region  of  the  liver,  perhaps 
referred  to  the  right  shoulder,  tenderness  about  the  liver,  a  mild  grade  of 
jaundice,  and  enlargement  of  the  liver.  The  enlargement  may  be 
nodular,  and  the  nodules  soft  and  perhaps  semifluctuating,  and  audible 
and  palpable  frictions  may  be  detected. 

The  so-called  tropical  abscess  of  the  liver,  although,  as  a  rule,  more 
readily  recognized,  may  be  very  indefinite  in  its  clinical  manifestations, 
and  escape  clinical  detection.  Generally,  the  onset  is  insidious:  some- 
times for  weeks  or  months  the  patient  may  complain  of  general  ill  health, 
malaise,  or  increasing  weakness — ^which  are  especially  significant  if  they 
constitute  part  of  the  poor  health  or  delayed  convalescence  following 
dysentery  or  other  intestinal  suppuration  or  ulceration.  In  some  cases 
the  onset  is  sudden,  attended  by  a  chill.  The  important  symptoms  are 
those  of  general  septicopyemia — chills,  fever,  sweats,  and  polynuclear 
leukocytosis,  to  which  local  signs  referable  to  the  liver  are  added. 
The  fever  may  be  quite  high  (104°  to  105°  F.),  and  distincUy  inter- 
mittent in  character.  Jaundice  occurs  in  about  16  per  cent,  of  the  cases, 
and  the  patient  may  develop  a  suggestive  icteroid  facial  aspect.     The 


CHRONIC  INTERSTITIAL  HEPATITIS  709 

liver  becomes  enlarged;  in  the  early  stages,  when  the  abscess  is  still 
well  within  the  substance  of  the  organ,  the  enlargement  may  be  tolerably 
uniform,  but  as  the  abscess  increases  in  size,  it  commonly  causes  dispro- 
portionate enlargement  upward,  usually  of  the  right  lobe — which  may 
assume  a  characteristic  dome  shape;  that  is,  the  upper  limit  of  hepatic 
dulness  rises  near  the  mammillary  line,  reaches  its  highest  point  (fourth 
or  third  rib)  near  the  midaxillary  line,  and  descends,  so  that  in  the  mid- 
scapular  hue  it  may  be  as  low  as  the  angle  of  the  scapula.  The  a:-rays 
may  disclose  the  extent  and  development  of  the  liver  enlargement  better 
than  percussion.  Nausea  and  vomiting  may  occur;  diarrhoea  is  rather 
common,  and  the  patient  emaciates.  Perforation  may  occur,  especially 
upward  through  the  diaphragm,  the  pleura,  and  the  lungs,  giving  rise  to 
a  so-called  hepatopulmonary  abscess;  the  expectoration  is  quite  charac- 
teristic and  has  been  likened  to  anchovy  sauce.  Rupture  may  occur  also 
into  the  gastro-intestinal  tract,  externally,  etc. 

Diagnosis. — The  diagnosis  is  often  difficult;  the  most  suggestive  signs 
consist  of  one  of  the  several  etiological  factors,  pain  in  the  region  of  the 
liver,  progressive  enlargement  and  tenderness  of  the  liver,  slight  jaundice, 
and  chills,  fever,  sweats,  and  polynuclear  leukocytosis.  Leukocytosis, 
however,  may  be  absent  in  slow-growing,  chronic,  and  well-encapsulated 
abscesses.  Malaria  may  be  excluded  by  a  history  of  antecedent  dysen- 
tery or  other  etiological  factor;  evening  rise  in  temperature  (that  of 
malaria  being  more  common  during  the  day);  disproportionate  enlarge- 
ment of  the  liver  as  compared  with  the  spleen  (the  reverse  being  the  case 
in  malaria);  absence  of  malarial  parasites  in  the  blood;  the  occurrence  of 
polynuclear  leukocytosis;  and  the  non-response  to  quinine.  Cholelithiasis 
and  Charcot's  biliary  intermittent  fever  may  be  excluded  by  the  absence 
of  a  history  of  cholecystitis,  cholelithiasis,  and  biliary  infection;  the 
absence  of  attacks  of  fever,  etc.,  separated  by  longer  or  shorter  periods 
of  apyrexia;  the  non-occurrence  of  increase  in  the  jaundice  after  each 
attack;  and  the  absence  of  serious  impairment  of  the  general  health 
despite  the  long  duration  of  the  disorder. 

Prognosis. — The  septicopyemia,  of  which  the  multiple  liver  abscesses 
are  merely  a  part,  is  almost  invariably  fatal.  Many  of  the  so-called 
single  or  tropical  abscesses  result  in  recovery  after  operation. 

Treatment. — The  treatment  of  the  multiple  septicopyemia  abscesses  is 
that  of  septicopyemia  in  general,  and  is  quite  as  ineffectual.  Perhaps 
treatment  by  specific  bacterins  may  yet  prove  of  service.  The  treatment 
of  the  large,  single  abscess  is  surgical  and  consists  of  thorough  evacua- 
tion and  drainage. 

CHRONIC  INTERSTITIAL  HEPATITIS:  THE  CIRRHOSES  OF  THE 

LIVER. 

Eliminating  from  consideration  cases  of  (1)  so-called  capsular  cir- 
rhosis (more  properly  called  perihepatitis  or  hepatic  capsulitis),  in  which 
the  liver  tissue  may  be  not  at  all  affected,  except  perhaps  secondarily  in 


710  DISEASES  OF  THE  LIVER 

consequence  of  compression  or  by  slight  ingrowth  of  new  connective 
tissue  from  the  capsule;  (2)  so-called  cardiac  cirrhosis  or  cardiac  liver, 
which  develops  in  consequence  of  long-standing  passive  congestion;  (3) 
syphilis  of  the  liver,  in  which  the  lesions  are  specific  and  peculiar  to  that 
infection;  and  (4)  circumscribed  or  focal  fibroses,  which  follow  limited 
inflammatory  and  degenerative  processes,  focal  necroses,  chronic  ob- 
struction of  the  biliary  ducts  (pericholangitis),  etc. — there  are  two  types 
of  chronic  diffuse  disorder  of  the  liver  attended  by  fibrosis,  to  which  the 
term  cirrhosis  may  be  limited.  One  of  these  disorders  is  very  common; 
it  is  usually  due  to  the  misuse  of  alcohol,  or  perhaps  other  poison  carried 
by  the  portal  circulation;  it  is  characterized  by  moderate  enlargement 
of  the  liver  (which  in  advanced  stages  may  become  reduced  in  size),  by 
newgrowth  of  connective  tissue,  especially  conspicuous  in  and  about  the 
portal  spaces,  by  phenomena  of  portal  obstruction  (notably  hematemesis 
and  ascites),  and  by  the  absence  or  unimportance  of  jaundice;  and  after 
the  development  of  symptoms  it  usually  runs  a  comparatively  short 
course  (Laennec's,  portal,  alcoholic,  atrophic,  or  multilobular  cirrhosis). 
The  second  of  these  disorders  is  rare;  it  is  of  unlinown  etiology;  it  is 
characterized  by  marked  and  persistent  enlargement  of  the  liver  and 
spleen,  by  chronic  jaundice,  by  periodic  attacks  of  abdominal  pain  and 
fever,  and  by  the  absence  of  manifestations  of  portal  obstruction  (notably 
ascites);  the  essential  lesion  is  a  radicular  cholangitis,  and  it  runs  a  com- 
paratively long  course  (Hanot's,  biliary,  hypertrophic,  or  monolobular 
cirrhosis. 

In  conditions  of  long-standing  obstruction  to  the  large  biliary  ducts, 
especially  from  gallstones,  more  or  less  fibrosis  develops  in  and  about  the 
smaller  biliary  ducts  in  the  liver,  and  may  spread  to  the  adjacent  liver 
tissue;  the  ensuing  induration  is  sometimes  spoken  of  as  obstructive 
biliary  cirrhosis  (more  properly  cholangitis  and  pericholangitis). 


PORTAL  CIRRHOSIS. 

Portal  cirrhosis  is  a  chronic  degenerative  and  inflammatory  disease  of 
the  liver  characterized  by  recurring  degeneration  and  regeneration  of  the 
hepatic  parenchyma  and  by  concomitant  and  consecutive  fibrosis  in  and 
about  the  interlobular  or  portal  spaces,  all  of  which  leads  ultimately  to 
obstruction  of  the  portal  circulation. 

Etiology. — Portal  cirrhosis  is  most  common  during  the  fifth  decade; 
although  it  is  by  no  means  rare  at  the  extremes  of  life.  A  number  of 
cases  occur  in  young  children,  in  whom  it  is  often  fatal  before  the  sixth 
year.  It  is  a  little  more  than  twice  as  common  in  men  as  in  women.  It 
is  undoubtedly  the  expression  of  the  activity  of  some  poison  or  poisons; 
these  are  various  in  nature,  and  may  reach  the  liver  by  way  of  the  portal 
vein,  the  hepatic  artery,  or  both.  In  the  great  majority  of  cases  it  follows 
addiction  to  alcohol,  especially  distilled  liquors  (whiskey,  gin,  brandy, 
etc.),  which  are  a  direct  poison  to  the  hepatic  parenchyma,  and  set  up 


PORTAL  CIRRHOSIS  711 

also  gastro-Intestinal  catarrh;  this  doubtless  results  iu  the  formation  of 
divers  autotoxins  that  may  injuriously  affect  the  liver.  A  special  form  of 
cirrhosis,  believed  to  be  due  to  highly  seasoned  food,  fermentative  dys- 
pepsia, etc.,  is  recognized  (Budd's  non-alcoholic  or  dyspeptic  cirrhosis). 
Infections  of  various  kinds,  such  as  malaria,  tuberculosis,  syphilis, 
uncinariasis,  distomatosis  (bilharziosis),  etc.,  may  be  followed  by  cir- 
rhosis, but  the  relationship  of  the  one  to  the  other  has  not  been  deter- 
mined; in  most  cases  the  necroses  and  fibroses  are  focal,  and  the  lesions 
are  not  really  cirrhotic  in  an  acceptable  sense.  Cirrhosis  is  also  asso- 
ciated with  a  type  of  hemolysis  (hemochromatosis). 

Pathology. — ^The  liver  varies  much  in  size  in  different  cases,  and  in 
the  same  case  at  different  times.  At  the  necropsy  it  may  be  very  small, 
weighing  only  980  grams  or  less;  or  it  may  be  very  large,  weighing  as 
much  as  4000  grams  or  more;  but  it  is  worthy  of  note  that  in  the  majority 
of  cases  at  the  necropsy  it  weighs  more  than  normally.  It  is  of 
increased  density,  increased  consistency,  and  lessened  elasticity.  The 
capsule  is  often  thickened  and  united  to  the  diaphragm  by  adhesions. 
The  surface  of  the  organ  is  distinctly  granular,  the  small  livers  more  so 
than  the  larger  ones:  grayish-white  depressions  alternate  with  pale, 
yellowish-brow^n,  sometimes  reddish-brown,  roundish  or  ovoid  elevations 
— the  so-called  coarsely  granular  or  "  hobnail  '^  liver.  The  cut  surface  of 
the  liver  reveals  interlacing  bands  of  whitish  or  grayish-white  fibrous  con- 
nective tissue  that  vary  somewhat  in  thickness,  pervade  the  entire  organ, 
and  are  continuous  with  the  grayish  opaque  depressions  on  the  surface 
of  the  liver.  These  bands  of  fibrous  connective  tissue,  which  obviously 
take  their  origin  in  the  periportal  spaces,  form  a  network  that  encloses  or 
surrounds  islets  of  liver  tissue  that  vary  in  size  from  that  of  a  pinpoint  to 
others  1  cm.  or  more  in  diameter;  the  larger  islets  are  made  up  of  several, 
often  eight,  ten,  or  more  liver  lobules  (or  remains  of  liver  lobules),  and  are 
pervaded  by  more  delicate  bands  of  connective  tissue  (so-called  multi- 
lobular cirrhosis).  The  liver  tissue  is  usually  pale  yellowish  in  color  or 
yellowish  brown  (/"/'pof,  yellowish);  occasionally  it  is  greenish  (from 
staining  with  bile),  or  reddish  or  brownish,  especially  in  the  centres  of  the 
lobules  (from  staining  with  blood  or  blood  pigment).  Microscopically, 
the  essential  lesions  consist  of  a  variable  degree  of  destroyed,  atrophic, 
hyperplastic,  and  rearranged  hepatic  parenchyma  and  of  newgrown 
fibrous  connective  tissue.  In  consequence  of  the  activity  of  some 
poison,  larger  or  smaller  areas  of  liver  cells  are  destroyed.  The  sur- 
viving cells  attempt  by  hyperplasia  to  compensate  for  the  cells  lost. 

The  continuing  activity  of  the  etiological  factor  leads  to  a  continuous 
or  recrudescing  death  of  certain  old  as  well  as  newly  formed  liver  cells, 
which  in  turn  is  followed  by  renewed  regeneration.  This  continuous 
degeneration  and  regeneration  ultimately  lead  to  complete  transforma- 
tion of  the  architecture  of  the  liver,  certain  lobules  are  entirely  destroyed, 
others  are  partly  or  completely  rearranged,  some  are  markedly  hyjier- 
plastic,  although  toleral)ly  well  arranged,  some  show  dendritic  and  other 
irregular  proliferation  (including  the  newly  formed,  so-called,  pseudo-bile 


712  DISEASES  OF  THE  LIVER 

ducts),  new  islets  of  liver  tissue  entirely  devoid  of  central  veins  appear, 
and,  what  is  especially  important,  new  circulatory  conditions — capillary 
and  venous — arise.  In  some  cases  there  is  considerable  fatty  infiltration 
of  the  liver  cells  (so-called  fatty  cirrhosis). 

Concurrent  with  the  degeneration  of  the  liver  cells,  the  interstitial  con- 
nective tissue  early  shows  more  or  less  round-cell  infiltration  and  other 
inflammatory  phenomena,  especially  in  and  about  the  portal  spaces; 
later  there  is  considerable  increase  in  the  amount  of  connective  tissue — 
in  part  the  result  of  organization  of  the  inflammatory  exudate,  in  part  a 
replacement  fibrosis  to  fill  up  potential  lacunse  left  by  destroyed  liver 
parenchyma,  in  part  the  tissue  originally  between  the  lobules  (the  con- 
nective tissue  of  Glisson's  capsule),  and  in  part  the  collapsed  and  other- 
wise altered  reticulum  of  certain  liver  lobules  the  cells  of  which  have  dis- 
appeared. This  newly  formed  connective  tissue  commonly  encloses 
rather  than  invades  the  liver  lobules;  sometimes  only  one  lobule  is  en- 
closed in  a  wide  band  of  connective  tissue,  sometimes  many  lobules — 
whence  the  designation  multilobular  cirrhosis.  There  is  usually  also 
considerable  increase  in  the  elastic  tissue.  This  fibrosis  ultimately  con- 
tracts, and  on  the  one  hand  causes  atrophic  changes  in  the  liver  cells,  and 
on  the  other,  obstruction  and  obliteration  of  some  of  the  interlobular  and 
intralobular  branches  of  the  portal  vein. 

The  spleen  becomes  enlarged  in  80  per  cent,  of  the  cases — the  conse- 
quence of  toxic  hyperplasia  and  of  passive  congestion.  The  gastro- 
intestinal tract  becomes  congested  and  chronically  inflamed,  and 
reveals  many  dilated  and  tortuous  veins,  which,  rupturing,  give  rise  to 
more  or  less  severe  hemorrhage.  The  kidneys  may  reveal  chronic  inter- 
stitial changes.  The  heart  and  the  pancreas  often  become  fibrosed. 
The  peritoneum  is  commonly  thickened,  and  not  infrequently  becomes 
the  seat  of  miliary  tuberculosis  (which  may  determine  the  final  lethal 
issue). 

Communications  between  the  portal  vein  and  the  systemic  circulation 
constitute  a  part  of  the  cirrhotic  process.  For  the  most  part  these  con- 
sist of  dilatations  of  normally  existing  anastomoses.  The  important  are 
(Rolleston):  (1)  A  general  anastomosis  between  the  veins  of  the  perito- 
neum and  those  of  the  abdominal  wall,  such  as  the  lumbar  and  renal. 
(2)  Those  around  or  in  connection  with  the  liver,  especially  the  para- 
umbilical veins  (Sappey)  of  the  falciform  ligament,  which  put  the  portal 
vein  in  communication  with  the  veins  of  the  anterior  abdominal  wall. 
This  anastomosis  may  show  itself  as  a  "caput  medusae,"  or  a  number 
of  dilated  veins  around  the  umbilicus.  This  must  be  distinguished  from 
the  more  marked  venous  anastomoses  which  result  from  obstruction  to 
the  passage  of  blood  along  the  inferior  vena  cava;  in  the  latter  the 
dilated  epigastric  and  mammary  veins  avoid  and  do  not  centre  around 
the  umbilicus.  (3)  Between  the  oesophageal  veins,  discharging  into  the 
azygos  veins  and  thence  into  the  superior  vena  cava,  on  the  one  hand, 
and  the  gastric  veins,  on  the  other.  These  veins  may  become  varicose 
(oesophageal  varices  or  piles),  and  are  a  common  cause  of  profuse  and 


PORTAL  CIRRHOSIS  713 

even  fatal  hemorrhage.  (4)  Between  the  superior  hemorrhoidal  veins, 
tributaries  of  the  inferior  mesenteric  vein,  and  the  middle  and  inferior 
hemorrhoidal  veins  which  open  into  the  internal  iliac  veins  (the  cause 
of  piles).  These  anastomoses  serve  both  a  useful  and  an  evil  purpose. 
On  the  one  hand,  as  long  as  the  collateral  circulation  is  efficient,  obstruc- 
tive symptoms  are  in  abeyance  and  the  disordered  liver  is  enabled  better 
to  perform  its  functions,  perhaps  enabled  to  regenerate,  whence  in  some 
cases  the  disease  remains  or  becomes  latent,  even  apparently  cured;  on 
the  other  hand,  (a)  the  dilated  veins  are  likely  to  rupture,  either  spon- 
taneously or  in  consequence  of  trauma,  and  lead  to  more  or  less  severe 
hemorrhage  (hematemesis,  enterorrhagia,  hematoma  of  the  abdominal 
wall  about  the  round  ligament);  and  (b)  much  of  the  blood  from  the 
gastro-intestinal  tract  being  thus  diverted  from  the  liver  to  the  general 
circulation,  conditions  somewhat  analogous  to  those  induced  by  the 
establishment  of  an  Eck's  fistula  (the  experimental  communication 
between  the  inferior  vena  cava  and  the  portal  vein),  supervene,  much 
of  the  products  of  digestion  is  not  brought  under  the  influence  of  the 
liver,  is  not  detoxified,  and  toxemia  ensues. 

Symptoms. — Cirrhosis  of  the  liver  may  remain  for  many  years  entirely 
latent;  indeed,  in  most  cases  the  lesions  in  the  liver  are  well  advanced 
before  the  onset  of  noteworthy  symptoms,  and  the  disease  not  infre- 
quendy  constitutes  an  unexpected  finding  at  the  necropsy  table.  Symp- 
tomatically,  the  disease  has  been  divided  into  the  preascitic  and  the 
ascitic  stage,  and  the  symptoms  are  described  as  being  (1)  obstructive, 
and  (2)  toxic.  As  long  as  the  collateral  circulation  is  efficient,  obstructive 
symptoms  are  in  abeyance. 

In  a  few  cases,  during  the  early  stages  of  the  development  of  the  dis- 
ease, phenomena  attributed  to  an  ill-defined,  so-called,  active  hyperemia 
of  the  liver  are  encountered;  that  is,  the  patient  complains  of  ill-defined 
or  vague  gastric  symptoms,  a  sense  of  weight  in  the  right  hypochon- 
drium,  perhaps  short  transitory  attacks  of  slight  fever,  slight  jaundice, 
and  actual  pain  in  the  region  of  the  liver;  and  the  liver  on  examination  is 
ound  to  be  enlarged  and  tender.  Such  attacks  may  last  several  days, 
disappear,  and  recur  at  longer  or  shorter  intervals. 

In  most  cases,  however,  the  early  symptoms  are  an  expression  of 
gastro-intestinal  catarrh — due  parUy  to  portal  congestion,  and  partly,  in 
many  cases  at  least,  to  chronic  alcoholism  with  acute  exacerbations. 
The  patient  complains  of  coated  tongue,  irregular  appetite,  flatulence, 
epigastric  distress,  especially  after  eating,  sometimes  of  nausea  and  vom- 
iting (often  in  the  morning,  and  usually  refera])le  to  alcoholism),  irregular 
action  of  the  bowels  (alternating  attacks  of  diarrhoea  and  constipation), 
or  habitual  constipation,  hemorrhoids,  etc.  The  increasing  portal 
obstruction  leads  to  increasing  congestion  of  the  gastro-intestinal  tract 
and  the  spleen,  the  congestion  being  doubtless  favored  by  Uie  absence  of 
valves  in  the  portal  tril)utaries.  This  congestion  reduces  tlie  functional 
capacity  of  the  stomach  and  intestines,  limiting  the  digestive  juices  and 
the  intestinal  secretions  (although  sometimes  increasing  the  mucus), 


714  DISEASES  OF  THE  LIVER 

reducing  the  absorbing  power  of  the  intestines,  and  often  inhibiting 
peristalsis.  Constipation  increases  and  tympanites  not  infrequently 
ensues,  and  both  may  become  of  high  grade  and  distressing;  occasional 
relief  is  sometimes  afforded  by  attacks  of  diarrhoea  which  relieve  the 
engorged  vessels.  These  phenomena,  while  not  diagnostic,  are  highly 
suggestive  of  the  disease,  especially  in  association  with  a  history  of  alco- 
holism. 

With  the  progress  of  the  disease  the  foregoing  evidences  of  derangement 
of  the  gastro-intestinal  tract  become  more  marked,  and  the  general  health 
becomes  impaired;  but  the  first  obtrusive  manifestation  of  the  disease, 
that  which  induces  the  patient  to  seek  medical  advice,  is  not  infrequently 
hematemesis  or  ascites. 

Hematemesis  is  an  initial  symptom  in  some  cases,  and  it  is  a  common 
event  some  time  in  the  course  of  most  cases.  Usually  it  occurs  early — 
while  the  liver  is  large;  when  not  the  initial  symptom,  it  is  often  the  first 
evidence  of  serious  disease  (33  per  cent,  of  the  cases) ;  but  it  may  occur 
late  in  the  disease,  that  is,  after  the  development  of  ascites  and  when  the 
liver  may  have  become  small.  With  the  hematemesis  there  is  usually 
blood  in  the  stools ;  but  blood  may  occur  in  the  stools  without  the  vom- 
iting of  blood,  especially  when  the  bleeding  into  the  stomach  is  slow,  and 
also  when,  as  is  not  uncommon,  the  source  of  the  blood  is  the  intestine 
or  the  rectum  or  hemorrhoids.  In  suspected  cases  of  cirrhosis  exami- 
nation of  the  stools  for  blood  (even  occult  blood)  should  be  early  resorted 
to.  Hemorrhage  from  or  into  other  parts  of  the  body  is  very  common, 
especially  epistaxis,  bleeding  from  the  gums,  larynx,  lungs,  and  into  the 
skin  and  mucous  membranes. 

Jaundice  is  not  a  part  of  portal  cirrhosis,  but  it  occurs  as  a  complication 
some  time  during  the  course  of  from  15  to  20  per  cent,  of  the  cases,  and  is 
usually  due  to  radicular  cholangitis. 

Toxic  symptoms  may  develop  at  any  time  during  the  course  of  the  dis- 
ease. Minor  symptoms  consist  of  restlessness,  weakness,  headache,  and 
itching;  the  itching  may  precede  or  be  unassociated  with  jaundice. 
More  severe  toxic  symptoms  comprise:  (1)  Apathy,  stupor,  and  coma; 
(2)  an  active  noisy  delirium;  and  (3)  convulsions,  paralyses,  contrac- 
tures, one  of  which  may  alternate  with  the  others. 

Cirrhosis  of  the  liver  may  be  afebrile  throughout  its  course;  during  the 
terminal  stage  the  temperature  maybe  subnormal;  but  attacks  of  fever 
(100°  to  102.5°  F.)  are  not  uncommon.  Sometimes  these  seem  to  be  part 
of  the  disease,  especially  when  it  advances  rapidly;  sometimes  they  are 
due  to  attacks  of  perihepatitis;  sometimes  they  are  due  to  complications. 
The  more  continuous  fever,  which  is  rather  common  late  in  the  disease,  is 
usually  due  to  tuberculosis — of  the  peritoneum,  lungs,  etc. 

Physical  Signs. — The  abdomen  is  more  or  less  markedly,  sometimes 
enormously,  distended,  and  is  in  notable  contrast  to  the  emaciated,  sub- 
icteroid  face  and  extremities.  The  abdominal  wall  reveals  enlarged  and 
varicose  veins  due  to  the  collateral  circulation.  The  liver  is  enlarged 
in  most  cases,  but  the  size  varies  considerably  in  different  cases  and  in  the 


PORTAL  CIRRHOSIS  715 

same  case  at  different  times.  Its  surface  may  be  distinctly  rough  to  pal- 
pation ("hobnails").  In  some  cases  late  in  the  course  of  the  disease  the 
liver  becomes  considerably  reduced  in  size.  The  spleen  is  usually  en- 
larged, palpable  two  or  three  fingers'  breadth  below  the  left  costal  margin. 
It  is  often  much  reduced  in  size  by  copious  gastro-intestinal  hemorrhage, 
severe  diarrhoea,  the  recurrence  of  ascites  after  tapping,  etc. 

Ascites  is  often  the  first  obtrusive  manifestation  that  leads  the  patient 
to  seek  medical  advice.  It  is  usually  a  late  event.  In  most  cases  the 
liver  is  larger  than  normally  at  the  time  of  development  of  the  ascites; 
but  a  large  liver  may  be  present  without  ascites;  a  small  liver  is  rarely 
found  without  ascites.  The  fluid  varies  in  amount — in  the  average  case 
from  4  to  8  or  10  liters,  but  it  may  be  as  much  as  20  liters.  It  is  due  to 
different  causes:  (1)  Portal  obstruction,  the  result  of  lessening  of  the 
portal  area  in  the  liver,  and  the  communication  of  the  hepatic-artery 
pressure  to  the  portal-vein  radicles;  (2)  a  complicating  perihepatitis  or 
more  widespread  peritonitis,  which  is  very  common  in  the  late  stages  of 
the  disease;  and  (3)  toxemia;  the  toxic  agent  is  not  known,  but  it  is 
believed  to  act  as  a  lymphagogue  on  the  peritoneum.  Varying  with  the 
•amount  of  fluid,  there  is  more  or  less  displacement  and  compression  of 
the  abdominal  and  thoracic  organs.  The  liver  and  the  diaphragm  are 
pushed  upward  and  cause  embarrassment  of  the  respiration  and  the 
heart  action,  and  not  infrequently  compression  and  consequent  con- 
gestion and  collapse,  and  perhaps  bronchopneumonia,  of  the  bases  of 
lungs,  particularly  the  right.  OEdema  is  common  late  in  the  disease, 
occasionally  it  may  precede  the  ascites,  in  which  event  it  is  toxic,  anemic, 
cardiac,  or  renal  in  origin.  The  blood  shows  the  changes  of  secondary 
anemia.  There  is  no  leukocytosis  unless  there  is  some  associated  infec- 
tion, which  is  not  rare.  Late  in  the  disease  evidences  of  considerable 
toxic  disorganization  of  the  blood  become  apparent — hydremia,  oedema, 
submucous  and  subcutaneous  hemorrhages,  etc.,  and  the  blood  findings 
rarely  may  simulate  those  of  pernicious  anemia. 

Complications. — ^Infections  of  various  kinds  are  common,  especially 
tuberculosis — of  the  lungs,  pleura,  or  peritoneum.  Tuberculous  perito- 
nitis is  very  common,  and  not  infrequently  determines  the  fatal  issue. 
It  is  suggested  by  fever,  tenderness  and  rigidity  of  the  abdominal  wall, 
perhaps  increase  in  the  amount  of  ascites  previously  stationary  (the 
fluid  may  become  hemorrhagic),  more  rapid  course,  and  speedy  death. 
Chronic  nephritis  occurs  in  about  one-half  of  the  cases. 

Diagnosis. — The  diagnosis  of  cii'rhosis  of  the  liver  in  the  early  stages  is 
not  always  an  easy  matter,  but  it  should  be  made  more  frequently  than 
it  is.  In  an  alcoholic  subject  with  dyspepsia,  an  enlarged  and  tender  liver 
suggests  the  diagnosis;  and  this  is  virtually  confirmed  if  to  these  there  be 
added  an  enlarged  spleen,  perhaps  recurring  attacks  of  pain  in  the  region 
of  the  liver,  with  slight  fever  or  slight  jaundice,  and  urobilinuria.  Later, 
when  hematemesis,  ascites,  the  hepatic  facies,  etc.,  have  developed,  the 
diagnosis  can  be  no  longer  in  doul^t.  When  the  liver  is  enlarged  and  there 
is  no  ascites,  one  must  exclude  other  causes  of  enlargement  of  the  liver, 


716  DISEASES  OF  THE  LIVER 

such  as  passive  congestion,  fatty  liver,  amyloid  liver,  leukemia,  malaria, 
and  syphilis.  The  occurrence  of  hematemesis  and  other  gastro-intestinal 
hemorrhages  necessitates  differentiation  from  gastric  and  duodenal  ulcer. 
When  ascites  has  developed,  one  must  exclude  other  causes  of  ascites, 
such  as  chronic  peritonitis  and  perihepatitis  (multiple  serositis),  throm- 
bosis of  the  portal  vein,  tumors  of  the  peritoneum  and  abdominal  organs, 
chronic  cardiac  disease,  and  cachectic  states.  Splenic  anemia  (Banti's 
disease)  also  must  be  considered  in  some  cases. 

There  are  several  special  types  of  portal  cirrhosis,  of  which  the  fol- 
lowing are  the  most  important:  (1)  Hemochromatosis  (bronzed  dia- 
betes), a  disorder  that  occurs  especially  in  male  adults,  and  is  characterized 
by  pigmentation  of  the  viscera  and  usually  also  of  the  skin;  cirrhosis  of 
the  liver;  and  fibrosis  of  the  pancreas,  with  involvement  of  the  islands 
of  Langerhans  and  consequent  diabetes.  The  pigmentation  is  usually 
attributed  to  increased  hemolysis.  The  noteworthy  symptoms  consist 
of  general  cutaneous  pigmentation  (suggesting  Addison's  disease), 
enlargement  of  the  liver  and  spleen,  and  the  ultimate  development  of 
diabetes.  Ascites  may  be  slight  or  absent;  hemorrhages  may  or  may 
not  occur,  but  death  may  result  from  rupture  of  oesophageal  varices. 
Diabetes,  when  it  supervenes,  is  severe  and  dominates  the  clinical  phe- 
nomena; acidosis  is  common  and  usually  leads  to  coma.  (2)  Malarial 
cirrhosis  is  said  by  those  of  experience  to  occur  in  the  tropics.  (3) 
Anthracotic  cirrhosis  is  very  rare.  (4)  Cirrhosis  in  children  is  usually  of 
the  portal  type.  The  symptoms  in  general  conform  to  those  in  the  adult. 
Hematemesis  is  less  common  (greater  distensibility  of  the  spleen  in  chil- 
dren), diarrhoea  and  slight  jaundice  are  more  common;  the  liver  and  the 
spleen  are  disproportionately  larger  than  in  adults  (relatively  greater 
volume  and  more  .ability  for  repair  in  children) ;  tuberculous  peritonitis 
is  common,  and  perhaps  accounts  for  most  of  the  ascites  and  the  not 
uncommon  fever. 

Prognosis. — The  prognosis  is  not  encouraging.  Ordinarily  the  disease 
runs  a  fatal  course  within  three  years  from  the  onset  of  symptoms. 
Doubtless  if  the  disease  were  earlier  recognized,  arrest  could  be  secured 
in  many  cases. 

Treatment. — The  only  trustworthy  treatment  is  based  upon  our  con- 
ception of  the  etiological  factors,  and  consists  essentially  in  the  avoidance 
of  all  causes  known  or  suspected  to  lead  to  the  disease.  Of  these,  the 
most  important  are  alcohol,  stimulating  and  highly  seasoned  foods,  foods 
likely  to  undergo  fermentation  in  the  intestinal  tract,  etc.,  all  of  which 
must  be  strictly  prohibited.  Milk  is  the  best  diet  for  a  month  or  six 
weeks,  and  from  time  to  time  alkaline  waters  may  be  added  to  it.  Later, 
one  may  give  also  eggs,  gruels,  cereals,  stewed  fruits,  fish,  and  green 
vegetables,  and  some  meat  from  time  to  time.  Good  results  sometimes 
follow  the  prolonged  use  of  the  iodides,  to  which  minute  doses  of  mercuric 
bichloride  may  be  added.  Nitrohydrochloric  acid  and  ammonium 
chloride  are  said  to  be  efficacious  in  some  cases.  Indigestion,  nausea, 
vomiting,  hematemesis,  constipation,  diarrhoea,  etc.,  are  to  be  treated 


BILIARY  CIRRHOSIS  717 

as  mentioned  under  those  headings  The  ascites,  if  not  relieved  by 
purgatives  (blue  mass  or  calomel  and  saline  cathartics),  diuretics  (alka- 
line diuretics,  theobromine,  spartein,  caffeine,  apocynum  cannabinum), 
the  Niemeyer  pill  (page  477),  and  a  dry  diet,  should  be  tapped.  The 
Talma-Morrison  operation  (omentopexy,  epiplopexy)  is  of  service  in 
carefully  selected  cases  early.  It  is  designed  to  relieve  the  portal  circu- 
lation, by  diverting  the  portal  blood  to  the  general  systemic  circulation 
through  the  medium  of  adhesions  set  up  between  the  liver,  the  omentum, 
and  the  parietal  peritoneum.  Associated  cardiac,  pulmonary,  or  renal 
disease,  repeated  tappings,  jaundice,  toxemia,  and  emaciation  are 
contra-indications  to  performing  operation. 


BILIARY  CIRRHOSIS. 

Biliary  cirrhosis  is  a  chronic  disorder  of  the  liver,  probably  infectious 
in  origin,  characterized  anatomically  by  radicular  cholangitis  and  con- 
nective-tissue hyperplasia,  and  clinically  by  chronic  jaundice  and  enlarge- 
ment of  the  liver  and  spleen. 

Etiology. — ^Biliary  cirrhosis  is  especially  common  during  adolescence 
and  early  adult  life;  most  cases  occur  between  the  twentieth  and  the 
thirtieth  year;  it  is  rare  after  the  fortieth  year,  but  it  is  quite  common  in 
children  (juvenile  type),  especially  in  India.  In  adults  about  85  per 
cent,  of  the  cases  occur  in  males;  in  children  it  is  equally  common  in 
the  two  sexes.     A  seeming  hereditary  influence  is  not  uncommon. 

The  exact  nature  of  the  disease  is  not  known.  Some,  but  not  all,  sub- 
jects are  alcoholic;  and,  on  the  whole,  it  seems  that  alcohol  plays  at  most 
a  minor  etiological  role.  In  the  cases  so  common  in  children  in  India 
it  is  not  in  any  way  an  etiological  factor.  In  other  cases,  perhaps,  it 
reduces  the  resisting  power  of  the  liver  and  thus  permits  of  the  more 
ready  operation  of  other  causes.  There  is  some  inconclusive  evidence 
that  the  disorder  is  the  consequence  of  a  general  blood  infection  that 
provokes  a  radicular  cholangitis;  but  no  definite  etiological  agent  has 
been  discovered.  An  infection  is  suggested  by  the  disorder  sometimes 
developing  after  infectious  diseases,  by  the  common  occurrence  of  attacks 
of  fever  and  leukocytosis,  and  the  not  rare  occurrence  of  general  lymph- 
node  enlargement. 

Pathology. — The  liver  is  enlarged  and  weighs  from  2000  to  4000  grams; 
its  shape  is  maintained,  its  consistency  increased,  and  its  elasticity  dimin- 
ished. The  surface  is  smooth  and  exhibits  very  fine  granulations  (in 
marked  contrast  to  the  coarse  granulations  of  portal  cirrhosis).  The 
liver  is  usually  dark  olive  green  in  color.  The  cut  surface  is  dark  greenish 
or  yellowish  green  in  color,  smooth,  or  very  slightly  granular  in  advanced 
cases;  usually  the  liver  lobules  are  more  or  less  obvious,  sometimes 
apparently  enlarged,  and  always  separated  by  widened  trabecuhe  of 
connective  tissue.  Microscopically,  the  obtrusive  feature  consists  of  an 
overgrowth  of  fibrous  connective  tissue,  which  occurs  in  delicate  fibrillar 


718  DISEASES  OF  THE  LIVER 

bands  that  not  only  course  between  the  lobules,  but  also  invade  the 
lobules  to  a  greater  or  less  extent  (so-called  monolobular,  unilobular, 
or  intralobular  cirrhosis).  In  some  advanced  cases  this  arrange- 
ment of  connective  tissue  is  not  so  regular.  The  basic  and  essential 
lesion  of  the  disorder,  however,  seems  to  be  a  radicular  cholangitis — 
which  is  disclosed  by  proliferation  and  desquamation  of  the  epithelium 
of  the  small  biliary  ducts.  This  leads  to  obstruction  and  consequent 
dilatation  of  the  biliary  canaliculi,  which  in  tiun  are  found  distended  with 
inspissated  bile  and  bile  thrombi.  Branching  columns  of  cells,  so- 
called  pseudobiliary  canaliculi,  in  and  about  the  periphery  of  the  liver 
lobules  (due  to  hyperplasia  of  the  liver  cells  as  well  as  of  preexisting 
ducts),  constitute  a  noteworthy  feature  of  the  lesions.  The  liver  cells 
exhibit  rather  inconspicuous  lesions,  but  acute  necrotic  autolytic  changes 
may  occur  at  any  time  and  determine  the  fatal  issue.  All  the  organs  of 
the  body  are  bile-stained.  The  spleen  is  enlarged,  and  commonly 
weighs  600  to  1500  grams  or  more;  in  children  it  may  be  as  large  as,  if 
not  larger  than,  the  liver.  The  lymph  nodes  in  the  portal  fissure  are 
enlarged,  oedematous,  and  congested,  but  they  exert  no  pressure  on  the 
biliary  ducts.  Occasionally  the  lymph  nodes  in  other  parts  of  the  body 
are  similarly,  although  less,  affected. 

Symptoms. — The  onset  of  the  disease  is  insidious;  for  a  long  time  there 
may  be  ill-defined  complaint  of  poor  health,  general  malaisC;  weakness, 
loss  of  flesh,  etc.;  or  there  maybe  a  sense  of  weight  or  distress,  perhaps 
actual  pain,  in  the  right  hypochondrium;  rarely  there  is  some  dyspepsia, 
coated  tongue,  poor  appetite,  perhaps  nausea,  diarrhoea,  etc.;  in  a  few 
cases  the  patient's  attention  may  be  first  directed  to  increase  in  the  size 
of  the  abdomen. 

In  the  great  majority  of  cases  the  first  obtrusive  symptom  is  jaundice. 
This  varies  in  degree  from  time  to  time,  periods  of  exacerbation  and  of 
regression  alternating;  but,  on  the  whole,  it  tends  to  increase  with  the 
progress  of  the  disease,  and  eventually  it  may  become  extreme,  usually 
greenish.  The  usual  concomitants  of  protracted  jaundice  are  seen; 
there  is  often  intense  itching^  eczema,  lichen,  sometimes  xanthelasma, 
etc.;  bleeding  from  the  nose  or  the  gums  or  other  mucous  membranes 
may  occur  from  time  to  time  for  a  long  period,  or  there  may  be  recurring 
attacks  of  purpura;  the  urine  shows  the  presence  of  bile  pigment.  The 
feces  also  contain  bile  pigments  and  may  be  very  dark  (in  contrast  to  the 
clay-colored  stools  of  obstructive  jaundice). 

In  addition,  the  disease  is  characterized  by  periodic  attacks  of  more 
or  less  severe  abdominal  pain,  especially  in  the  region  of  the  liver,  some- 
times attended  by  nausea  and  vomiting,  and  associated  with  fever, 
leukocytosis,  and  increase  of  the  jaundice.  These  attacks  occur  without 
regularity  and  without  demonstrable  cause,  and  they  last  variable  periods 
— ^several  days  to  several  weeks.  Usually  the  fever  does  not  go  above 
102°;  in  some  cases  there  is  slight  fever  for  long  periods.  Occasionally 
these  exacerbations  are  attended  by  the  nervous  and  other  phenomena  of 
icterus  gravis,  and  with  high  fever,  delirium,  coma,  etc.,  the  patient  may  die. 


TUMORS  OF  THE  LIVER  719 

Examination  reveals  the  liver  to  be  uniformly  enlarged,  reaching  some- 
times to  or  below  the  transumbilical  line;  it  presents  a  smooth  or  finely 
granular  surface.  The  spleen  also  is  enlarged,  much  more  so  than  in 
portal  cirrhosis.  It  is  said  that  the  enlargement  of  the  spleen  sometimes 
antedates  that  of  the  liver.  In  children  the  spleen  may  be  actually  larger 
and  heavier  than  the  liver — the  juvenile  type  of  biliary  cirrhosis  (cirrhose 
biliaire  splenomegalique  of  Gilbert  and  Fournier).,  The  blood  reveals 
oligocythemia,  leukocytosis  (increased  at  the  time  of  the  periodic  exacer- 
bations), and  diminished  coagulability. 

Rarely,  a  bulbous  enlargement  involving  the  soft  tissues  of  the  fingers 
and  toes  (Hippocratic  fingers)  occurs.  In  children,  growth  is  stunted, 
a  type  of  infantilism  develops,  and  the  onset  of  puberty  is  delayed. 

Diagnosis. — The  important  diagnostic  features  consist  of  the  occur- 
rence in  a  young,  usually  non-alcoholic  subject  of  chronic  progressive 
jaundice,  with  considerable  and  persistent  enlargement  of  the  liver  and 
spleen,  and  periodic  attacks  of  abdominal  pain,  fever,  and  leukocytosis, 
with  subsequent  increase  in  the  jaundice,  and  no  sign  of  cholelithiasis 
or  portal  obstruction.  There  should  be  no  difficulty  in  differentiating 
the  more  common  or  portal  cirrhosis — ^which  occurs,  as  a  rule,  in  older 
and  alcoholic  subjects  and  is  attended  by  more  marked  dyspeptic  symp- 
toms and  by  evidences  of  portal  obstruction  (dilatation  of  the  subcu- 
taneous veins  of  the  abdomen  and  ascites),  which  are  absent  in  biliary 
cirrhosis.  In  portal  cirrhosis^  hemorrhages,  especially  hematemesis, 
often  occur  early  and  are  commonly  profuse;  whereas  in  biliary  cirrhosis 
hemorrhages  are  usually  a  late  manifestation  and  small.  Jaundice 
sometimes  occurs  in  portal  cirrhosis,  but  it  is  a  complication  and  catarrhal 
in  nature;  in  biliary  cirrhosis  it  is  the  conspicuous  feature,  and,  although 
permanent,  it  is  not  associated  with  absence  of  bile  from  the  feces. 
Portal  cirrhosis  usually  runs  a  fatal  course  within  three  years  or  less; 
biliary  cirrhosis  not  uncommonly  lasts  from  five  to  ten  years  or  more. 

Prognosis. — The  outlook  as  regards  cure  is  hopeless,  but  the  disease 
may  last  for  many  years  and  the  general  health  may  be  well  maintained. 

Treatment. — ^The  treatment  is  largely  symptomatic.  The  hygienic 
conditions  should  be  the  best  obtainable.  The  diet  should  be  generous, 
but  dietetic  indiscretions,  alcohol,  etc.,  should  be  avoided.  The  prob- 
able infectious  nature  of  the  disorder  has  suggested  the  use  of  antiseptics, 
such  as  the  salicylates  and  hexamethylenamin,  which  are  eliminated 
with  the  bile;  apparent  improvement  has  been  reported  in  some  cases. 
Good  results  are  said  also  to  have  followed  drainage  of  the  gall-bladder 
and  the  biliary  ducts,  but  the  diagnoses  in  some  of  these  cases  is  open  to 
question. 

TUMORS  OF  THE  LIVER. 

Etiology. — Carcinoma  of  the  liver  may  l^e  primary  or  secondary  (to 
carcinoma  of  the  stomach,  pancreas,  intestine,  rectum,  female  genitalia, 
breast,  etc.).     A   primary   growth    is    very   rare,  the  secondary  being 


720  DISEASES  OF  THE  LIVER 

from  twenty-five  to  forty  times  as  common.  Both  occur  in  adult  life 
and  old  age.  The  primary  tumor  seems  to  be  slightly  more  common  in 
men  than  in  women,  the  secondary  slightly  more  common  in  women. 
Sarcoma  and  so-called  benign  growths  are  rare. 

Pathology. — Primary  carcinoma  appears  under  three  forms:  (1)  Nod- 
ular or  multiple  carcinoma  (65  per  cent,  of  the  cases) — numerous  grayish- 
white  nodules  scattered  throughout  the  liver;  (2)  massive  carcinoma  (23 
per  cent,  of  the  cases) — a  large  mass  occupying  almost,  if  not  quite,  an 
entire  lobe;  and  (3)  infiltrating  or  diffuse  carcinoma  (12  per  cent,  of  the 
cases) — so-called  cirrhosis  with  multiple  adenoma  or  carcinoma.  The 
growth  may  develop  from  the  hepatic  cells  or  the  biliary  epithelium.  In 
some  cases  the  sequence  of  events  is  represented  by  hepatic-cell  hyper- 
plasia, adenoma,  carcinoma.  Secondary  carcinoma  appears  as  multiple 
grayish  nodules  scattered  throughout  the  organ;  these  often  become 
necrotic,  softened,  and  umbilicated.  Primary  sarcoma  may  occur  as  a 
nodular  or  a  diffuse  growth;  secondary  sarcoma  is  usually  melanotic  in 
type,  and  follows  a  primary  growth  in  the  choroid  coat  of  the  eye. 

Symptoms. — ^The  symptoms  do  not  differ  notably  whether  the  growth  be 
primary  or  secondary,  and  carcinomatous  or  sarcomatous.  Usually  the 
onset  is  insidious;  the  patient  may  complain  of  general  ill  health,  languor, 
anemia,  emaciation,  etc.,  for  a  long  time  before  the  true  nature  of  the 
disorder  is  disclosed;  in  many  cases,  certainly  in  at  least  one-third  of  the 
cases  of  secondary  carcinoma,  the  actual  conditions  are  recognized  only 
at  autopsy.  In  some  cases,  symptoms  referable  to  the  primary  growth 
precede,  for  a  variable  time,  symptoms  significant  of  involvement  of  the 
liver;  but  in  a  considerable  number  of  cases,  carcinoma  of  the  stomach, 
rectum,  etc.,  may  be  for  a  long  time  latent,  or  the  symptoms  are  not 
obtrusive,  and  the  first  noteworthy  manifestations  may  be  referable  to 
the  liver.  In  a  small  percentage  of  cases  the  primary  growth  remains 
insignificant;  the  lesions  are  most  marked  in  the  liver,  and  the  symptoms 
almost,  if  not  exclusively,  hepatic.  They  consist  of  local  pain  and  dis- 
tress, jaundice,  ascites,  and  enlargement  of  the  liver.  The  local  discom- 
fort (or  sense  of  weight)  is  usually  proportionate  to  the  size  and  rapidity  of 
growth  of  the  carcinoma;  in  some  large  carcinomas,  however,  there  may 
be  no  actual  pain.  Jaundice  occurs  in  more  than  one-half  of  the  cases; 
it  varies  in  degree  at  first,  but  tends  to  increase  and  to  become  perma- 
nent. If  a  large  duct  becomes  obstructed,  the  stools  become  more  or  less 
pale,  perhaps  even  clay-colored.  Progressive  enlargement  of  the  liver  is 
the  phenomenon  that  determines  the  diagnosis.  The  enlargement  may 
be  moderate  or  great;  it  usually  involves  especially  the  right  lobe,  and 
it  is  characteristically  nodular — the  nodules  often  becoming  umbilicated 
(softening,  necrosis,  or  hemorrhage).  Ascites  occurs  in  about  20  per 
cent,  of  the  cases,  being  due  to  portal  obstruction  or  perihepatitis. 

In  the  course  of  time  secondary  nodules  may  develop  along  the  falci- 
form ligament  and  become  palpable  through  the  linea  alba  or  at  the 
umbilicus,  or  in  consequence  of  penetration  of  a  branch  of  the  hepatic 
vein,  more  distant  metastases  may  supervene  (lungs,  etc.);  the  patient 


CONGENITAL  OBLITERATION  OF   THE  BILIARY  DUCTS     721 

loses  strength,  and  becomes  anemic,  emaciated,  and  cachectic;  and  phe- 
nomena attributable  to  hepatic  insufficiency  (cholemia)  may  develop. 

Diagnosis. — ^The  diagnosis  is  not  always  possible,  especially  in  the  cases 
of  secondary  growths  in  which  the  deposits  are  few  in  number,  small  in 
size,  and  deep  within  the  substance  of  the  liver.  In  cases  in  which  a 
primary  growth  is  obvious  or  found  on  examination,  and  in  which 
there  is  persisting  severe  jaundice,  emaciation,  cachexia,  and  a  rapidly 
enlarging  and  nodular  liver,  the  diagnosis  can  often  be  made  on  inspec- 
tion alone,  especially  if  the  patient  be  made  to  take  a  deep  inspiration 
(whereupon  the  irregular  nodular  liver,  covered  only  by  a  thin  layer  of 
skin,  will  be  seen  to  descend).  In  the  differential  diagnosis  one  must 
exclude  tumors  of  adjacent  organs,  as  well  as  other  causes  of  enlarge- 
ment of  the  liver,  especially  cirrhosis,  syphilis,  abscess,  and  hydatid 
disease. 

Prognosis. — The  outlook  is  hopeless.  The  average  duration  of  life 
after  the  development  of  symptoms  referable  to  the  liver  is  seven  months. 

Treatment. — ^The  treatment  is  purely  palliative  and  symptomatic. 


DISEASES  OF  THE  GALL-BLADDER  AND 
BILIARY  DUCTS. 

CONGENITAL  OBLITERATION  OF  THE  BILIARY  DUCTS. 

Congenital  obliteration  of  the  biliary  ducts  is  a  disorder  characterized 
anatomically  by  obliteration  or  atresia  of  the  biliary  ducts  and  biliary 
cirrhosis  of  the  liver,  and  clinically  by  persistent  jaundice  and  so-called 
cholemia,  which  proceed  to  a  fatal  issue.  The  nature  of  the  disorder  has 
not  been  definitely  determined,  at  least  for  all  cases.  It  may  be  the  con- 
sequence of  an  anomaly  of  development,  or  it  may  be  due  to  syphilis,  to 
foetal  peritonitis  and  adhesions,  or  to  a  form  of  hepatic  cirrhosis  with 
descending  and  obliterative  cholangitis.  Clinically,  the  disorder  is  char- 
acterized by  jaundice,  which  is  present  at  or  develops  soon  after  birth, 
although  rarely  it  may  be  delayed  for  several  months;  it  becomes  pei^ 
sistent  and  intense.  The  stools  become  acholic,  if  not  acholic  from 
birth;  the  urine  contains  bile  pigments;  the  liver  and  the  spleen  are 
enlarged;  vomiting  often  ensues;  and  hemorrhages  occur  from  the 
umbilical  cord  and  into  the  subcutaneous  and  the  submucous  tissues. 
Gradually  the  infant  emaciates;  stupor,  coma,  or  convulsions  (cholemia) 
develop,  and  death  ensues.  The  course  of  the  disorder  is  rarely  less  than 
a  week;  usually  it  lasts  for  several  weeks  or  several  months.  The  more 
benign  icterus  neonatorum  may  be  distinguished  usually  by  the  presence 
of  bile  in  the  feces  and  by  the  less  marked  jaunflice  which  soon  fades. 
Syphilis  may  be  excluded  by  the  absence  of  a  history  of  syphilis  in  a 
parent,  the  absence  of  other  evidences  of  syphilis,  and  the  non-response 
to  antisyphilitic  treatment. 
46 


722    DISEASES  OF  THE  GALL-BLADDER  AND  BILIARY  DUCTS 

ACUTE  CATARRHAL  CHOLANGITIS, 

(Catarrhal  Jaundice.) 

Etiology. — ^Acute  catarrhal  cholangitis  is  a  common  disorder  in  young, 
especially  male,  adults,  although  it  occurs  at  all  ages.  It  is  usually  due 
to  dietetic  indiscretions,  such  as  eating  too  much  food,  or  indigestible 
or  tainted  food,  or  overindulgence  in  alcohol — ^which  set  up  a  duodenal 
catarrh,  which  spreads  to  the  biliary  papilla  and  causes  swelling  of  the 
mucosa  and  obstruction  to  the  free  flow  of  bile.  Similar  conditions 
sometimes  occur  in  infections  like  pneumonia,  typhoid  fever,  etc.,  in  passive 
congestion  of  the  duodenum,  etc.     Epidemics  are  sometimes  observed. 

Pathology. — The  lesions  consist  of  congestion,  swelling,  oedema,  and 
increased  production  of  mucus  at  the  lower  end  of  the  common  bile  duct 
and  of  the  duodenal  mucosa  adjacent  to  the  diverticulum  of  Vater.  In 
some  cases  the  swelling  itself  is  sufficient  to  obstruct  the  flow  of  bile,  but 
in  other  cases  a  plug  of  inspissated  tenacious  mucus  effectually  blocks 
the  diverticulum  of  Vater.  Eppinger  found  hyperplasia  of  the  lymphoid 
tissue  of  the  mucosa  of  that  part  of  the  common  biliary  duct  that  runs  in 
the  wall  of  the  intestine;  this  had  led  to  complete  occlusion  of  the  com- 
mon duct  and  dilatation  of  the  rest  of  the  biliary  system. 

Symptoms. — ^In  most  cases  the  early  symptoms  are  those  of  the  pro- 
voking gastro-intestinal  catarrh;  loss  of  appetite,  bad  taste  in  the  mouth, 
coated  tongue,  foul  breath,  epigastric  distress,  especially  after  eating, 
flatulence,  nausea,  and  perhaps  vomiting;  there  may  be  constipation,  or 
perhaps  diarrhoea  from  extension  of  the  intestinal  catarrh;  and  the  patient 
complains  of  headache,  vertigo,  mental  depression,  general  malaise,  etc. 
Rarely  there  is  an  acute  onset,  jaundice  being  the  first  symptom  noticed; 
but  in  most  cases  after  the  mentioned  symptoms  have  lasted  for  a  few 
days  to  a  week,  the  patient  notices,  or  his  attention  is  directed  to  the  fact, 
that  he  is  slightly  jaundiced.  The  jaundice  is  of  slow  and  insidious  onset, 
and  gradually  increases.  With  the  appearance  of  the  jaundice,  some- 
times before  there  is  any  obvious  jaundice,  the  stools  become  pale  in 
color  and  soon  are  devoid  of  bile  pigment;  the  urine  becomes  scanty, 
dark  in  color,  deposits  an  abundant  sediment,  and  shows  the  presence  of 
bile  pigments.  Usually  the  bile  pigments  can  be  detected  in  the  urine 
before  the  appearance  of  the  jaundice  in  the  sclerotics.  Pruritus  is 
often  marked;  sometimes  it  even  precedes  the  development  of  the  jaun- 
dice. The  itching  is  sometimes  so  extreme  as  to  induce  severe  eczema, 
in  consequence  of  uncontrollable  scratching.  The  pulse  usually  is 
slowed,  60  or  less  per  minute,  and  may  reveal  the  dicrotism  of  low 
vascular  tension. 

In  most  cases  neither  the  liver  nor  the  gall-bladder  is  palpably  enlarged 
or  tender.  Fever  (101°)  is  occasionally  present,  but  it  is  rarely  due 
directly  to  the  cholangitis,  except  in  the  epidemic  infectious  cases;  that 
which  sometimes  occurs  at  the  beginning  of  the  attack  and  lasts  a  day  or 
two  is  probably  due  to  the  gastro-enteritis ;  when  conspicuous  or  when 


ACUTE  CATARRHAL  CHOLANGITIS  723 

it  lasts  more  than  several  days,  it  suggests  some  one  of  the  types  of  toxic 
or  infectious  jaundice  (of  which,  in  reality,  it  may  be  a  mild  manifes- 
tation). 

At  the  end  of  about  a  week,  sometimes  not  until  later,  the  evidences  of 
gastro-intestinal  irritation  subside;  gradually  the  evidences  of  biliary 
obstruction  lessen,  bile  pigments  appear  in  the  feces,  and  disappear,  first 
from  the  urine  and  then  from  the  skin,  where,  however,  traces  may  be 
found  for  several  months.  Restoration  of  the  general  health  is  often 
much  delayed;  although  the  appetite  may  return  at  the  end  of  a  week 
or  two,  improvement  in  the  general  health  does  not  occur  until  the  bile 
pigments  begin  to  be  removed  from  the  tissues. 

Diagnosis. — In  most  cases  the  diagnosis  is  readily  made  from  the  youth 
of  the  patient,  an  antecedent  gastro-intestinal  catarrh  provoked  by  some 
more  or  less  obvious  cause,  and  the  absence  of  local  pain  and  of  serious 
involvement  of  the  general  health  (emaciation,  etc.);  the  diagnosis  is 
further  confirmed  by  the  benign  and  favorable  course  of  the  disorder, 
which  in  many  cases  definitely  determines  the  diagnosis.  Doubt  re- 
garding its  catarrhal  nature  should  always  be  awakened  by  the  occur- 
rence of  jaundice  in  a  middle-aged  or  elderly  person,  if  it  becomes  deep 
or  olive-tinted,  and  if  it  lasts  more  than  six  weeks;  this  is  much  more 
likely  to  be  due  to  impaction  of  a  gallstone  or  to  carcinoma  compressing 
the  common  duct. 

Prognosis. — ^As  a  rule,  the  prognosis  is  good;  the  disease  of  itself  does 
not  endanger  life,  and  recovery  is  usually  complete  and  lasting  at  the  end 
of  three  to  four  or  six  weeks. 

Treatment. — The  treatment  is  essentially  that  of  the  gastro-intestinal 
catarrh,  commonly  provocative  of  the  cholangitis.  The  diet  should  be 
reduced  and  for  several  days  should  consist  of  a  moderate  amount  of 
milk,  preferably  skimmed  milk,  or  broth.  The  natural  alkaline  waters 
are  serviceable;  but  alkalies,  especially  sodium  bicarbonate,  may  be 
added  to  ordinary  water.  The  bowels  should  be  opened  freely.  Custom 
sanctions  the  use  of  calomel,  which  may  be  given  in  a  single  large  dose  or 
in  repeated  small  doses  (a  blue  pill  is  equally  eflBcacious);  it  should  be 
followed  by  a  saline  aperient.  They  should  be  given  in  sufficient  dose  to 
cause  one  or  two  free  evacuations  daily;  more  are  undesirable.  Injec- 
tions into  the  rectum  of  cold  water  are  sometimes  very  efficacious  in 
stimulating  intestinal,  and  perhaps  also  gall-bladder,  peristalsis.  As  the 
biliary  stasis  begins  to  subside,  dilute  nitrohydrochloric  acid  and  bitter 
tonics  render  excellent  service.  Excessive  flatulence  is  sometimes  dis- 
tressing; it  may  be  relieved  by  the  use  of  bismuth  salicylate,  soda-mint, 
aromatic  spirit  of  ammonia,  chloroform  water,  and  antifermentatives; 
magnesia  or  rhu})arb  with  sodium  bicarbonate  and  charcoal  also  are  of 
much  service,  and  relieve  the  constipation.  The  pruritus  may  be  relieved 
by  cold  sponging,  or  a  carbolic-acid  lotion  (1  to  40),  or  the  internal  use  of 
the  bromides. 


724     DISEASES  OF  THE  GALL-BLADDER   AND  BILIARY  DUCTS 


SUPPURATIVE  CHOLANGITIS. 

Etiology. — Suppurative  cholangitis  results  from  virulent  bacterial  infec- 
tion of  the  biliary  ducts.  The  common  infectious  agents  are  Bacillus  coli 
communis,  staphylococci,  streptococci,  pneumococci,  Bacillus  typhosus, 
Bacillus  aerogenes  capsulatus,  etc.  The  infection  may  occur  by  way  of 
the  portal  or  the  general  systemic  circulation  (descending  infection),  or 
by  way  of  the  duodenum  and  the  diverticulum  of  Vater  (ascending 
infection).  In  the  great  majority  of  cases  there  is  some  local  disease  of 
the  biliary  tract,  which  acts  as  an  almost  necessary  predisposing  factor; 
this  comprises  all  disorders  that  interfere  with  the  free  circulation  of  the 
bile  (that  is,  cause  stagnation),  and  reduce  the  resistance  of  the  biliary 
ducts,  especially  gallstones  and  tumors  obstructing  the  duct.  Usually 
there  is  associated  disease  of  the  gall-bladder. 

Pathology. — The  biliary  ducts  are  dilated,  congested,  oedematous,  and 
filled  with  purulent  material,  usually  bile-stained;  and  about  the  terminal 
branches  of  the  biliary  ducts  within  the  liver  there  are  few  or  many,  small 
or  moderately  sized,  abscesses.  The  liver  tissue  is  the  seat  of  cloudy 
swelling  and  more  or  less  necrosis. 

Symptoms. — Usually  there  is  a  history  of  antecedent  cholelithiasis  or 
vague  symptoms  that  may  be  interpreted  as  due  to  gallstones;  in  other 
cases  there  is  some  impairment  of  the  general  health,  which,  in  the  light 
of  subsequent  events,  may  be  ascribed  to  malignant  disease;  in  still  other 
cases  the  patient  suffers  from,  or  has  recendy  suffered  from,  some  general 
infection,  such  as  tj-phoid  fever,  pneumonia,  etc.  The  onset  is  often 
insidious;  occasionally  the  first  noteworthy  symptom  is  slight  jaundice, 
but  in  perhaps  most  cases,  especially  in  cases  in  which  there  has  been 
antecedent  jaundice  due  to  other  causes,  the  onset  of  the  disease  is  an- 
nounced by  constitutional  phenomena,  such  as  chills,  fever,  and  sweats. 
These  are  usually  severe,  more  or  less  frequently  repeated  at  irregular 
intervals,  and  soon  lead  to  considerable  impairment  of  the  general 
nutrition,  emaciation,  loss  of  appetite,  nausea,  perhaps  vomiting,  diar- 
rhoea, etc.;  variable  afebrile  periods,  however,  are  not  uncommon. 
Jaundice  is  almost  always  present,  but  it  is  variable  in  degree;  usually 
it  is  slight  or  moderate  only,  except  in  cases  in  which  the  cholangitis  is 
associated  with  other  conditions  that  cause  intense  jaundice.  There 
may  be  dull  aching  or  discomfort  in  the  region  of  the  liver  (tension  of 
the  liver  capsule);  now  and  then  there  is  more  severe  pain  due  to  acute 
cholecystitis,  cholelithiasis,  obstruction  of  the  ducts  by  tumors  or  worms, 
perihepatitis,  peritonitis,  etc.  The  liver  is  enlarged  and  usually  con- 
tinues to  enlarge  under  observation.  Usually  the  gall-l)ladder  also  is 
enlarged  and  tender  (acute  cholecystitis).  The  spleen  may  be  enlarged. 
Examination  of  the  blood  reveals  polynuclear  leukocytosis,  more  marked 
during  and  just  after  the  febrile  periods;  sometimes  it  is  absent  during 
the  afebrile  periods. 


CHRONIC  CATARRHAL  CHOLANGITIS  725 

Diagnosis. — The  diagnosis  is  usually  apparent  from  a  history  of  ante- 
cedent gallstones  or  other  disorder  of  the  biliary  tract,  or  of  typhoid  fever 
or  other  infection,  and  the  development  of  chills,  fever,  sweats,  jaundice, 
local  pain,  progressive  enlargement  of  the  liver,  perhaps  also  of  the 
gall-bladder  and  spleen,  and  leukocytosis. 

Prognosis. — The  prognosis  is  bad,  but  may  be  improved  by  thorough 
drainage  of  the  gall-bladder  and  ducts  undertaken  early. 

Treatment. — Attempts  should  be  made  to  prevent  the  disorder  by 
thorough  and  efficient  treatment  of  all  forms  and  grades  of  biliary  infec- 
tion (including  gallstones).  \Mien  suppurative  cholangitis  has  devel- 
oped, the  treatment  is  essentially  surgical,  and  consists  of  the  establish- 
ment of  free  drainage.  The  only  available  medical  treatment  comprises 
the  use  of  antiseptics,  such  as  the  salicylates,  hexamethylenamin,  and 
other  remedies,  to  disinfect  the  biliary  tract  and  promote  the  free  flow  of 
bile. 

CHRONIC  CATARRHAL  CHOLANGITIS. 

Etiology.- — Chronic  catarrhal  cholangitis  may  result  from  repeated 
attacks  of  acute  catarrh,  or  from  a  low  grade  chronic  infection.  Usually 
it  is  found  in  association  with  gallstones;  but  it  may  be  found  also  in 
chronic  duodenal  catarrh,  and  in  obstruction  due  to  tumors  or  strictures 
of  the  ducts. 

Pathology. — The  lesions  of  chronic  catarrhal  cholangitis  (of  the  larger 
ducts)  consist  of  congestion  and  swelling  of  the  mucosa,  increased  pro- 
duction of  mucus,  round-cell  infiltration,  and  proliferation  of  the  sub- 
mucosa  and  muscularis,  wuth  the  production  of  new  fibrous  connective 
tissue;  these  lead  to  thickening  and  induration  of  the  walls  of  the  ducts 
and  to  pericholangitis.  There  may  be  partial  or  complete  obstruction 
of  the  ducts.  In  the  event  of  complete  obstruction,  the  ducts  become 
enormously  dilated  (up  to  the  size  of  a  thumb  or  larger);  the  gall- 
bladder and  some  of  the  intrahepatic  ducts  also  become  dilated.  The 
contents  of  the  biliary  tract  is  usually  a  clear,  almost  colorless,  often 
sterile  mucus;  when  the  mucus  is  sterile,  the  mucosa  of  the  biliary  tract 
is  usually  quite  smooth.  In  the  event  of  incomplete  obstruction,  the 
ducts,  and  especially  the  gall-bladder,  are  less  dilated,  the  contents 
are  usually  turbid  and  often  contain  bacteria,  and  the  mucosa  may  be 
more  or  less  ulcerated. 

Symptoms. — The  symptoms  are  those  of  chronic  relapsing  jaundice. 
Rarely,  this  may  represent  a  direct  continuation  of  an  acute  catarrhal 
jaundice,  being  more  insidious  in  onset,  and  subject  to  exacerbations  and 
remissions.  "^I'hc  attending  phenomena  are  those  of  acute  catarrhal 
cholangitis — prolonged.  In  the  cases  of  comph^te  obstruction,  the  con- 
tents of  tlic  l)iliary  tract  being  sterile,  there  is  usually  no  fever,  and 
remissions  in  the  jaundice  are  slight.  In  the  cases  of  incomplete  ob- 
struction, remissions  in  the  jaundice  are  more  marked,  and  the  contents 
of  the  biliary  tract  being  infected,  attacks  of  chill,  fever,  and  sweats  are 


726     DISEASES  OF  THE  GALL-BLADDER  AND  BILIARY  DUCTS 

common.  These  attacks  by  no  means  warrant  a  diagnosis  of  suppura- 
tion of  the  biliary  tract,  although  they  are  evidences  of  infection.  This 
chronic  catarrhal  cholangitis  may  lead  to  suppurative  cholangitis  (of 
which  it  is  often  only  a  minor  manifestation),  acute  infectious  jaundice, 
acute  yellow  atrophy  of  the  liver,  etc. 

Diagnosis. — In  cases  of  persisting  jaundice  that  begin  seemingly  as 
acute  catarrhal  cholangitis,  one  must  attempt  to  eliminate  cholelithiasis 
and  malignant  disease  obstructing  the  ducts.  Often  it  is  quite  impos- 
sible to  differentiate  non-calculous  from  calculous  cholangitis  with  a 
gallstone  in  the  common  duct;  attempts  to  do  so  are  usually  only  of 
academic  interest.  A  history  of  antecedent  gallstone  colic  is  suggestive, 
but  by  no  means  conclusive.  Hypertrophic  biliary  cirrhosis  may  be 
eliminated  by  the  absence  of  marked  enlargement  of  the  liver  and  spleen. 

Prognosis. — ^The  prognosis  is  dependent  upon  the  associated  lesions. 

Treatment. — The  treatment  is  essentially  that  of  acute  catarrhal  cho- 
langitis. In  protracted  cases  operation  should  be  undertaken  with  a 
view  to  drain  the  biliary  ducts;  this  is  the  more  urgently  demanded  in 
view  of  the  impossibility  often  of  excluding  obstruction  due  to  a  gallstone. 


ACUTE  CHOLECYSTITIS. 

Etiology. — It  is  largely  artifice  that  leads  to  a  distinction  between 
cholangitis  and  cholecystitis;  the  one  like  the  other  is  an  expression  of 
infection  of  the  biliary  tract.  In  some  cases  the  infection  may  remain 
confined  to  the  ducts  or  the  gall-bladder.  In  other  cases,  developing  in 
the  one  or  the  other,  the  process  may  extend  to  that  not  primarily  in- 
volved; and  it  may  persist  in  the  gall-bladder  and  subside  in  the  ducts, 
or  vice  versa. 

Acute  cholecystitis  may  result  from  the  microorganisms  already  men- 
tioned as  causative  of  acute  cholangitis.  Special  importance  attaches 
to  Bacillus  typhosus.  Bacillus  coli,  and  the  pyococci.  These  usually 
reach  the  gall-bladder  by  way  of  the  portal  circulation,  less  commonly 
by  way  of  the  general  systemic  circulation,  and  sometimes,  perhaps,  by 
way  of  the  diverticulum  of  Vater.  Important  contributing  factors  com- 
prise those  that  reduce  the  vitality  and  resisting  power  of  the  gall-bladder 
and  those  that  interfere  with  the  free  flow  of  bile. 

Significance  attaches  to  the  fact  that  the  gall-bladder  once  having 
become  infected,  may  harbor  the  invading  bacteria  for  many  years 
(so-called  "chronic  carriers,"  especially  important  in  relation  to  typhoid 
fever);  these  bacteria  being  continuously  or  intermittently  discharged 
from  the  gall-bladder,  are  often  the  source  of  epidemics. 

Pathology. — ^Various  types  of  acute  cholecystitis  may  be  differentiated 
— catarrhal,  suppurative,  phlegmonous,  gangrenous,  and  membranous. 
Properly  interpreted,  these  are  varying  manifestations  of  the  one  process 
(an  infection),  which  results  from  variations  in  the  virulence  of  the  in- 
fecting agent,  in  the  local  and  general  resistance,  and  in  the  freedom  of 


ACUTE  CHOLECYSTITIS  727 

the  circulation  of  the  bile;  they  differ  in  degree  rather  than  in  nature, 
and  pass  sometimes  almost  imperceptibly  the  one  into  the  other.  In 
the  mild  cases  the  gall-bladder  is  distended  and  tense;  the  wall  is  swollen, 
cedematous,  and  softened,  and  the  mucosa  is,  in  addition,  congested  and 
covered  with  a  layer  of  mucus,  perhaps  bile-stained;  in  many  cases  the 
inflammatory  phenomena  invade  also  the  peritoneal  covering,  which  then 
is  dull,  lustreless,  or  opaque,  and  covered  with  a  thin  layer  of  fibrin, 
which  may  serve  to  unite  the  gall-bladder  to  adjacent  structures.  The 
cystic  duct  usually  is  partially  obstructed  from  swelling  of  the  mucosa; 
sometimes  it  is  completely  obstructed,  but  usually  only  in  the  event  of 
recurrent  attacks  of  inflammation  or  of  cicatrization  of  ulcerations.  The 
contents  of  the  gall-bladder  usually  consist  of  turbid  bile.  Gallstones 
may  be  encountered,  especially  in  recurrent  attacks;  but  usually  not  in 
cases  of  less  than  four  to  six  months'  duration  (during  most  of  which  time 
the  infection  may  be  latent).  The  adjacent  lymph  nodes,  especially 
those  in  the  portal  fissure,  are  usually  enlarged  and  softened.  The  more 
severe  cases  exhibit  all  gradations  to  severe  suppurative,  ulcerative,  and 
gangrenous  lesions,  with  more  or  less  suppurative  contents  (acute  and 
chronic  empyema  of  the  gall-bladder). 

Symptoms. — Initial  nausea  and  vomiting,  fever,  pain,  and  tenderness 
in  the  region  of  the  gall-bladder,  rigidity  of  the  overlying  abdominal 
muscles,  and  an  enlarged  and  tender  gall-bladder  constitute  the  impor- 
tant clinical  manifestations  of  acute  cholecystitis.  These  may  be  of 
sudden  or  rather  insidious  onset.  The  nausea  and  vomiting  are  usually 
moderate  in  grade  and  soon  subside,  except  in  the  event  of  perichole- 
cystic  or  more  general  peritonitis  and  concomitant  paresis  of  the  intestine. 
In  catarrhal  cholecystitis  the  fever  is  slight  and  lasts  only  a  short  time; 
in  the  cases  complicating  some  general  infection  there  may  be  little  if  any 
added,  fever,  but  if  occurring,  for  instance,  during  convalescence  from 
typhoid  fever,  the  onset  of  the  cholecystitis  is  often  announced  by 
fever,  which  may  be  high.  The  pain  usually  occurs  first  in  the  epigas- 
trium, sometimes  directly  in  the  midline,  and  later  becomes  more  localized 
to  the  right  hypochondrium;  it  varies  much  in  character,  and  may  be 
colicky.  Jaundice  is  not  a  part  of  cholecystitis,  but  it  may  occur  in  the 
event  of  complicating  cholecystitis,  or  obstruction  of  the  common  duct. 

The  consequences  of  acute  cholecystitis  are  many:  Persistent  mild 
infection  (chronic  bacillus  cairiers)  with  acute  exacerbations;  gall- 
stones; pericholecystic  adhesions;  or  progression  to  severe  types  of  the 
affection,  with  ulceration  and  perforation  (sudden  increase  of  the  local 
pain,  more  or  less  collapse,  increased  pulse  rate,  and  increase  of  the 
local  abdominal  symptoms — that  is,  peritonitis). 

Diagnosis. — The  diagnosis  of  acute  cholecystitis  presents  no  serious 
difficulties  in  the  great  majority  of  cases;  nausea  and  vomiting,  pain  and 
tenderness  in  the  region  of  the  gall-bladder,  rigidity  of  the  overlying 
abdominal  muscles,  and  an  enlarged  and  tender  gall-bladder  constitute  a 
complex  of  symptoms  that  can  scarcely  be  attributed  to  anything  else. 
The  phenomena  of  gallstone  colic  are  properly  attributable  in  most  cases 


728     DISEASES  OF  THE  GALL-BLADDER  AND  BILIARY  DUCTS 

to  an  acute  cholecystitis,  perhaps  acute  exacerbation  of  a  chronic  chole- 
cystitis. In  the  severe  cases,  with  well-marked  peritonitis  of  the  upper 
abdomen,  one  must  exclude  other  causes  of  such  peritonitis,  especially 
perforated  gastric  or  duodenal  ulcer,  acute  pancreatitis,  etc. 

Prognosis. — In  the  majority  of  cases  the  prognosis  is  good,  the 
process  tending  to  subside,  under  appropriate  treatment,  within  ten  days 
or  a  fortnight.  Sequels,  especially  gallstones  and  adhesions,  however, 
are  almost  certain  to  occur,  so  that  the  subsequent  outlook  is  not  the  best; 
in  other  cases  a  low-grade  infection  may  persist  and  the  patient  become 
a  subject  of  chronic  infection  and  recurring  attacks  of  cholecystitis.  In 
the  more  severe  forms,  suppurative,  phlegmonous,  and  gangrenous 
cholecystitis,  the  tendency  toward  spontaneous  cure  is  slight;  in  this 
event  the  prognosis  is  grave,  since  not  only  are  the  lesions  of  the  gall- 
bladder serious  in  themselves,  but  a  localized  abscess  or  general  peri- 
tonitis may  ensue  and  a  fatal  issue  result,  unless  recourse  is  had  to 
surgical  intervention. 

Treatment. — ^The  treatment  is  that  recommended  for  gallstone  colic 
(page  735),  which  virtually  is  an  attack  of  more  or  less  acute  cholecystitis. 
In  the  severe,  suppurative,  and  gangrenous  cases,  surgical  intervention  is 
called  for. 

CHRONIC  CHOLECYSTITIS. 

Chronic  cholecystitis  may  be  the  residual  manifestations  of  an  acute 
cholecystitis,  or  the  process  may  be  chronic  from  the  beginning.  The 
etiological  factors,  therefore,  are  those  of  acute  cholecystitis,  the  chron- 
icity  of  the  process  being  a  manifestation  of  lingering  infection,  or  the 
consequence  of  a  low-grade  infection  with  almost,  but  not  quite,  sufficient 
biliary  drainage.  In  the  great  majority  of  cases  the  condition  is  asso- 
ciated with  gallstones  the  one  process  sustaining  the  other;  that  is, 
most  cases  are  calculous.  In  a  few  cases  the  lesions  extend  throughout 
the  biliary  tract;  that  is,  cholangitis  and  cholecystitis  are  associated. 
In  the  absence  of  gallstones,  the  lesions  may  be  catarrhal  and  the  gall- 
bladder may  be  distended.  In  most  long-standing  cases  the  gall- 
bladder becomes  reduced  in  size,  thickened,  and  sclerotic;  it  may  be 
represented  by  a  mass  of  thickened,  contracted  connective  tissue,  perhaps 
enclosing  gallstones.  Symptomatically,  the  condition  cannot  be  dis- 
tinguished with  certainty  from  cholelithiasis. 


CHOLELITHIASIS. 

(Gallstones. ) 

Etiology. — Cholelithiasis  is  an  exceedingly  common  condition,  being 
found  at  the  necropsy  in  from  5  to  10  per  cent,  of  subjects  dead  from  all 
causes.  It  occurs  at  all  ages,  but  the  incidence  increases  progressively 
with  advancing  years;  75  per  cent,  or  more  of  the  cases  are  found  in 


CHOLELITHIASIS  729 

persons  over  forty  years  of  age,  and  less  than  1  per  cent,  in  those  under 
twenty  years;  but  this  age  incidence  does  not  correctly  represent  the 
time  of  the  formation  of  gallstones,  since  in  many  cases,  having  formed, 
they  remain  latent  for  years  and  are  found  only  when  the  subject  dies  at  a 
more  advanced  age  from  the  consequences  of  gallstones  or  other  causes. 
Doubtless,  therefore,  many,  if  not  most,  gallstones  are  formed  in  early 
adult  life,  before  the  fortieth  year,  corresponding  with  the  period  of 
greatest  frequency  of  typhoid  and  other  infections.  They  are  more 
common  in  women  than  in  men  (the  ratio  being  variously  stated  as  5  to 
1  (Schroeder),  to  4  to  3  (Rolleston).  The  essential  cause  is  a  low-grade 
catarrhal  inflammation  of  the  biliary  tract,  which  is  usually  provoked 
by  the  typhoid  or  colon  bacilli,  or  attenuated  pyococci;  a  contributing 
factor  is  some  obstruction  to  the  free  flow  of  bile.  This  ensues  in  con- 
ditions of  biliary  obstruction,  and  is  promoted  by  a  sedentary  life,  obesity, 
muscular  inactivity,  lax  abdominal  muscles  (as  after  pregnancy),  hepato- 
ptosis,  etc.  Whether  a  third  factor,  disorders  of  metabolism  (disorders 
dependent  upon  diet),  is  active,  has  not  been  determined  with  certainty. 
Pathology. — Gallstones  may  be  found  in  any  part  of  the  biliary  tract, 
but  they  are  most  common  in  the  gall-bladder.  There  may  be  one  or 
many  stones;  they  vary  much  in  size — from  the  smallest  particle  (biliary 
sand  or  gravel)  to  those  larger  than  a  normal  gall-bladder;  and  they 
vary  in  shape.  Single  stones  are  usually  ovoid,  spheroid,  or  pear-shaped; 
multiple  stones  are  usually  cuboidal  or  polyhedral,  and  are  faceted 
(from  mutual  compression).  Stones  within  the  intrahepatic  ducts  con- 
form to  the  ducts  in  shape,  and  are  ovoid  or  cylindrical;  occasionally 
they  are  branched,  as  are  the  ducts.  Although  usually  smooth,  the  sur- 
face of  gallstones  may  be  rough,  irregular,  or  nodular  (mulberry  cal- 
culus). In  consequence  of  the  bacterial  infection  of  the  biliary  tract,  a 
low-grade  catarrhal  inflammation  is  set  up;  this,  on  the  one  hand,  leads 
to  obstruction  of  the  free  flow  of  bile  from  swelling  of  the  mucous  mem- 
brane, and  the  products  of  this  inflammation,  on  the  other  hand,  contain 
the  essential  constituents  of  gallstones.  In  the  gall-bladder  the  catarrhal 
inflammation  leads  to  desquamation  of  the  lining  epithelium,  an  allni- 
minous  exudation,  and  an  increased  formation  of  mucus  and  of  choles- 
terin;  and  in  the  gall-bladder  dynamic  factors  frequently  favor  the  stag- 
nation of  bile.  The  increased  cholesterin  is  derived  not  from  the  bile, 
but  from  catarrhal  disintegration  of  the  mucous  cells  lining  the  wall  of 
the  gall-bladder.  Bacmeister  and  Exner  and  Heyrovsky,  however,  have 
shown  that  bacteria,  notably  the  typhoid  and  the  colon  bacillus  (but  not 
streptococci),  may  effect  directly  a  decomposition  of  the  bile  with  the 
precipitation  of  cholesterin.  Exner  and  Heyrovsky  attribute  this  to 
decomposition  of  the  bile  acid  salts  (the  solvent  menstruum),  in  conse- 
quence of  which  the  normal  amount  of  cholesterin  can  no  longer  be  held 
in  solution.  The  bilirubin  calcium  is  derived  from  the  bile,  being  pre- 
cipitated by  bacterial  growth  or  by  the  albuminous  exudation  of  the 
inflammatory  process.  Bilirubin  calcium  is  believed  by  Naunyn  to  act 
as  a  cement  substance,  binding  together  the  cholesterin,  desquamated 


730    DISEASES  OF  THE  GALL-BLADDER  AND  BILIARY  DUCTS 

epithelium,  etc.,  the  whole  forming  the  nucleus  of  the  gallstone.  Agglu- 
tinated typhoid  and  other  bacteria  also  may  apparently  act  as  the  nucleus. 

The  following  varieties  of  gallstones  are  distinguished  by  Naunyn:  (1) 
Pure  cholesterin  stones,  which  consist  of  nearly  pure  cholesterin,  and  are 
uncommon.  They  vary  in  size  from  that  of  a  cherry  to  that  of  a  pigeon's 
egg,  are  hard,  oval,  or  roughly  spherical,  seldom  faceted,  have  a  smooth 
or  nodular  surface,  and  are  pure  white  or  yellowish  and  translucent,  or 
rarely  brown,  greenish,  of  brownish-black  on  the  surface.  On  section 
they  are  white,  and  crystalline  throughout,  or  show  brown  deposits  be- 
tween the  crystals;  they  are  not  stratified.  (2)  Laminated  cholesterin 
stones,  which  consist  of  about  90  per  cent,  of  cholesterin,  together  with 
bilirubin  calcium,  biliverdin  calcium,  and  calcium  carbonate.  In  general 
appearance  they  resemble  the  pure  cholesterin  calculi,  but  they  may  be 
brittle  and  friable,  and  they  are  often  faceted.  On  section,  they  are 
more  or  less  distinctly  laminated,  layers  of  almost  pure  white  alternating 
with  others  that  are  yellow,  brown,  green,  or  red.  The  centre  may  be 
crystalline,  but  the  external  layers  are  usually  vitreous  or  earthy.  (3) 
The  common  (or  mixed  cholesterin)  stones,  which  vary  much  in  size, 
although  they  seldom  equal  a  large  cherry;  they  may  be  small  and  very 
numerous,  and  are  usually  faceted.  The  surface  is  usually  yellow,  but 
often  brown  or  white.  When  fresh,  they  are  often  soft  and  greasy;  when 
dried,  they  undergo  shrinkage  and  become  harder.  On  section,  the 
centre  is  often  soft  and  may  contain  a  cavity.  (4)  Mixed  bilirubin  cal- 
cium stones,  which  may  consist  roughly  of  75  per  cent,  of  bilirubin  calcium 
and  about  25  per  cent,  of  cholesterin.  They  are  as  large  as  a  cherry,  or 
larger,  and  may  occur  singly  or  in  groups  of  three  or  four  in  the  gall- 
bladder or  larger  ducts.  Their  shape  depends  upon  their  situation; 
when  multiple,  they  may  be  faceted.  They  consist  of  concentric  layers 
of  reddish-brown  or  dark  brown  material,  which  is  seldom  quite  hard, 
and  contracts  on  drying,  often  with  the  formation  of  fissures  or  cracks. 
(5)  Pure  bilirubin  calcium  stones,  which  vary  in  size  from  that  of  a  grain 
of  sand  to  that  of  a  pea.  There  are  two  types:  small,  solid,  brownish- 
black  concretions,  with  rough,  irregular  surfaces  and  wax-like  consistency, 
and  exhibiting  a  disposition  to  become  welded;  and  harder,  smooth  con- 
cretions of  a  grayish-black  metallic  lustre  and  an  internal  spongy  struc- 
ture. (6)  Rarer  stones,  such  as  amorphous  and  incompletely  crystalline 
cholesterin  gravel  (resembling  pearls);  calcareous  stones;  concretions 
with  included  bodies  and  conglomerate  stones;  and  casts  of  the  bile  ducts. 

Symptoms. — ^The  characteristic  and  significant  symptoms  are:  (1) 
Chronic,  long-continued,  or  recurring  indigestion,  and  (2)  the  phenomena 
designated  gallstone  colic.  The  symptoms  of  chronic  long-continued  or 
recurring  indigestion  are  of  the  utmost  importance  and  are  commonly 
misinterpreted.  This  stands  in  relationship  with  the  facts — that  gall- 
stones are  present  in  very  many  subjects  and  are  commonly  believed  not 
to  cause  noteworthy  symptoms  (in  not  more  than  5  per  cent,  of  the  sub- 
jects); that  symptoms,  having  once  occurred,  are  exceedingly  likely  to 
recur;  and  that  the  symptoms  are  often  paroxysmal  and  very  severe. 


CHOLELITHIASIS  731 

Gallstones  are  sometimes  latent,  particularly  in  elderly  subjects,  in  whom 
the  original  infection  has  died  out,  and  in  whom  more  or  less  atrophy, 
especially  of  the  muscular  coat  of  the  gall-bladder  and  biliary  ducts,  has 
occurred;  but  there  can  be  no  doubt  that  symptoms  commonly  denomi- 
nated "stomach  trouble,"  "indigestion,"  "dyspepsia,"  etc.,  are  often 
due  to  gallstones  and  disease  of  and  about  the  biliary  tract. 

Gallstone  colic  usually  develops  suddenly  with  severe,  often  agonizing, 
pain  in  the  right  hypochondrium  or  the  epigastrium,  radiating  around 
the  chest  or  to  the  right  scapular  region,  nausea,  vomiting,  and  prostra- 
tion— weak,  rapid  pulse,  rapid  heart  action,  profuse  perspiration,  etc. 
Sometimes  the  attack  is  preceded  by  local,  less  acute  pain  or  discomfort, 
chilliness,  fever,  etc. ;  more  commonly  (60  per  cent,  or  more  of  the  cases) 
chilliness  and  fever  accompany  and  follow  the  pain.  In  some  cases 
the  severe  pain  lasts  for  a  few  moments  only;  usually  it  lasts  from 
two  to  twelve  hours;  in  unusual  cases  it  may  last  much  longer,  but  in 
these  circumstances  the  phenomena  are  more  correctly  interpreted  as  a 
succession  of  paroxysms.  Often  the  pain  ceases  as  suddenly  as  it  began, 
but  usually  following  the  agonizing  pain,  more  or  less  dull  aching  con- 
tinues for  a  variable  period.  The  colic  may  recur  at  varying  intervals — 
days,  weeks,  months,  or  years;  occasionally  there  is  only  one  attack; 
usually  there  are  many.  With  succeeding  attacks  the  likelihood  of  other 
attacks  increases.  In  some  cases  the  pains  are  not  colicky;  that  is,  the 
classical  gallstone  colic  does  not  occur.  The  pains,  of  whatever  nature, 
are  usually  due  to  an  acute  cholecystitis,  or  reactivation  of  a  more  or  less 
quiescent  cholecystitis;  but,  as  pointed  out  by  Riedel,  the  colicky  pains 
may  be  due  to:  (1)  Adhesions  of  a  gall-bladder  no  longer  containing 
stones;  (2)  adhesions  when  large  stones  are  present  in  the  gall-bladder 
and  the  cystic  duct  is  patent;  (3)  inflammatory  processes  in  a  gall- 
bladder distended  by  fluid  or  stones,  when  the  cystic  duct  is  occluded  by 
inflammation  or  by  the  presence  of  a  stone  in  the  neck  of  the  gall-bladder; 
(4)  the  transit  of  a  stone  through  the  bile  passages;  and  (5)  the  inflam- 
mation of  a  dilated,  calculous  common  duct  or  its  tributaries,  without 
impaction  of  a  stone. 

Jaundice  may  occur,  but  is  entirely  absent  in  at  least  one-third  of  the 
cases.  It  varies  much  in  degree  and  duration  with  the  local  conditions. 
It  may  be  due  to:  (1)  Gallstones  in  the  hepatic  or  the  common  bile  duct; 
(2)  spasm  of  the  musculature  or  inflammatory  swelling  of  the  mucosa  of 
the  biliary  ducts,  and  (3)  compression  of  the  common  duct  or  of  th§  exti-a- 
hepatic  part  of  the  hepatic  duct  by  a  large  stone  in  the  cystic  duct, 
swollen  lymph  nodes,  regional  tumors,  inflammatory  exudations,  adhe- 
sions, kinking  of  the  ducts,  etc.  The  gall-bladder  may  be  enlarged  and 
palpable  in  early  cases;  but  in  advanced  cases,  when  the  gall-bladder  has 
become  thickened  and  cicatrized  and  is  manifestly  incapable  of  dis- 
tending, it  is  usually  not  palpable.  Courvoisier  stated  that  in  cases  of 
chronic  jaundice,  contraction  of  the  gall-bladder  is  suggestive  of  gall- 
stones, and  that  dilatation  of  the  gall-bladder  is  suggestive  of  biliary 
obstruction,  caused  by  factors  other  than  gallstones;  that  is,  pressure 


732    DISEASES  OF  THE  GALL-BLADDER  AND  BILIARY  DUCTS 

from  without  (most  often  enlargement,  carcinoma,  of  the  head  of  the 
pancreas).  This,  so-called  Courvoisier's  law,  is  applicable  in  perhaps- 
two-thirds  of  the  chronic  cases. 

Fever  is  common,  and  should  be  correctly  interpreted — as  a  manifes- 
tation of  infection,  and  not  as  due  to  reflex  causes,  etc.  In  many  cases, 
concurrently  with  the  development  of  the  gallstone  colic,  there  is  a  sud- 
den elevation  of  the  temperature,  followed  sometimes  by  an  equally 
sudden  fall;  in  other  cases,  the  fever  is  of  longer  duration — obviously 
due  to  acute  cholecystitis,  or  an  acute  exacerbation  of  a  chronic  chole- 
cystitis; in  still  other  cases,  especially  cases  of  calculus  in  the  common 
duct,  the  fever  is  that  known  as  Charcot's  intermittent  hepatic  (or  biliary) 
fever — periodic  attacks  of  chill,  fever  (103°  to  104°F.),  and  sweats,  usually 
accompanied  by  pain  in  the  epigastrium  or  right  hypochondrium,  re- 
currence or  increase  of  jaundice,  perhaps  nausea  and  vomiting,  and 
often  leukocytosis. 

Obstkuction  of  the  Cystic  Duct. — The  calculus  is  usually  lodged 
in  the  beginning  of  the  duct  or  in  the  termination  of  the  neck  of  the  gall- 
bladder. The  following  conditions  may  ensue:  (1)  Acute  cholecystitis 
(catarrhal,  suppurative,  phlegmonous,  or  gangrenous).  (2)  Chronic 
dilatation  of  the  gall-bladder,  a  condition  that  follows  complete  obstruc- 
tion to  the  entrance  of  bile  into  the  gall-bladder,  which  soon  becomes 
distended  with  mucus,  at  first  bile-stained,  but  ultimately  quite  clear 
(so-called  hydrops).  (3)  Chronic  fibrous  or  atrophic  cholecystitis — - 
the  usual  sequel  of  hydrops  when  the  obstruction  is  not  complete  and 
the  infection  dies  out.  The  gall-bladder  gradually  lessens  in  size  and 
may  ultimately  be  reduced  to  a  mass  of  fibrous  tissue,  which  usually 
tightly  encircles  a  calculus. 

Obstruction  of  the  Common  Bile  Duct. — The  obstruction  may 
be  complete  or  incomplete,  and  may  or  may  not  be  associated  with 
cholangitis.  When  the  obstruction  is  complete,  a  stone  is  usually 
tightly  impacted  in  the  common  duct;  when  the  obstruction  is  incom- 
plete, the  stone  may  be  more  or  less  fixed,  but  permits  the  flow  of  bile 
around  it,  or  it  may  circulate  in  the  common  duct  and  imitate  the  con- 
ditions in  a  ball  valve.  Dilatation  of  the  biliary  ducts  usually  ensues,  and 
to  the  common  cholangitis  and  pericholangitis  more  or  less  fibrosis 
of  the  adjacent  liver  tissue  and  atrophy  of  the  liver  cells  often  ensue — a 
condition  sometimes  spoken  of  as  obstructive  biliary  cirrhosis  In  the 
event  of  complete  obstruction  without  infection,  deep  and  permanent 
jaundice  is  produced,  and  is  unattended  by  fever.  Incomplete  obstruc- 
tion may  last  for  many  years  without  leading  to  jaundice.  Usually, 
however,  jaundice  is  present;  it  lasts  a  long  time,  varies  in  intensity 
with  the  degree  of  obstruction,  is  subject  to  more  or  less  fluctuation, 
which  is  very  characteristic;  and  there  is  fever,  periodic,  intermittent, 
or  remittent,  or  more  or  less  continuous  (indicative  of  the  usually  asso- 
ciated biliary  infection).  Osier  has  emphasized  the  importance  of  the 
followinij  signs  in  the  diagnosis  of  a  ball-valve  calculus  in  the  diverticu- 
lum  of  Vater  (where  it  occurs  most  frequently),  or  in  the  common  bile 


CHOLELITHIASIS  733 

duct:  "  (a)  Ague-like  paroxysms  of  chill,  fever,  and  sweating — the  hepatic 
intermittent  fever  of  Charcot;  (6)  jaundice  of  varying  intensity,  which 
persists  for  months  or  even  years,  and  deepens  after  each  paroxysm ;  and 
(c)  at  the  time  of  the  paroxysm,  pain  in  the  region  of  the  liver,  with  gas- 
tric disturbance.  .  .  .  Pain,  which  is  sometimes  severe  and  colicky, 
does  not  always  occur.  There  may  be  vomiting  and  nausea.  As  a  rule, 
there  is  no  progressive  deterioration  of  health.  In  the  intervals  between 
the  attacks  the  temperature  is  normal." 

Complications  and  Sequels. — Of  the  many  complications  and  sequels  of 
cholelithiasis,  some  infectious,  some  purely  mechanical,  but  most  of  them 
infectious  and  mechanical,  the  following  are  the  most  important:  (1) 
Infectious  (Inflammatory)  Lesions  of  the  Biliary  Tract  and  Adjacent 
Yiscera.  These  comprise  especially  varying  grades  of  acute  and  chronic, 
suppurative  and  non-suppurative,  cholangitis  and  cholecystitis,  pro- 
gressing perhaps  to  ulceration,  gangrene,  perforation,  etc.  The  inflam- 
matory phenomena  may  extend  to  adjacent  structures,  and  set  up  local 
peritonitis  (with  abscess  formation)  or  a  more  widespread  peritonitis, 
pylephlebitis,  pancreatitis,  etc.  (2)  Chronic  Pericholecystic  Adhesions. 
These  represent  the  sequels  of  postsubacute  and  chronic,  sometimes 
acute,  inflammation  that  has  spread  to  the  adjacent  peritoneum.  Similar 
adhesions  may  follow  disease  of  the  stomach  and  duodenum;  and  any 
of  these  adhesions  may  be  responsible  for  ''stomach  ache,"  "indigestion," 
"  biliousness,"  etc.  (3)  Biliary  Fistulce.  Fistulous  communications  be- 
tween the  biliary  tracts  and  adjacent  viscera,  as  well  as  the  exterior  of  the 
body,  frequently  result  from  cholelithiasis  and  the  associated  inflam- 
matory and  ulcerative  processes.  Courvoisier  in  a  study  of  499  cases, 
found  that  fistulous  communications  had  been  established  as  follows: 
between  difl^erent  parts  of  the  biliary  passages  in  8;  into  the  portal  vein 
in  5;  into  the  peritoneal  cavity  in  70;  into  peritoneal  adhesions  in  49; 
into  the  retroperitoneum  in  3;  with  the  stomach  in  13;  with  the  duo- 
denum in  83;  with  the  jejunum  in  1;  with  the  ileum  in  1;  with  the  colon 
in  39;  with  the  urinary  tract  in  7;  with  the  pleura  and  lung  in  24;  and 
externally  in  196.  (4)  Intestinal  Obstruction.  This  is  a  rare  event, 
that  may  follow  ulceration  of  a  gallstone  from  the  gall-bladder  into  the 
duodenum,  or,  less  commonly,  the  colon.  The  obstruction  occurs  most 
commonly  in  the  ileum  (near  the  ileocecal  valve),  and  may  be  suspected 
in  a  person  in  advanced  life  with  a  history  of  past  gallstones. 

Diagnosis. — The  diagnosis  of  cholelithiasis  comprises  the  recognition 
of  the  gallstone  colic  and  of  the  many  and  varied  associated  lesions  and 
sequels.  Severe  pain  in  the  epigastrium  or  the  right  hypochondriuni, 
radiating  around  the  chest  or  to  the  right  scapula,  accompanied  by 
nausea  and  vomiting  and  enlargement  and  tenderness  of  the  gall-bladder 
and  followed  by  jaundice  and  the  detection  of  a  gallstone  in  the  feces, 
are  characteristic  of  the  passage  of  a  gallstone;  but  jaundice  is  by  no 
means  always  present,  and  the  other  symptoms  may  be  provoked  by 
cholecystitis  in  the  absence  of  a  gallstone;  indeed,  with  increasing  expe- 
rience, it  becomes  often  more  and  more  difficult  to  say  whether  or  not 


734    DISEASES  OF  THE  GALL-BLADDER  AND  BILIARY  DUCTS 

gallstones  are  present  in  certain  individual  cases  of  obvious  chronic 
biliary  infections.  Recourse  to  the  a:-rays  is  seldom  of  much  diagnostic 
utility,  since  the  cholesterin  stones  produce  scarcely  any  shadow,  usually 
not  more  than  the  adjacent  liver;  in  the  rare  cases  of  calcium  stones, 
more  shadow  is  cast,  but  this  also  is  obscured  by  the  shadow  of  the 
liver. 

The  severe  pain  of  gallstone  colic  may  be  imitated  by  renal  colic  or 
intestinal  colic;  but  in  renal  colic  the  pain  is  usually  in  the  back,  loin, 
or  groin,  and  radiates  down  the  ureter  to  the  testicle,  which  may  become 
retracted;  strangury  or  frequent  micturition  is  common;  the  kidney  is 
usually  tender  (the  tenderness  being  in  the  loin  rather  than  anteriorly  in 
the  region  of  the  gall-bladder);  and  the  urine  subsequently  contains 
blood  and  a  proportionate  amount  of  albumin,  perhaps  crystals  or  a 
calculus,  and  pus  and  epithelium  from  the  pelvis  of  the  kidney;  and  it 
does  not  contain  bile.  Intestinal  colic  is  usually  due  to  some  more  or 
less  obvious  cause;  the  pain  is  usually  about  the  umbilicus;  it  radiates 
in  different  directions,  remits  and  intermits,  and  subsides  with  the 
removal  of  the  exciting  cause,  often  with  belching  or  the  discharge  of 
feces  or  gas  or  mucus  by  the  bowel;  and  there  is  no  localized  tenderness 
in  the  region  of  the  gall-bladder.  In  lead  colic  there  is,  in  addition,  the 
history  of  exposure  to  the  poison,  a  blue  line  on  the  gums,  anemia, 
basophilic  degeneration  of  the  erythrocytes,  and  perhaps  other  present  or 
past  evidences  of  the  intoxication,  such  as  persistent  abdominal  discom- 
fort or  pain  and  constipation,  wrist-drop,  etc.  ^-Mien  the  symptoms, 
especially  the  pain,  are  less  acute,  and  do  not  merit  the  designation 
gallstone  colic,  difficulty  may  be  experienced  in  differentiating  disorders 
of  the  stomach,  especially  gastric  and  duodenal  ulcer.  The  persistence 
of  jaundice  may  suggest  malignant  disease  of  the  ducts  or  of  the  pancreas, 
but  in  cholelithiasis  there  is  less  impairment  of  the  general  health;  there 
is  usually  periodic  variation  in  the  intensity  of  the  jaundice  (of  much  diag- 
nostic importance);  and  fever,  especially  intermittent  hepatic  fever,  is 
likely  to  be  present. 

Prognosis. — ^The  prognosis,  as  a  rule,  depends  more  upon  the  associated 
conditions  than  upon  the  mere  presence  of  the  gallstones.  The  prog- 
nosis in  gallstone  colic  is  virtually  that  of  a  more  or  less  acute  cholecys- 
titis; the  outlook  as  regards  permanent  health  depends  upon  the  chronic 
gall-bladder  infection.  A  first  gallstone  colic  is  sometimes  the  last  and 
the  infection  subsides.  Usually,  however,  there  are  subsequent  attacks, 
if  not  of  severe  colic,  of  more  or  less  disturbance  with  digestion,  and 
general  impairment  of  health  due  to  the  toxic  absorption,  etc.;  some 
subjects  pass  into  chronic  invalidism  from  unrecognized  chronic  biliary 
infections.  The  occurrence  of  intermittent  hepatic  fever,  especially  of 
severe  ague-like  paroxysms,  renders  the  prognosis  bad,  since  it  shows 
active  infection,  which,  although  it  may  persist  for  years  without  sup- 
puration, may  nevertheless  lead  to  serious  consequences.  The  prog- 
nosis as  to  final  recovery  of  health  is  bad  without  operative  intervention 
in  pericholecystic  adhesions,  fistulas,  and  intestinal  obstructions. 


CHOLELITHIASIS  735 

Treatment. — The  fact  that  gallstones  are  most  common  in  women,  in 
the  obese,  in  those  that  lead  a  sedentary  life,  eat  too  much,  are  consti- 
pated, and  addicted  to  alcohol,  suggests  the  correction  of  certain  very 
obvious  etiological  factors.  Women  vi^ho  have  been  repeatedly  preg- 
nant and  have  lax  abdominal  walls  should  wear  proper  supports.  Men 
and  women  who  lead  a  sedentary  life  should  take  properly  regulated 
exercise;  they  should  practise  deep  breathing  (to  promote  the  move- 
ments of  the  diaphragm),  bathe  frequently,  be  much  in  the  open  air, 
etc. ;  that  is,  they  should  apply  to  themselves  the  general  principles  of 
hygienic  living.  Constipation  should  be  overcome,  and  the  diet  should 
be  such  as  will  be  presently  pointed  out. 

^^Tien  gallstones  have  formed,  the  main  indications  for  treatment  may 
be  said  to  be:  (1)  To  cause  solution  of  the  stone  or  stones;  (2)  to  cause 
the  discharge  of  the  stone  or  stones;  and  (3)  to  treat  the  complicating 
infection. 

It  is  quite  impossible  to  cause  solution  of  gallstones  in  the  gall-bladder, 
olive  and  other  oils,  turpentine,  ether,  etc.,  being  without  effect  in  this 
regard.  The  many  stones  said  to  have  been  passed  by  the  bowel  after 
the  administration  of  olive  oil  are  merely  masses  of  saponified  oleic  acid, 
resembling  gallstones  in  outward  appearance.  Olive  oil,  however,  is 
often  of  service  in  relieving  the  commonly  attendant  hyperchlorhydria. 
To  attempt  the  discharge  of  gallstones  from  the  gall-bladder,  even  were 
this  possible  to  effect,  is  not  a  worthy  object  of  rational  treatment.  The 
special  function  of  the  physician  is  to  treat  the  associated  biliary  infection. 

The  'pain  of  gallstone  colic  is  usually  so  severe  as  to  require  the  admin- 
istration of  morphine,  which  not  only  relieves  the  pain  (and  mitigates  the 
attendant  shock),  but,  by  relaxing  the  spasm  of  the  biliary  musculature, 
favors  the  exit  of  bile  from  the  tense  gall-bladder  and  the  transit  of  the 
calculus  through  the  ducts  (if  it  be  already  therein).  Usually,  \  grain 
(0.015  gram)  with  -^-^  grain  (0.0013  gram)  of  atropine,  or  ^-^  (0.0006 
gram)  grain  of  nitroglycerin  suffices;  sometimes  after  the  lapse  of  fifteen 
to  thirty  minutes  a  second  smaller  dose  may  seem  necessary,  but  in  these 
circumstances  a  few  whiffs  of  chloroform,  or  spirit  of  chloroform  or  of 
ether  (1  dram,  4  c.c),  to  which  tincture  of  belladonna  (5  to  10  minims, 
0.3  to  0.6  c.c),  may  be  added,  will  usually  carry  the  patient  through 
the  painful  period  until  the  morphine  has  had  time  to  act;  or,  and  this 
is  often  attended  by  excellent  results,  an  additional  dose  of  atropine 
(tf¥  gi'3'in,  0.0006  gram)  may  be  administered  Hypodermically.  Should 
resort  be  had  to  chloroform  inhalation,  one  should  not  induce  complete 
anesthesia  in  the  hope  of  thus  relaxing  the  biliary  musculature  and  freeing 
the  calculus;  such  objects  are  not  thus  achieved.  In  many  cases  relief 
may  also  be  afforded  by  hot  fomentations  over  the  region  of  the  gall- 
bladder and  by  lavage  of  the  stomach  with  water  as  hot  as  can  well  be 
borne.  Should  the  vomiting  persist  and  be  manifest  especially  by  inef- 
fectual retching,  resort  should  be  had  to  lavage,  if  it  has  not  been  pre- 
viously used ;  sodium  bicarbonate  may  be  added  to  the  hot  water.  The  hot 
full  bath  may  also  be  resorted  to  at  the  very  beginning  of  the  attack,  with 


736    DISEASES  OF  THE  GALL-BLADDER  AND  BILIARY  DUCTS 

hope  of  excellent  result.  In  other  cases  the  vomiting  may  be  relieved 
by  bismuth,  carbolic  acid,  creosote,  dilute  hydrocyanic  acid,  cerium 
oxalate,  sips  of  hot  water  and  brandy,  champagne,  etc.  In  some  cases 
the  pain  leads  to  extraordinary  depression  of  the  patient,  which,  if  it  is 
not  relieved  by  the  morphine,  should  be  met  with  whisky  or  brandy  in 
hot  water,  or  the  hypodermic  use  of  camphor. 

Upon  the  subsidence  of  the  pain,  as  well  as  in  the  absence  of  a  definite 
gallstone  colic,  the  medical  treatment  of  cholelithiasis  is  that  of  the 
chronic  biliary  infection.  The  diet  should  be  regulated;  large  amounts 
of  an  alkaline  water  should  be  taken,  and  the  saline  cathartics  should  be 
administered  daily.  Salicylic  acid  seems  to  augment  the  flow  of  bile  by 
stimulating  its  production,  and  since  it  also  possesses  antiseptic  properties 
and  is  excreted  with  the  bile,  it  exerts  a  most  desirable  influence  on  the 
biliary  infection.  No  preparation  is  better  than  chemically  pure  sali- 
cylic acid;  it  may  be  combined  with  an  equal  amount  of  sodium  bicar- 
bonate or  sodium  benzoate;  or  the  salicylates  or  other  preparations  of 
salicylic  acid  may  be  given. 

Hexamethylenamin  also  is  excreted  in  the  bile  and  through  the  wall 
of  the  gall-bladder,  and  serves  to  disinfect  the  biliary  passages.  It 
should  be  given  in  generous  dose — 40  to  60  grains  (2.5  to  4  grams) — 
within  twenty-four  hours,  from  time  to  time;  but  its  general  effect  should 
be  carefully  observed.  Oxgall  also  stimulates  the  secretion  and  out- 
pouring of  bile,  and  thus  favors  drainage  of  the  biliary  tract;  it  should 
be  administered  as  salts  of  the  bile  acids,  such  as  sodium  glycocholate, 
10  to  15  grains  (0.6  to  1  gram)  daily.  Ammonium  chloride  also  is 
sometimes  extolled  for  its  effect  upon  inflamed  mucous  membranes;  by 
promoting  the  free  flow  of  thin  bile  it  may  assist  in  the  much  desired 
flushing  of  the  biliary  tract. 

Surgical  treatment  is  indicated  in  all  cases  in  which  quiescence  or 
latency  of  the  infection  cannot  be  brought  about  by  medicinal  measures; 
in  the  event  of  recurring  attacks  of  gallstone  colic;  in  the  cases  that  run 
their  course  under  the  guise  of  "indigestion,"  "biliousness,"  etc.,  and  in 
which  recurrence  of  attacks  is  common;  in  cases  of  persisting  jaundice, 
with  or  without  Charcot's  biliary  intermittent  fever;  and  in  all  cases  of 
complicating  or  severe  suppurative,  ulcerative,  or  gangrenous  chole- 
cystitis. 

CARCINOMA  OF   THE  GALL-BLADDER  AND  BILIARY  DUCTS. 

Carcinoma  may  develop  in  any  part  of  the  biliary  tract,  but  it  is  most 
common  in  the  gall-bladder.  It  is  usually  associated  with  gallstones, 
commonly  involves  the  fundus,  and  may  be  a  fungus-like  or  an  infil- 
trating growth  (cylindrical  or  cuboidal  cell).  Extension  to  the  liver 
occurs  in  more  than  50  per  cent,  of  the  cases.  In  the  biliary  ducts 
carcinoma  is  most  common  in  the  common  duct,  but  may  occur  any- 
where, even  in  the  ampulla  of  Vater  (choledochopancreatic  duct);  it  is 
usually  an  infiltrating  growth. 


HEMORRHAGES  INTO  THE  PANCREAS  737 

Symptoms. — The  symptoms  of  carcinoma  of  the  gall-bladder  consist 
usually  of  antecedent  phenomena  referable  to  cholecystitis  and  chole- 
lithiasis, to  which  become  added  a  progressive,  irregular,  and  nodular 
enlargement  of  the  gall-bladder  (more  than  one-half  of  the  cases), 
jaundice  (three-fourths  of  the  cases),  and  impairment  of  the  general 
health — emaciation,  anemia,  and  cachexia.  Ascites  occurs  in  about 
one-fourth  of  the  cases,  being  due  to  portal  obstruction  or  perihepatitis. 
In  carcinoma  of  the  extrahepatic  biliary  ducts,  jaundice  is  usually  the 
first  noteworthy  symptom;  it  is  progressive,  soon  becomes  extreme,  and 
is  permanent.  The  stools  become  acholic.  The  gall-bladder  becomes 
enlarged  (smooth,  pear-shaped),  and  metastasis  may  occur  to  the  liver 
(palpable  nodules),  to  the  portal  lymph  nodes  (causing  ascites),  etc.;  and 
the  patient  becomes  cachectic. 

Pro^osis. — ^Death  usually  occurs  within  six  months  of  the  onset  of 
serious  symptoms. 

Treatment. — ^The  treatment  is  essentially  surgical. 


DISEASES  OF  THE  PANCREAS. 

Pathological  Physiology. — Some  reference  has  been  made  in  the  intro- 
ductory remarks  on  diseases  of  the  intestine  to  the  pathological  physi- 
ology of  the  pancreatic  juice,  and,  under  diabetes,  to  disturbances  in  the 
internal  secretion  of  the  pancreas.  The  chief  results  of  disturbances 
(deficiency)  of  the  pancreatic  juice  consist  of  imperfect  tryptic  digestion 
— the  occurrence  of  unchanged  muscle  fibers  in  the  stools  (azotorrhoea), 
especially  the  non-digestion  of  the  muscle  fiber  nuclei  (Schmidt's  test); 
imperfect  digestion  of  carbohydrates,  due  to  lessening  or  absence  of  pan- 
creatic amylase;  and  imperfect  fat-splitting,  due  to  lessening  or  absence 
of  steapsin.  The  stools  are  voluminous;  pale,  grayish,  slate-colored,  or 
clay-colored;  pasty,  fetid,  and  acid.  The  fat  content  may  be  as  high 
as  80  or  90  per  cent,  (steatorrhoea),  instead  of  the  normal  7  to  10  per 
cent.  In  addition,  the  urine  may  contain  sugar,  rarely  a  fat-splitting 
ferment  (Opie),  or  it  may  reveal  the  so-called  Cammidge  reaction. 

HEMORRHAGES  INTO  THE   PANCREAS. 

Hemorrhage  into  the  pancreas  occurs  in  a  variety  of  conditions  such  as 
determine  hemorrhage  in  other  organs — infectious  diseases,  sepsis,  hem- 
orrhagic diathesis,  purpura,  in  association  with  tumors  and  cysts,  and 
following  traumas.  In  addition,  however,  there  is  a  class  of  cases  in 
which  hemorrhage  into  the  pancreas  constitutes  the  only  noteworthy 
lesion  at  necropsy  in  cases  of  sudden  death  occurring  in  persons  pre- 
viously healthy — so-called  pancreatic  apoplexy.  Many  of  these  are 
doubtless  cases  of  hemorrhagic  pancreatitis,  being  reported  in  the  older 
literature,  when  observations  were  more  or  less  imperfect  and  the  nature 
47 


738  DISEASES  OF  THE  PANCREAS 

of  hemorrhagic  pancreatitis  ill  understood.  From  these,  however,  may 
be  separated  cases  occurring  in  atheroma,  and  in  association  with  throm- 
bosis and  embolism.  Symptomatically,  however,  they  cannot  be  differ- 
entiated from  acute  or  hemorrhagic  pancreatitis. 


ACUTE  PANCREATITIS. 

Etiology. — Acute  pancreatitis  is  most  common  in  adult  males,  although 
it  occurs  in  women  and  has  been  observed  even  in  infants.  Some  of  the 
patients  have  given  a  history  of  addiction  to  alcohol;  others  have  suffered 
from  gastro-intestinal  derangements,  cholelithiasis,  or  diabetes  mellitus. 
In  most  cases  the  disease  is  associated  with  cholelithiasis  and  concomitant 
infection  of  the  biliary  tract.  Usually  the  gallstone  obstructs  the  com- 
mon bile  duct,  and  thus  permits  the  ready  access  of  the  bile  to  the  pan- 
creas. Flexner,  Pearce,  and  others  have  demonstrated  that  the  injecting 
of  bile,  artificial  gastric  juice,  and  other  irritating  substances,  into  the 
pancreatic  duct  may  cause  pancreatitis,  even  in  the  absence  of  bacterial 
infection.  In  some  cases  ulcerative  and  suppurative  processes  of  adja- 
cent organs  or  of  remote  organs  (by  metastasis)  may  set  up  the  pancreatitis. 

Pathology. — Since  the  time  of  Fitz's  original  observations  it  has  been 
customary  to  distinguish  three  varieties  of  acute  pancreatitis — hemor- 
rhagic, suppurative,  and  gangrenous.  In  many  cases,  however,  it  is 
impossible  to  differentiate  between  so-called  pancreatic  hemorrhage, 
hemorrhagic  pancreatitis,  and  gangrenous  pancreatitis,  and  in  most 
cases  these  are  but  different  stages  or  varying  manifestations  of  the 
one  disease.  In  hemorrhagic  'pancreatitis  the  pancreas  is  enlarged, 
softened,  and  mottled,  dark  reddish  brown  or  black  in  color — the  result 
of  infiltration  of  the  interstitial  tissue  with  blood.  In  some  cases  the 
hemorrhagic  infiltration  extends  also  to  the  neighboring  peripancreatic 
tissues,  and  the  mesentery,  mesocolon,  and  omentum.  An  essential 
feature  of  the  disease  is  extensive  necrosis  of  all  the  constituents  of  the 
gland — the  parenchyma,  the  interstitial  tissue,  and  the  bloodvessels, 
with  which  inflammatory  phenomena  (polynuclear  leukocytic  infiltra- 
tion and  serofibrinous  exudation)  are  associated.  The  hemorrhage  is 
attributed  to  necrosis  and  consequent  rupture  of  the  bloodvessels.  The 
necrotic  foci  are  sharply  demarcated  from  the  surrounding  living  tissue 
by  a  narrow  zone  of  reactive  inflammation.  Opie  draws  attention  to  the 
occurrence  of  hyaline  thromboses  within  the  relatively  intact  tissue 
adjoining  the  necrotic  zones,  and  he  believes  that  "it  is  not  improbable 
that  the  ferments  of  the  pancreatic  juice,  notably  trypsin,  acting  upon 
cells  injured  by  contact  with  various  irritant  substances  which  can 
produce  hemorrhagic  pancreatitis,  have  a  part  in  the  production  of  the 
widespread  disintegration  of  the  parenchyma  which  results." 

Gangrenous  pancreatitis  follows  hemorrhagic  pancreatitis,  and  no 
sharp  line  of  demarcation  can  be  drawn  between  them.  The  initial 
lesions  are  similar  to  those  of  hemorrhagic  pancreatitis — necrosis  and 


ACUTE  PANCREATITIS  739 

consequent  hemorrhage;  inflammatory  alterations  soon  develop,  and  in 
the  course  of  time,  concurrent  with  bacterial  invasion,  the  appearances 
recognized  as  gangrene  result.  The  pancreas  is  swollen,  soft,  friable,  and 
mottled  grayish-black  (slate-colored)  or  reddish  brown  or  black  in 
color.  In  some  cases  it  consists  of  a  dark,  mottled,  slate-colored,  foul- 
smelling  necrotic  mass;  whereas,  in  a  few  cases,  late  in  the  course  of 
the  disease,  it  may  consist  of  a  rather  firm  and  dry  mass  covered  with  blood. 
Inflammation  of  the  lesser  peritoneal  cavity  results,  and  is  often  followed 
by  the  development  of  a  large  abscess  cavity  containing  dark,  grumous, 
malodorous,  chocolate-colored,  purulent  material,  and  in  some  cases 
the  partly  or  fully  sequestered  gangrenous  pancreas.  Rupture  of  the 
abscess  into  the  intestine  may  ensue. 

Suppurative  pancreatitis  is  a  secondary  condition,  and  not  the  cause 
of  the  gangrene.  There  may  be  a  single  large  abscess  or  many  small 
abscesses — the  pancreas  being  correspondingly  enlarged  and  softened. 
The  suppuration  may  extend  to  the  adjacent  tissues,  or  rupture  may 
occur  into  the  lesser  peritoneal  cavity  (giving  rise  to  a  large  abscess 
cavity),  or  into  the  stomach  or  the  duodenum;  or  pylephlebitis  and  liver 
abscess  may  result. 

Fat  necrosis  is  a  common  concomitant  of  acute  hemorrhagic  and 
gangrenous  pancreatitis,  and  may  be  observed  also  in  association  with 
chronic  suppurative  and  chronic  interstitial  pancreatitis.  It  occurs 
as  disseminated  or  multiple  minute  foci  in  or  upon  the  pancreas,  and  as 
larger  foci  (2  to  3  mm.  in  diameter)  in  the  fat  of  the  omentum,  and  of 
the  subperitoneal  and  retroperitoneal  tissues,  and  sometimes  in  the  peri- 
cardial and  subcutaneous  fat.  Extremely  large  foci  have  occasionally 
been  observed.  The  foci  are  whitish  or  yellowish  and  opaque  (in  marked 
contrast  to  the  translucent  yellow  of  the  normal  fat),  and  they  are  fre- 
quently surrounded  by  a  narrow  zone  of  hemorrhage.  They  consist  of 
lime  and  certain  fatty  acids.  Flexner  has  demonstrated  the  presence 
of  the  fat-splitting  ferment  (presumably  that  of  the  pancreatic  juice) 
in  distant  necrotic  foci  (subcutaneous  and  peritoneal  fat),  as  well  as 
in  the  foci  in  the  immediate  vicinity  of  the  pancreas.  Fat  necrosis 
is  believed  to  result  from  diffusion  of  the  pancreatic  ferment  in  conse- 
quence of  hemorrhagic  destruction  of  the  gland  or  obstruction  of  the  ducts. 

Symptoms. — As  a  rule,  the  patient  presents  a  history  of  long-standing 
gastro-intestinal  derangement;  sometimes  of  more  or  less  distinct  and 
recurring  attacks  of  colicky  pain,  nausea,  and  vomiting,  attributable  in 
some  cases  to  cholelithiasis,  in  others,  perhaps,  to  minor  attacks  of  pan- 
creatitis from  which  the  patient  has  recovered.  Acute  pancreatitis 
itself  is  characteristically  acute  in  onset,  with  sudden,  severe,  continuous 
pain  in  the  epigastrium,  nausea,  and  vomiting,  soon  followed  by  collapse, 
subnormal  temperature,  rapid  pulse,  and  sometimes  death  within  twenty- 
four  to  forty-eight  hours.  The  pain,  though  continuous,  is  subject  to 
paroxysmal  exacerbations,  and  is  intensified  l)y  motion  and  vomiting; 
as  a  rule,  it  is  not  very  well  localized — spreading  from  the  epigastrium 
over  the  upper  part  of  the  abdomen  (doubtless  due  to  stretching  and 


740  DISEASES  OF  THE  PANCREAS 

tearing  of  the  cceliac  plexus).  Occasionally  the  pain  is  more  marked  to 
the  left  of  the  median  line — when  the  lesions  are  more  marked  in  the 
tail  of  the  pancreas.  The  epigastrium  is  exquisitely  tender,  especially 
on  deep  pressure.  Should  the  patient  not  die,  evidences  of  peritonitis 
of  the  upper  part  of  the  abdomen  soon  develop.  The  pain  and  tender- 
ness continue;  rigidity  of  the  abdominal  muscles  becomes  marked;  and 
distention,  due  to  paresis  of  the  stomach  and  intestine,  ensues.  The  bowels 
are  markedly  constipated  (whence  the  condition  may  be  mistaken  for 
intestinal  obstruction),  the  temperature  rises  and  may  reach  104°  F. 
(though  this  is  unusual),  the  pulse  becomes  rapid  and  thready,  hiccough 
and  thirst  may  increase  the  distress  of  the  patient,  the  features  become 
pinched  and  pallid,  the  expression  anxious,  and  some  mental  wandering 
and  delirium  may  supervene.  Physical  examination  may  disclose  a 
deep-seated  swelling  or  merely  induration — tympanitic  on  percussion 
because  of  the  overlying  stomach  and  intestine.  A  chill  sometimes  occurs 
at  the  onset,  but  is  more  common  and  is  likely  to  be  repeated  later, 
and  to  be  associated  with  sweating  and  leukocytosis,  when  suppura- 
tion has  supervened.  Slight  jaundice  is  observed  in  some  cases,  and 
is  attributed  to  obstruction  of  the  common  bile  duct  or  this  and  the 
pancreatic  duct  by  a  gallstone  in  the  diverticulum  of  Vater,  by  swelling 
of  the  duodenal  mucous  membrane,  by  the  enlarged  and  swollen  pancreas, 
or  by  an  abscess  which  may  develop.  The  urine  is  lessened  in  amount, 
and  may  contain  albumin  and  casts,  but  rarely  sugar.  Opie  has  sug- 
gested that  the  fat-splitting  ferment  may  be  found  in  the  urine  in  some 
cases  and  recommends  this  as  a  test  of  possible  diagnostic  value.  An 
abscess  may  rupture  into  the  intestine,  and  blood  and  pus,  and  even  a 
portion  of  the  necrotic  pancreas,  may  appear  in  the  stools.  If  the  disease 
is  not  fatal  within  several  days,  the  acute  symptoms  subside,  and  rarely 
the  patient  may  eventually  recover  or  the  disease  may  become  chronic. 
Usually,  however,  if  not  relieved  by  operation,  the  patient  dies  from 
exhaustion  and  sepsis  in  the  course  of  several  days  or  weeks. 

Diagnosis. — "Acute  pancreatitis  is  to  be  suspected  when  a  previously 
healthy  person  or  a  sufferer  from  occasional  attacks  of  indigestion 
is  suddenly  seized  with  a  violent  pain  in  the  epigastrium  followed  by 
vomiting  and  collapse,  and  in  the  course  of  twenty-four  hours  by  a 
circumscribed  swelling,  tympanitic  or  resistant,  with  slight  elevation  of 
temperature.  Circumscribed  tenderness  in  the  course  of  the  pancreas 
and  tender  spots  throughout  the  abdomen  are  valuable  diagnostic  signs" 
(Fitz).  The  different  forms  of  acute  pancreatitis  cannot  be  differentiated 
the  one  from  the  other,  though  suppuration  is  suggested  by  the  ordinary 
evidences  of  sepsis.  Other  causes  of  peritonitis  in  the  upper  part  of  the 
abdomen  should  be  taken  into  consideration, 'but  it  is  often  impossible 
to  differentiate  before  operation,  perforation  of  a  gastric  or  a  duodenal 
ulcer,  though  the  history  sometimes  affords  a  clue.  In  cholecystitis  the 
pain  is  less  severe,  is  located  over  the  gall-bladder,  and  radiates  to  the 
right  and  the  back;  muscular  rigidity  is  less  widespread;  and  tympany, 
if  it  occurs,  is  delayed  and  less  marked.    A  history  of  previous  biliary 


CHRONIC  PANCREATITIS  741 

colic  and  jaundice  is  inconclusive,  since  it  may  be  present  in  pancreatitis 
as  well  as  in  cholecystitis.  Irritant  (and  ptomaine)  poisoning  is  suggested 
by  the  history  of  the  case,  analysis  of  the  vomit,  generalized  abdominal 
pain,  and  diarrhoea  (as  contrasted  with  constipation). 

Treatment  — ^The  nature  of  the  disease  precludes  the  possibility  of 
medicinal  treatment  being  of  much  avail.  At  the  onset,  attempts  should 
be  made  to  relieve  the  pain  by  hot  fomentations  locally  and  morphine 
h}^^odermicly,  and  to  counteract  the  collapse  by  stimulants  and 
external  heat.  The  treatment  of  the  disease  itself  is  essentially  surgical — 
exploration  and  drainage  of  the  lesser  peritoneal  cavity.  In  some  cases 
this  may  be  undertaken  with  hope  of  ultimate  success,  if  the  patient 
survives  the  initial  shock.  The  supervention  of  suppuration,  of  course, 
calls  for  operative  intervention. 


CHRONIC   PANCREATITIS. 

Etiology. — Chronic  interstitial  pancreatitis  (fibrosis  of  the  pancreas) 
is  more  common  in  men  than  in  women,  especially  between  the  fortieth 
and  the  sixtieth  year  (two-thirds  of  the  cases).  Its  etiological  factors 
are:  (1)  Bacterial  infections,  the  consequence  of  ascending  infection 
of  the  ducts  from  the  duodenum,  or  of  infection  transported  by  the 
bloodvessels  or  the  lymphatics,  as  in  syphilis,  tuberculosis,  etc.  (2) 
Intoxications,  especially  alcohol,  probably  answerable  for  the  rather 
common  association  of  interstitial  lesions  in  the  pancreas  and  cirrhosis 
of  the  liver.  (3)  Mechanical  factors.  Opie,  who  has  studied  the 
subject  attentively,  states  that  "the  most  common  cause  of  chronic 
pancreatitis  is  obstruction  of  the  duct  of  Wirsung,  due  to  pancreatic 
calculi,  to  biliary  calculi  in  the  terminal  part  of  the  common  bile  duct, 
or  to  carcinoma  invading  the  head  or  body  of  the  gland.  Obstruc- 
tion of  the  duct  may  be  followed  by  the  invasion  of  bacteria,  and 
these  take  part  in  the  production  of  the  resulting  lesion.  Ascending 
infection  of  the  unobstructed  duct  of  Wirsung  may  follow  an  acute  lesion 
of  the  duodenum  or  of  the  bile  passages,  and  may  cause  chronic  inflam- 
mation. In  cases  which  give  a  history  of  long-standing  vomiting,  chronic 
diffuse  pancreatitis  may  be  found  at  necropsy,  and  is  probably  the 
result  of  an  ascending  infection  of  the  gland." 

Pathology. — The  noteworthy  lesion  consists  of  enlargement  and 
induration  of  the  head  of  the  pancreas,  in  some  cases  of  the  entire 
organ.  Opie  distinguishes  two  varieties  of  chronic  pancreatitis:  (1) 
Interlobular  pancreatitis,  the  result  of  obstruction  of  the  ducts,  and 
sometimes  of  ascending  infection,  and  characterized  by  proliferation 
of  connective  tissue  between  the  lobules,  only  secondary  invasion  of 
the  lobules,  and  non-implication  of  the  islands  of  Langerhans,  except 
in  a  very  advanced  stage  of  the  disease;  and  (2)  interacinar  (or  intra- 
lobular) pancreatitis,  much  less  common  than  interlobular  pancrea- 
titis, and  characterized  by  proliferation  of  the  interacinar  connective 


742    ■  DISEASES  OF  THE  PANCREAS 

tissue  with  early  invasion  and  hyaline  degeneration  of  the  islands  of 
Langerhans.  This  accompanies  atrophic  or  Laennec's  cirrhosis  of  the 
liver,  arteriosclerosis,  and  hemochromatosis.  A  congenital  syphilitic 
pancreatitis,  characterized  by  diffuse  interstitial  connective-tissue  hyper- 
plasia and  atrophy  of  the  parenchyma,  but  with  preservation  of  the 
islands  of  Langerhans,  is  also  described. 

Symptomatology. — The  symptoms  of  chronic  pancreatitis  are  quite 
obscure,  and  in  many  cases  the  condition  is  merely  an  interesting 
finding  at  the  necropsy.  Occasionally,  however,  local  symptoms 
due  to  the  situation  of  the  organ,  evidences  of  interference  with  the 
motility  of  the  stomach  and  duodenum,  and  disturbances  with  the  func- 
tions (the  internal  and  the  external  secretions)  of  the  gland,  permit  an 
inference  as  to  the  presence  of  chronic  inflammatory  alterations.  The 
symptoms  develop  insidiously,  rarely  following  an  acute  attack,  and 
consist  of  gradually  increasing  dyspepsia,  loss  of  appetite,  nausea, 
flatulence,  and  epigastric  distention.  Deep-seated  pain,  tending  to 
radiate  to  the  left  and  the  back,  is  occasionally  complained  of,  and  on 
palpation,  deep-seated  tenderness  and  sometimes  a  sensation  of  increased 
resistance,  corresponding  to  the  pancreas,  may  be  elicited.  Vomiting 
sometimes  results  from  motor  insufficiency  and  dilatation  of  the  stomach, 
induced  by  enlargement  and  induration  of  the  head  of  the  pancreas ;  occa- 
sionally it  is  frequent  and  persistent.  Jaundice,  which  may  be  slight  or 
marked  and  prolonged,  is  common  also  in  conditions  of  enlargement  and 
induration  of  the  head  of  the  pancreas  (as  well  as  in  tumor  formations), 
and  results  from  obstruction  of  the  common  bile  duct.  Some  cases  of 
so-called  catarrhal  jaundice  have  been  attributed  by  Mayo  Robson  to 
enlargement  of  the  head  of  the  pancreas.  Obstruction  of  the  portal 
vein  may  lead  to  the  development  of  ascites.  Glycosuria  and  other 
evidences  of  diabetes  mellitus  occur  in  a  few  cases — especially  when 
the  islands  of  Langerhans  are  destroyed;  and  since  this  may  happen 
without  much  involvement  of  the  glandular  structure  of  the  organ, 
disturbances  of  pancreatic  digestion  in  the  intestine  may  be  absent  in  the 
presence  of  glycosuria.  Alimentary  glycosuria  has  been  observed  in  many 
cases.  The  stools  are  voluminous  and  contain  undigested  muscle  fibers 
(azotorrhoea)  and  visible  fat  (steatorrhoea),  but  azotorrhoea  is  found  also 
in  conditions,  such  as  obstruction  of  the  ducts,  from  a  tumor,  a  cyst,  or  a 
calculus,  interfering  with  the  flow  of  the  pancreatic  juice  into  the  intestine; 
and  steatorrhoea  occurs  in  obstruction  of  the  bile  duct  as  well  as  the  pan- 
creatic duct,  and  after  the  ingestion  of  large  quantities  of  fat.  The  chemical 
constitution  of  the  fat,  however,  may  be  of  some  diagnostic  value,  since  the 
investigations  of  Miiller  seem  to  show  that  normally  (as  well  as  in  conditions 
causing  deficiency  or  absence  of  bile  from  the  intestine)  75  per  cent,  of 
the  fat  in  the  feces  is  split  up  into  fatty  acids  and  soaps,  whereas  in  dis- 
ease of  the  pancreas  (causing  deficiency  or  absence  of  the  pancreatic 
juice  in  the  intestine)  the  fat  is  present  largely  as  free  neutral  fat.  It 
has  been  suggested  that  in  such  cases  a  useful  test  of  the  presence 
or  absence  of  the  pancreatic  juice  might  result  from  the  giving  of  pan- 


CYSTS  OF  THE  PANCREAS  743 

creatic  preparations  with  the  subsequent  disappearance  from  the  stools 
of  unchanged  muscle  fibers  and  fat.  However,  a  marked  difficulty  in 
the  diagnosis  of  pancreatic  disorders  consists  in  the  fact  that  the  functions 
of  the  pancreas  are  shared  by  other  organs.  Diarrhoea  is  rather  common; 
secondary  anemia  and  emaciation  are  features  of  some  cases;  the  skin 
may  become  pigmented;  and  profuse  salivation  (pancreatic  sialorrhoea) 
occasionally  occurs  and  may  become  distressing. 

Diagnosis. — ^The  diagnosis  is  always  difficult,  and  frequently  is  scarcely 
more  than  a  surmise.  The  most  trustworthy  symptoms  consist  of 
chronic  indigestion,  more  or  less  jaundice,  a  disposition  to  diarrhoea 
and  large  stools,  and  emaciation.  Carcinoma  of  the  pancreas,  carcinoma 
of  the  bile  ducts,  a  calculus  in  the  common  bile  duct,  and  perigastric 
adhesions  (following  gastric  ulcer  or  carcinoma),  must  be  considered  in 
the  differential  diagnosis. 

Prognosis. — The  outlook  is  good  in  the  event  of  surgical  intervention. 

Treatment. — ^The  treatment,  aside  from  operative  intervention,  is 
largely  hygienic  and  dietetic.  Diastatic  ferments-,  or  pancreatic  prepara- 
tions, are  sometimes  of  service  in  aiding  digestion.  The  causative  factors 
should  receive  attention  in  all  cases.  Of  these,  gallstones  are  of  prime 
importance — ^whence  the  good  effects  of  operative  intervention  (drainage 
of  the  biliary  ducts  as  a  preventive,  as  well  as  a  curative  measure). 


CYSTS  OF  THE  PANCREAS. 

Cysts  of  the  pancreas  are  about  equally  common  in  the  two  sexes — of 
121  of  the  134  cases  collected  by  Oser,  60  were  in  men,  and  61  in  women. 
Sixty-two  of  the  cases  (51  per  cent.)  occurred  between  the  ages  of  twenty 
and  forty  years,  but  the  greatest  number  (21  cases)  occurred  in  men  during 
the  fourth  decade,  and  the  greatest  number  in  women  (21  cases)  during 
the  third  decade.  The  condition,  however,  has  been  observed  in  infancy. 
Korte  distinguishes  three  varieties :  (1)  Traumatic  cysts,  following  blows 
and  oft-repeated  pressure  on  the  abdomen;  (2)  postinflammatory 
cysts;  and  (3)  cysts  of  unknown  origin.  Mayo  Robson  distinguishes 
anatomically:  (1)  Retention  cysts;  (2)  proliferation  cysts — cystic  ade- 
noma and  epithelioma;  (3)  hydatid  cysts;  (4)  congenital  cysts;  (5) 
hemorrhagic  cysts;  and  (6)  pseudocysts.  The  cyst  may  develop  from  any 
part  of  the  pancreas,  though  probably  most  frequently  from  the  tail, 
and  it  varies  much  in  size  and  in  situation  in  different  cases.  It  may  be 
single  or  multiple,  and  microscopic  in  size  or  so  large  as  to  accommodate 
many  liters  of  fluid  (a  cyst  containing  14  liters  has  been  reported).  The 
fluid  contents  is  usually  slightly  opaque  and  straw-colored,  though  in 
traumatic  cases  it  may  be  hemorrhagic.  Its  reaction  is  alkaline;  its 
specific  gravity  varies  between  1007  and  1028  (Oser) ;  and  microscopicly 
it  contains  fat  granules,  cell  detritus,  blood-coloring  matter,  and 
sometimes  cholesterin.  Occasionally,  but  often  not  in  the  older  cases, 
the  fluid  digests  albumin  and  fibrin  (important),  and  emulsifies  fat  and 


744  DISEASES  OF  THE  PANCREAS 

converts  starch  into  glucose  (of  relatively  little  importance,  since  other 
fluids  of  the  body  sometimes  possess  the  same  qualities).  Most  cysts 
develop  in  the  lesser  peritoneal  cavity,  displace  the  stomach  upward  and 
to  the  right,  and  present  between  the  stomach  and  the  transverse  colon; 
in  some  cases  the  cyst  presents  above  the  stomach,  which  it  displaces 
downward;  occasionally  it  develops  in  the  transverse  mesocolon  and 
presents  below^  the  colon;  and  in  still  rarer  cases  it  presents  toward  the 
splenic  or  the  nephritic  region. 

Symptoms.- — ^The  early  symptoms  vary,  depending  on  the  etiology.  In 
traumatic  cases,  initial  pain,  tenderness,  and  vomiting,  as  well  as  other 
evidences  of  local  inflammation  may  be  present.  In  other  cases  the 
early  symptoms  are  more  mild  and  not  to  be  differentiated  from  the 
symptoms  of  chronic  pancreatitis.  In  most  cases  the  presence  of  a  cyst 
is  not  suspected  until  it  begins  to  cause  enlargement  of  the  abdomen. 
Clinically  the  cyst  appears  as  a  spheroidal,  smooth,  rather  resistant, 
usually  immobile  mass,  presenting  in  the  hj'pochondriac  region  between 
the  stomach  and  the  colon,  though,  as  already  mentioned,  it  may  present 
below  the  colon — hence  below  the  mnbilicus.  Other  s}Tnptoms  result 
from  the  absence  of  the  pancreatic  juice  from  the  intestine  (azotorrhoea, 
steatorrhcea),  as  well  as  glycosuria.  Certain  s}TQptoms  result  from  press- 
ure of  the  cyst  or  adliesions,  such  as  neuralgic  pains  from  pressure  on  the 
regional  nerves,  jaundice  from  obstruction  of  the  common  bile  duct,  diffi- 
culty in  emptying  the  stomach  and  consequent  dilatation  of  the  stomach 
from  obstruction  of  the  pylorus  or  the  duodenum,  ascites  and  intes- 
tinal hemorrhage  from  pressure  on  the  portal  or  the  mesenteric  vein, 
oedema  of  the  lower  extremities  from  obstruction  of  the  vena  cava, 
hydronephrosis  from  obstruction  of  the  ureter,  etc.  Ruptiu-e  of  the  cyst 
into  the  peritoneal  cavity,  the  stomach,  or  the  intestine  may  result  in 
(sometimes)  sudden  decrease  in  the  size  of  the  abdomen,  and  watery 
discharges  from  the  bowel. 

Treatment. — ^The  treatment  consists  of  operation — drainage  or  extir- 
pation of  the  cyst. 


TUMORS    OF   THE   PANCREAS. 

Of  the  tiunors  of  the  pancreas,  in  themselves  comparatively  rare, 
carcinoma  is  the  most  frequent,  though  sarcoma  and  adenoma  have 
been  observed.  Carcinoma  of  the  pancreas  is  more  common  in  men 
than  in  women,  and  occurs  most  frequently  from  the  fortieth  to  the 
sixtieth  year,  but  it  has  been  observed  in  infancy  and  in  advanced  life. 
It  is  most  common  in  the  head  of  the  pancreas,  but  it  may  be  wide- 
spread or  limited  to  the  body  or  the  tail.  It  may  be  small  or  very  large, 
and  frequently  extends  to  adjacent  structures  by  contiguity  of  structure, 
and  gives  metastasis  to  the  regional  lymph  nodes  and  the  liver.  The 
growth  is  commonly  an  adenocarcinoma,  usually  of  the  so-called  scirrhus 
variety. 


PANCREATIC  CALCULI  745 

Symptoms. — The  early  symptoms  do  not  differ  essentially  from 
those  of  chronic  pancreatitis.  Epigastric  pain  is  present  in  most 
cases,  and  is  often  paroxysmal.  Jamidice,  due  to  obstruction  of  the 
diverticulum  of  Vater  or  of  the  common  bile  duct,  is  a  conspicuous  symp- 
tom; it  may  develop  gradually  or  suddenly,  is  intense  and  persistent, 
and  is  usually  associated  with  enlargement  of  the  gall-bladder  (in  con- 
trast with  an  impacted  calculus  in  the  common  bile  duct,  in  which,  in 
consequence  of  infection  and  consequent  atrophy,  the  gall-bladder  is 
usually  small :  Courvoisier's  law).  Other  symptoms  due  to  pressure  on  or 
adhesions  to  regional  structures  occur,  but  these  are  not  different  from 
those  mentioned  in  connection  with  pancreatic  cyst,  although  duodenal 
stenosis  and  consequent  gastric  dilatation  (with  nausea  and  vomiting) 
is  probably  the  most  common.  Symptoms  due  to  absence  of  the  pan- 
creatic juice  are  similar  to  those  mentioned  under  chronic  pancreatitis. 
In  a  small  proportion  of  cases  a  tumor  is  palpable,  and  sooner  or  later 
the  well-known  anemia,  emaciation,  and  cachexia  of  carcinoma  intervene. 

Diagnosis.— In  the  early  stages,  and,  indeed,  in  the  late  stages  in  many 
cases,  the  disease  is  not  susceptible  of  diagnosis.  The  most  suggestive 
symptoms  are  pain,  a  palpable  tumor,  jaundice  (with  enlarged  gall- 
bladder), anemia,  emaciation,  and  cachexia.  Carcinoma  of  adjacent 
viscera  (pylorus,  liver,  colon,  etc.)  must  be  considered  in  the  differential 
diagnosis. 

Treatment. — The  treatment  is  purely  symptomatic.  Cholecystenter- 
ostomy  and  even  removal  of  the  carcinoma  have  been  practised  in  a  few 
cases  with  good  temporary  results. 

PANCREATIC    CALCULI. 

Etiology. — Pancreatic  calculi  are  rare,  scarcely  more  than  one  hun- 
dred cases  having  been  reported.  It  occurs  especially  between  the 
ages  of  thirty-five  and  forty-five  years,  and  is  apparently  much  more 
common  in  men  than  in  women  (26  cases  in  men,  and  6  cases  in 
women,  in  Oser's  collection).  As  a  rule,  the  calculi  are  small,  often 
so  small  as  scarcely  to  be  discernible,  but  very  large  calculi  (up  to  2  to 
4  cm,  in  diameter)  have  been  observed.  Usually  there  is  more  than 
one  calculus,  sometimes  very  many  (upward  of  a  hundred  or  more). 
They  may  be  round,  oblong,  or  irregular  in  shape,  and  smooth  or  rough. 
Usually  they  are  composed  of  calcium  carbonate,  either  alone  or  in  com- 
bination with  calcium  phosphate.  They  are  sometimes  found  in  the 
pancreatic  ducts  at  necropsy  (a  personal  observation  of  my  own); 
sometimes  they  become  impacted  in  the  duct  of  Wirsung,  or  in  the  com- 
mon bile  duct,  or  in  the  diverticulum  of  Vater.  Thus  they  cause:  (1) 
Chronic  interstitial  pancreatitis  with  marked  overgrowth  of  the  fibroid 
connective  tissue  and  atrophy  of  the  glandular  tissue,  and  sometimes  lead 
to  dilatation  of  the  ducts  and  large  cyst-like  formations,  which  rarely 
establish  fistulous  communications  with  adjacent  organs,  such  as 
the  stomach,  the  intestine,  etc.    (2)  In  consequence  of  secondary  infec- 


746  DISEASES  OF  THE  PERITONEUM 

tion,  they  sometimes  lead  to  abscess  of  the  pancreas.  (3)  Sometimes, 
analogous  to  a  similar  process  in  the  gall-bladder,  they  are  said  to  result 
in  carcinoma  of  the  pancreas.  The  exact  cause  of  the  calculus  formation 
is  not  known,  although  there  is  some  evidence  that  bacterial  infection 
of  the  mucous  membrane  results  in  their  formation — analogous  to  the 
process  in  the  gall-bladder.  Indeed,  calculi  in  the  biliary  passages  and 
in  the  pancreas  are  sometimes  associated. 

Symptoms. — Pancreatic  calculi  often  occasion  few,  if  any,  symptoms, 
especially  when  they  lie  dormant.  Like  gallstones,  they  produce  symp- 
toms when  they  move  on  from  their  place  of  birth  (pancreatic  colic),  and 
when  they  produce  secondary  results  in  and  about  the  pancreas. 

Pancreatic  colic  is  characterized  by  sudden  severe  pain  in  the  epi- 
gastrium, radiating  to  the  left  mammary  region,  the  left  margin  of  the 
ribs,  and  the  left  shoulder,  vomiting,  and  sometimes  collapse.  In  some 
cases  the  pain  is  more  diffuse,  radiates  to  both  sides,  and  is  not  to  be 
differentiated  from  some  attacks  of  gallstone  colic.  Following  the 
attack,  pancreatic  calculi  have  occasionally  been  found  in  the  stools. 
Confirmatory  symptoms  consist  of  salivation,  hunger  and  thirst  (said  to 
come  on  after  the  colic),  fatty  diarrhoea,  glycosuria,  and  other  evidences 
of  interference  with  the  functional  activity  of  the  pancreatic  juice.  As  a 
matter  of  fact,  aside  from  pancreatic  colic,  the  presence  of  pancreatic 
calculi  is  altogether  insusceptible  of  diagnosis,  the  symptoms  being  those 
of  its  results — chronic  pancreatitis,  pancreatic  abscess,  etc.  In  the  event 
of  marked  dilatation  of  the  ducts  a  tumor  may  be  palpable. 

Diagnosis. — ^The  diagnosis  is  suggested  by  epigastric  pain  (colic)  often 
recurring  and  of  obscure  causation,  and  associated  with  glycosuria, 
and  many  muscle  fibers  and  marked  increase  of  neutral  fat  in  the  stools, 
and  the  absence  of  evidence  of  a  newgrowth.  The  calculi  are  sometimes 
susceptible  of  recognition  by  the  x-rays. 

Treatment. — The  treatment  of  the  colic  does  not  differ  from  that  of 
gallstone  colic — hot  application  to  the  abdomen,  morphine  and  atropine 
hypodermicly,  and  partial  or  complete  anesthesia  (ether  or  chloroform)  if 
necessary.  Impaction  of  the  stone  with  dilatation  of  the  ducts  or  abscess 
formation  calls  for  surgical  intervention.  Otherwise,  the  treatment 
is  that  of  chronic  pancreatitis,  which  also  is  largely  operative. 


DISEASES  OF  THE  PERITONEUM. 

ASCITES. 

( Hydro-peritoneum . ) 

Etiology. — ^Ascites,  the  accumulation  of  serous  fluid  in  the  peritoneum, 
may  be  due  to  general  or  local  causes.  The  general  causes  comprise: 
(1)  Those  that  determine  dropsy  in  other  parts  of  the  body,  such  as 
chronic  cardiac  disease,   sometimes  antedated  by  chronic  pulmonary 


ASCITES  747 

disease  (such  as  emphysema),  or  pleural  or  mediastinal  lesions;  and 
(2)  anemic  and  cachectic  states,  such  as  high-grade  anemia,  leukemia, 
chronic  nephritis,  amyloidosis,  etc.  The  local  causes  comprise:  (1) 
Portal  obstruction,  such  as  may  occur  in  cirrhosis  of  the  liver,  advanced 
passive  congestion  of  the  liver,  pylethrombosis,  or  compression  or  kinking 
of  the  portal  vein;  (2)  chronic  inflammation  of  the  portal  vein,  tuber- 
culosis or  so-called  simple;  (3)  abdominal  tumors,  such  as  carcinoma 
of  the  peritoneum,  ovarian  tumors,  the  enlarged  spleen  of  leukemia,  etc. 

Symptoms. — ^The  chief  manifestation  consists  of  a  uniform  or  sym- 
metrical enlargement  of  the  abdomen.  Secondary  symptoms,  due  largely 
to  embarrassed  cardiac  and  pulmonary  action  from  compression,  are 
usually  also  present. 

Examination  reveals  the  abdomen  to  be  more  or  less  enlarged.  In  the 
recumbent  posture,  there  is  bulging  of  the  flanks;  the  umbilicus  may 
protrude;  the  superficial  veins  are  often  dilated  and  tortuous;  the  anas- 
tomosis between  the  epigastric  and  the  mammary  veins  may  carry  the 
blood  upward;  in  cirrhosis,  a  plexus  of  veins  may  centre  in  the  umbilicus 
(caput  medusae).  Percussion  reveals  dulness  in  both  flanks  and  low 
down  in  the  hypogastric  and  the  inguinal  regions,  and  tympany  above 
— around  the  umbilicus;  both  the  dulness  and  the  tympany  shift  with 
change  in  the  posture  of  the  patient.  Palpation  reveals  a  distinct  sense 
of  fluctuation  (which  must  not  be  confounded  with  a  somewhat  similar 
sensation  transmitted  by  a  fat  and  relaxed  abdomen). 

Diagnosis. — The  diagnosis,  as  a  rule,  is  readily  made.  One  must  ex- 
clude ovarian  cyst,  pancreatic  cyst,  a  distended  urinary  bladder,  and  fluid 
feces  in  a  dilated  colon. 

The  fluid  is  usually  pale  amber  in  color,  clear,  somewhat  opalescent,  and 
alkaline.  That  which  occurs  in  anemic  and  cachectic  states  has  a  spe- 
cific gravity  of  1010  or  less,  and  contains  less  than  1  per  cent,  of  albumin; 
that  of  obstruction  (liver  cirrhosis,  etc.)  has  a  specific  gravity  of  1010  to 
1015,  and  contains  from  1  to  3  percent,  of  albumin;  and  that  of  inflam- 
matory processes  (exudates)  has  a  specific  gravity  of  1015  to  1020  or 
more,  and  contains  from  3  to  5  per  cent,  or  more  of  albumin.  Occa- 
sionally the  fluid  contains  traces  of  urea,  urobilin,  purin  bodies,  sugar,  etc. 
Inflammatory  fluid  is  likely  also  to  be  turbid.  Bacteriological  studies  show 
the  fluid  to  be  sterile,  in  the  absence  of  infectious  processes.  Cytological 
studies  reveal  the  cellular  constituents  of  ordinary  ascites  (transudates) 
to  be  few  and  to  consist  of  lymphocytes  and  endothelial  cells,  with  a  few 
erythrocytes  and  leukocytes;  inflammatory  fluids  may  reveal  more  poly- 
nuclear  neutrophilic  leukocytes.  Cryoscopy  reveals  the  freezing  point 
to  vary  with  the  amount  of  albumin. 

Occasionally  the  fluid  is  chylous,  in  consequence  of  obstruction  and 
rupture  of  the  lymphatics  (it  contains  considerable  albumin,  less  than 
0.9  per  cent,  of  fat,  and  perhaps  some  sugar);  or  it  may  be  chyliform 
(no  sugar,  but  considerable  fat— 5  per  cent,  or  more);  or  it  may  be  hemor- 
rhagic (traumatism,  rupture  of  minute  vessels,  petechial  hemorrhages  in 
the  serous  membrane,  some  forms  of  tuberculosis,  carcinoma,  etc.). 


748  DISEASES   OF  THE  PERITONEUM 

The  percentage  of  albumin  may  be  calculated  by  Reuss'  formula — 
the  percentage  of  albumin  equals  three-eighths  of  the  last  two  figures  of 
the  specific  gravity,  minus  2.8.  Rivalta's  reaction  may  also  be  resorted  to 
to  differentiate  transudates  from  exudates :  to  50  c.c.  of  distilled  water  one 
drop  of  50  per  cent,  acetic  acid  is  added,  and  then  one  drop  of  the  ascitic 
fluid;  in  the  event  of  the  fluid  being  inflammatory,  on  coming  in  contact 
with  the  acidulated  water,  it  assumes  the  form  of  a  bluish- white  opalescent 
ring,  which,  as  it  broadens  out,  may  become  striated  by  many  bluish- white 
lines. 

ACUTE  PERITONITIS. 

Etiology. — ^Acute  peritonitis  may  perhaps  occur  as  a  primary  disorder, 
but  it  is  very  rare.  Usually  the  condition  is  secondary — to  disease  of  any 
of  the  abdominal  organs;  less  commonly  to  diseases  of  more  distant 
organs  (by  metastasis).  The  most  important  antecedent  conditions  are 
appendicitis,  salpingitis,  gastric  and  duodenal  ulcer,  cholecystitis,  and 
pancreatitis;  but  any  inflammatory,  suppurative,  or  ulcerative  lesion  of 
the  gastro-intestinal  tract,  the  female  genitalia,  the  liver,  spleen,  urinary 
organs,  etc.,  may  be  followed  by  peritonitis.  The  important  micro- 
organismal  causes  are:  Bacillus  coli,  streptococci,  staphylococci,  Ba- 
cillus pyocyaneus,  Diplococcus  pneumoniae.  Bacillus  proteus.  Micro- 
coccus gonorrhoeae.  Bacillus  typhosus,  etc.;  mixed  infections  are  common. 

Pathology. — ^The  lesions  may  be  circumscribed  or  diffuse;  and  fibri- 
nous, serofibrinous,  purulent,  or  hemorrhagic  in  character;  rarely  also 
putrid;  or  there  may  be  only  a  small  amount  of  thin,  serous  fluid;  or  the 
peritoneum  may  be  only  opaque  and  lustreless,  no  exudate  having 
formed.  The  lesions  may  extend  to  the  peritoneum  from  continuity  of 
tissue,  or  from  perforation  into  the  peritoneum  of  a  hollow  viscus  or 
abscess  of  a  solid  organ.  Special  interest  attaches  to  localized  peri-appen- 
dicular  peritonitis,  to  pelvic  peritonitis  (the  consequence  of  antecedent 
infection  of  the  uterus  or  Fallopian  tubes),  to  peritonitis  about  the 
pylorus,  duodenum,  and  gall-bladder,  and  to  subphrenic  peritonitis. 
From  these  local  lesions  the  peritonitis  may  become  diffuse;  but  it  may 
become  diffuse  also  with  such  antecedent  localizations  as,  for  instance, 
after  perforation  in  tj^hoid  fever. 

Symptoms. — In  the  localized  forms  of  peritonitis  the  symptoms  are 
largely  those  of  the  antecedent  disorder,  many  of  the  manifestations  of 
which  are  due  to  the  associated  peritonitis.  The  most  important  com- 
prise abdominal  pain,  tenderness,  and  rigidity  of  the  overlying  muscles. 
Nausea,  vomiting,  and  constipation  are  often  present;  and  there  is  more 
or  less  fever,  a  rapid  pulse  (sometimes  the  hard,  wiry  pulse  of  the  older 
^^^:•ite^s),  and  leukocytosis;  and  a  mass  may  be  palpable.  In  the  per- 
forative cases  sudden  severe  abdominal  pain  and  collapse  are  usually 
observed.  In  the  diffuse  cases  the  pain  and  tenderness  become  more 
widespread,  the  abdomen  distended  and  tympanitic,  and  free  fluid  may 
be  more  or  less  readily  detected  (physical  signs  of  ascites).     The  pulse 


CHRONIC  PERITONITIS  749 

becomes  very  rapid  and  weak,  and  the  fever  moderate  or  high  (rarely 
only  slight  fever);  nausea  and  vomiting  may  persist,  and  constipation  is 
usually  obstinate.  The  face  becomes  pinched,  the  eyes  sunken,  and 
the  expression  anxious  (Hippocratic  facies);  the  skin  takes  on  a  pallid, 
cyanotic  hue,  and  may  be  bathed  in  continuous  or  frequently  repeated 
sweats;  the  patient  usually  becomes  delirious,  and  soon  dies. 

Diagnosis. — The  diagnosis  is  usually  quite  apparent  from  the  afore- 
mentioned symptoms.  Special  attention  should  be  directed  to  ascer- 
taining the  antecedent  condition  answerable  for  the  peritonitis.  In  addi- 
tion to  these  disorders,  in  some  cases  it  may  be  necessary,  for  a  time  at 
least,  to  consider  the  different  types  of  colic  (intestinal,  renal,  and  gall- 
stone), intestinal  obstruction,  ruptured  tubal  pregnancy,  embolism  or 
thrombosis  of  the  superior  mesenteric  artery,  etc.  Subphrenic  abscess 
usually  follows  gastric  (or  duodenal)  ulcer  or  carcinoma,  or  other  suppu- 
rative or  ulcerative  lesions  of  the  intestine;  it  is  characterized  by  a  collec- 
tion of  pus,  or  of  pus  and  gas  (subphrenic  pyopneumothorax)  between 
the  liver  and  the  diaphragm;  and  it  is  suggested  by  severe  pain,  nausea, 
vomiting,  embarrassed  respiration,  chills,  fever,  sweats,  and  leukocytosis, 
and  the  physical  signs  of  fluid  or  of  fluid  and  air  above  the  liver. 

Prognosis. — In  diffuse  peritonitis  death  usually  ensues  within  forty- 
eight  hoiu's.  In  the  circumscribed  cases  the  outlook  varies  with  the 
extent  and  severity  of  the  lesions  and  the  treatment  adopted. 

Treatment. — The  treatment,  although  modified  somewhat  by  the  ante- 
cedent disorder,  is  virtually  that  described  for  appendicitis.  In  the 
majority  of  cases  the  treatment  is  essentially  and  solely  surgical. 

CHRONIC  PERITONITIS. 

Etiology. — Clu'onic  peritonitis  is  perhaps  rarely  a  primary  process,  in 
which  event  it  is  usually  set  up  by  the  tubercle  bacillus.  Commonly  the 
condition  is  secondary  to  disease  of  any  of  the  abdominal  viscera,  or  it 
may  be  part  of  a  multiple  serositis. 

Pathology. — Like  acute  peritonitis,  the  lesions  may  be  circumscribed 
or  dift'use.  The  circimiscril)ed  lesions  often  represent  the  residue  of 
postacute  localized  peritonitis,  and  consist  of  more  or  less  thick  or  thin 
fibrous  adhesions  or  bands.  These  are  especially  common  about  the 
appendix,  the  female  genitalia,  the  gall-bladder,  pylorus,  and  duodenum, 
the  liver,  and  the  spleen;  occasionally  they  involve  the  intestine,  the 
mesentery,  etc.  They  bind  the  organs  involved  to  adjacent  organs  or 
tissues,  and  more  or  less  seriously  interfere  with  their  functional  activity. 
The  diffuse  lesions  may  consist  of:  (a)  Widespread  thickening  and  adhe- 
sions, which,  uniting  the  intestines  to  the  abdominal  parietes  and  viscera, 
may  lead  to  complete  obliteration  of  the  peritoneum  (obliterative  or 
deforming  peritonitis).  (1))  Serous  effusion,  which  may  be  slight, 
moderate,  or  great  in  amount,  and  is  likely  to  be  tuberculous  in  nature 
(p.  103).  (c)  Hemorrhagic  effusion,  which  is  most  common  in  tuber- 
culosis or  carcinoma  of  the  peritoneum. 


750    '  DISEASES  OF   THE  PERITONEUM 

Symptoms. — The  circumscribed  adhesions  are  responsible  for  much 
of  the  so-called  chronic  "indigestion,"  especially  the  adhesions  about  the 
appendix,  the  gall-bladder,  the  pylorus,  and  the  duodenum.  Pain  may 
be  dull  and  more  or  less  persistent,  or  colicky.  Eventually  more  or 
less  general  impairment  of  health  and  invalidism  may  ensue.  A  coil 
of  intestine  may  become  caught  beneath  a  fibrous  band  and  intestinal 
obstruction  and  strangulation  ensue. 

The  diffuse  cases  with  much  fluid  exudation  are  characterized  by  the 
physical  signs  of  ascites;  and,  since  most  of  the  cases  are  tuberculous, 
there  is  usually  also  some  fever,  local  pain  and  tenderness,  and  perhaps 
also  muscular  rigidity,  emaciation,  etc.  A  tuberculous  focus  elsewhere 
in  the  body  may  be  detectable.  Chronic  obliterative  or  deforming  peri- 
tonitis is  suggested  by  palpable  tumor-like  masses  and  sacculated  fluid, 
but  it  is  rarely  recognized  during  life. 

Diagnosis. — The  "dyspeptic"  cases  should  be  recognized  by  bearing  in 
mind  their  etiological  factors  and  associated  conditions.  Ascites  and 
fever  are  significant  of  the  more  diffuse  lesions  (usually  tuberculous). 

Prognosis. — Some  of  the  ascitic  cases  in  young  subjects  tend  to  undergo 
spontaneous  recovery,  but  in  general  the  outlook  in  all  cases  is  not 
reassuring. 

Treatment. — ^The  treatment  of  the  tuberculous  cases  is  mentioned  on 
page  105;  otherwise  the  treatment  is  surgical. 


MULTIPLE  SEROSITIS. 

{Multiple  Progressive  Hyaloserositis,  Nicholls;  Polyorrhomenitis;  Polyserositis;  Indu- 
rative Mediastino'pericarditis;  Chronic  Hyperplastic,  Hyaline,  or  Deforming 
Peritonitis;  Zuckergussleber ;  Zuckergussmilz;  Zuckergussherz;  Zucker- 
gusslunge;  Pericarditic  Pseudocirrhosis  of  the  Liver,  Peck.) 

Etiology. — The  cause  of  multiple  serositis  is  not  well  understood.  Cer- 
tain of  the  infective  diseases,  such  as  typhoid  fever,  pertussis,  malaria, 
syphilis,  and  rheumatism,  are  set  down  as  etiological  factors  in  a  number 
of  the  reported  cases.  In  some  cases  the  lesions  are  of  an  extremely 
obscure  and  unknown  etiology,  whereas  in  other  cases  the  provoking 
agent  is  certainly  the  tubercle  bacillus;  other  cases  occur  during  the 
course  of  chronic  nephritis. 

Pathology. — ^Anatomically  the  distinguishing  feature  of  these  cases  is 
a  chronic  fibrous  (usually  hyperplastic)  inflammation  of  the  several 
serous  membranes  of  the  body — a  multiple  serositis.  In  some  cases  the 
inflammation  may  remain  localized  to  one  or  two  serous  membranes, 
but  there  is  a  marked  tendency  for  all  the  serous  membranes  to  become 
involved.  The  several  serous  membranes  may  become  involved  equally 
or  unequally;  usually  the  lesions  are  most  marked  in  the  pericardium 
and  on  both  sides  of  the  diaphragm.  In  some  cases  extensive  calcifica- 
tion of  the  pericardium  occurs.  In  cases  in  which  there  is  but  partial 
obliteration  of  the  pleural  or  the  pericardial  sacs  there  is  usually  also 


MULTIPLE  SEROSITIS  751 

some  fluid  present.  In  many  cases,  however,  not  only  is  the  pericardium 
thickened  and  obliterated,  but  it  has  also  formed  adhesions  with  the  chest 
wall  and  the  structures  of  the  mediastinum,  one  or  both  pleurae  are  thick- 
ened and  obliterated,  and  the  peritoneum  is  more  or  less  thickened  and 
adherent  and  contains  a  large  quantity  of  fluid.  In  many  cases  the  liver 
is  adherent  not  only  to  the  under  surface  of  the  diaphragm,  but  also  to 
the  stomach,  the  colon,  the  omentum,  the  anterior  abdominal  wall,  etc. 
The  lesions  involve  also  the  spleen,  especially  in  those  cases  in  which 
there  are  extensive  adhesions  in  the  left  pleura.  A  distinguishing  feature 
of  the  lesions  is  the  development  of  thick,  fibrous,  almost  cartilaginous, 
masses  of  connective  tissue,  that  encase,  compress,  and  often  distort  the 
organs,  and  give  rise  to  an  appearance  suggesting  confectioner's  icing — 
whence  the  designation  "iced  liver,"  or  sugar-iced  liver  (Zuckerguss- 
leber),  etc.  In  many  cases  of  primary  pericarditis  the  liver  is  enlarged, 
smooth,  and  has  sharp  edges;  later,  with  the  development  of  the  peri- 
hepatitis, the  liver  lessens  in  size,  its  surface  becomes  somewhat  irregular, 
its  edges  rounded,  and  sometimes  the  entire  organ  becomes  much  dis- 
torted; still  later,  or  in  some  cases  earlier,  the  appearances  characterized 
as  nutmeg,  with  or  without  atrophic  alterations,  may  supervene.  Al- 
though some  slight  connective-tissue  proliferation  and  some  extension  of 
newly  formed  connective  tissue  from  the  thickened  capsule  sometimes 
occur,  the  common  absence  of  marked  connective-tissue  proliferation 
in  the  liver  is  noteworthy.  In  some  cases  the  lesions  of  cirrhosis  are 
encountered. 

Symptoms. — Although  the  disease  is  characterized  by  slow,  insidious, 
and  intermittent  course,  the  perihepatitis  and  the  peritonitis  dominate  the 
clinical  picture  of  the  well-developed  disease.  Aside  from  this,  that  is, 
aside  from  the  ascites,  the  clinical  picture  varies,  depending  upon  the 
point  of  origin  of  the  disease.  In  some  cases  the  disease  is  ushered  in 
with  acute  pericarditis,  pleuritis  (which  may  necessitate  repeated  tap- 
pings), or  perihepatitis  (circumscribed  peritonitis),  which  subsides  and 
leaves  the  patient  apparently  well  for  a  number  of  years.  Usually,  how- 
ever, the  lesions  of  the  pericardium  and  of  the  pleurae  are  latent,  and  the 
first  sensible  evidence  of  the  disease  is  ascites.  In  some  cases  of  primary 
pericarditis  slight  and  transient  oedema  of  the  legs  may  be  present 
early,  but  this  is  not  observed  in  many  cases,  inasmuch  as  the  pericar- 
ditis is  usually  latent.  When  oedema  does  occur  early,  it  usually  soon 
subsides  and  does  not  recur  until  the  ascites  has  been  present  for  a  long 
time,  or  until  shortly  before  death;  except  shortly  before  death,  it  is  in- 
conspicuous when  contrasted  with  the  excessive  ascites.  Associated 
with  early  oedema,  slight  swelling  of  the  spleen  and  disturbance  of  the 
gastro-intestinal  tract  may  develop,  l)ut  these  usually  subside  with  the 
ascites,  and  the  disease,  as  a  rule,  is  characterized  by  the  entire  absence 
of  such  symptoms  until  shortly  before  death.  The  ascites  is  characterized 
by  the  fact  that  it  is  excessive,  that  it  necessitates  repeated  tappings, 
that  it  recurs  rapidly  after  tapping,  and  that  it  may  remain  stationary 
(not  necessitating  tapping)  for  many  years.     After  repeated  tappings  it 


752  DISEASES  OF  THE  PERITONEUM 

may  be  impossible  to  draw  off  much  fluid  again  on  account  of  the  devel- 
opment of  many  adhesions. 

In  a  few  cases  lesions  of  the  peritoneum  appear  to  be  entirely  absent, 
whereas,  in  other  cases  they  are  so  slight  as  to  appear  inadequate  to 
cause  the  ascites.  These  may  be  likened  to  similar  cases  of  valvular 
disease  of  the  heart,  in  which  disproportionate  ascites  is  the  striking 
clinical  feature,  and  in  which  the  ascites  is  doubtless  due  directly  to  the 
congestion  of  the  liver  and  its  consequences,  as  maintained  by  Pick.  In 
some  cases  both  factors — the  congestion  of  the  liver  and  the  peritonitis 
— are  operative.  In  those  in  which  the  congestion  is  the  major  factor 
we  should  expect  more  or  less  swelling  of  the  spleen  and  disturbances  of 
the  gastro-intestinal  tract;  in  those  in  which  the  serositis  is  the  major 
factor,  we  should  expect  an  absence  of  such  symptoms.  Some  distinction 
— anatomically,  at  least — may  be  drawn  between  cases  in  which  the 
lesions  are  confined  to  the  peritoneum  and  cases  in  which  the  lesions  are 
more  widespread.  The  cases  in  which  the  pericardium  is  unaffected 
reveal  no  congestive  alterations  in  the  liver;  clinically,  however,  the  two 
classes  of  cases  are  very  much  alike,  and  the  "  Zuckergussleber"  may 
occur  in  both. 

Diagnosis. — Recurring  ascites  in  a  person  in  otherwise  good  health, 
together  with  the  disposition  and  ability  to  be  up  and  about  between  tap- 
pings, should  suggest  the  diagnosis.  ■  Of  especial  diagnostic  significance 
are:  a  history  of  a  previous  attack  of  pericarditis,  pleuritis,  or  perihepa- 
titis; the  early  occurrence  and  subsequent  disappearance  of  oedema  of  the 
legs;  marked  ascites  with  little  or  no  oedema  of  the  legs;  an  enlarged  liver 
early  (this  may  not  occur),  and  a  small  and  distorted  but  otherwise 
smooth  liver  late  in  the  course  of  the  disease;  the  absence  or  very  late 
occurrence  of  marked  enlargement  of  the  spleen;  a  tendency  to  the  re- 
peated occurrence  of  attacks  of  pain,  tenderness,  rigidity,  and  possibly 
palpable  and  audible  friction  in  the  right  hypochondriac  region — attribu- 
table to  attacks  of  perihepatitis;  and  the  rapid  recurrence  of  ascites 
after  tapping.  One  should  determine  whether  the  lesions  are  confined 
to  the  region  about  the  liver  or  are  more  widespread,  involving  the  peri- 
cardium and  the  pleura.  In  these  cases  one  must  endeavor  to  dissociate 
the  symptoms  due  to  the  serositis  from  those  due  to  failure  of  the  circu- 
lation induced  by  the  pericardial  part  of  the  serositis  and  its  consequences. 
In  most  of  these  cases  prime  importance  attaches  to  the  recognition  of 
an  adherent  pericardium  (page  485). 

From  cirrhosis  of  the  liver  the  condition  may  be  distinguished  by  the 
signs  of  adherent  pericardium;  the  absence  of  the  etiological  factors  of 
cirrhosis  of  the  liver;  the  slow,  insidious,  protracted,  and  intermittent 
course;  the  long  periods  during  which  the  ascites  may  remain  stationary 
and  the  patient  in  good  condition;  the  entire  absence  or  transient  presence 
of  slight  jaundice;  the  absence,  in  most  cases,  of  portal  congestion  and 
gastro-intestinal  disturbances;  in  some  cases,  the  association  of  an  en- 
larged, smooth,  and  firm  liver,  with  marked  ascites;  and  the  fact  that  in 
many  cases  the  patient  survives  a  large  number  of  tappings. 


MULTIPLE  SEROSITIS  753 

Prognosis. — The  prognosis  as  to  eventual  recovery  is  bad,  but  the 
patient  may  live  for  many  years. 

Treatment. — The  treatment  is  almost  wholly  symptomatic.  Diuretics 
may  effect  the  discharge  of  the  too  abundant  fluid  or  a  similar  object  may 
be  achieved  by  free  catharsis.  Potassium  iodide  and  mercury  may  be 
tried  when  there  is  a  trustworthy  history  of  syphilis,  as  well  as  in  doubtful 
cases,  since  they  hold  out  some  hope  of  benefit.  Tapping  must  be 
performed  when  necessary;  usually  it  has  to  be  done  frequently,  although 
occasionally  the  fluid  remains  at  a  standstill  for  long  periods  of  time. 


4S 


SECTION   IX. 
DISEASES  OF  THE  UEINARY  SYSTEM. 


Pathological  Physiology. — The  kidneys,  together  with  the  intestines, 
lungs,  hver,  and  perhaps  the  skin,  are  charged  with  the  function  of 
excretion;  that  is,  of  removing  from  the  body  waste  products  of  no 
further  use  in  the  economy.  Perhaps  the  kidneys  produce  also  a  secre- 
tion, that  is,  a  substance  of  service  in  the  processes  of  metabolism;  but 
this  has  not  yet  been  definitely  determined.  The  substances  excreted 
by  the  healthy  kidneys  are  especially  the  waste  products  of  nitrogenous 
metabolism,  certain  mineral  salts,  pigments,  and  water.  All  of  these 
are  normally  present  in  the  blood,  from  which  they  are  removed  by  the 
healthy  kidney — the  water  and  the  mineral  salts  probably  by  the  glomer- 
uli, and  the  waste  products  of  nitrogenous  metabolism  probably  by  the 
epithelium  of  the  convoluted  tubules.  In  disease  the  functional  activity 
of  the  kidneys  fails  or  becomes  perverted,  so  that  on  the  one  hand,  sub- 
stances normally  eliminated  are  retained  and  accumulate  in  the  blood, 
whereas,  on  the  other  hand,  the  kidney  becomes  pervious  to  substances 
that  ordinarily  do  not  pass  it.  This  failure  of  excretion  is  in  some  way 
related  to  the  predominating  symptoms  of  nephritis — oliguria,  uremia 
(in  part,  perhaps,  retention  of  waste  products  of  nitrogenous  metabolism), 
and  oedema  (in  part,  retention  of  sodium  chloride);  and  the  abnormal 
permeability  of  the  renal  epithelium  is  answerable  for  the  other  significant 
manifestation  of  nephritis — albuminuria.  The  albumin  discharged  with 
the  urine  in  disease  is  the  albumin  of  the  blood,  serum  albumin  and 
globulin;  this  fact  (and  others)  shows  a  selective  action  on  the  part  of 
the  cells  of  the  glomeruli,  which  in  health  never  excrete  serum  albumin, 
although  they  may  excrete  a  foreign  protein,  such  as  egg-albumen,  pep- 
tone, or  the  Bence-Jones  albumose  (myelopathic  albumosuria),  etc.  Fur- 
thermore, although  when  diseased  the  kidney  usually  suffers  as  a  whole, 
certain  parts  seem  to  be  unduly  susceptible  to  the  action  of  certain 
poisons,  as  the  glomeruli  to  the  toxin  of  scarlatina — which  provokes  a 
so-called  glomerulonepln'itis,  especially  characterized  by  oliguria. 

The  urine,  the  totality  of  the  excretory  activity  of  the  kidneys,  is 
a  measure  not  only  of  the  functional  capacity  of  the  kidneys  themselves, 
but  also  of  other  organs  more  or  less  remote  from,  though  variously 
related  to,  the  kidneys,  and  of  the  general  metabolism.      In  diseased 


756  DISEASES  OF  THE  URINARY  SYSTEM 

conditions,  then,  the  urine  may  exhibit  (1)  variations  in  its  normal 
constituents,  or  (2)  substances  foreign  to  it  in  health  (quantitatively  or 
qualitatively);  and  these  latter  may  be  significant  of  (a)  disease  of 
the  kidney  and  the  urinary  tract,  or  (h)  disorders  of  general  metabolism 
or  of  organs  other  than  the  kidney. 

Variations  in  the  Normal  Constituents  of  the  Urine. — ^The 
total  daily  volume  of  the  urine  is  a  measure  of  the  local  renal  and  the  gen- 
eral blood  pressure,  of  the  amount  of  blood  circulating  through  the  kidneys, 
and  of  the  activity  of  the  renal  epithelium  and  of  the  skin.  The  reciprocal 
relations  existing  between  the  kidneys  and  the  skin  are  of  much  im- 
portance in  determining  the  amount  of  water  in  the  urine :  other  things 
being  equal,  the  more  the  sensible  and  insensible  perspiration  (activity 
of  the  skin)  the  less  the  water  in  the  urine,  and  vice  versa.  In  health  the 
renal  epithelium  responds  to  the  amount  of  blood  that  circulates  through 
the  kidneys :  an  increased  amount  of  blood  results  in  an  increased  amount 
of  urine,  and  the  reverse.  Thus,  for  instance,  when  in  consequence 
of  cold,  the  cutaneous  vessels  become  constricted  and  the  kidneys  (and 
other  abdominal  organs)  receive  an  increased  supply  of  blood,  as  well 
as  when,  in  consequence  of  vasomotor  relaxation  (nervousness,  fright), 
more  blood  is  determined  to  the  kidneys,  the  urine  is  increased.  In 
acute  inflammation,  however,  the  increased  amount  of  blood  is  associated 
with  swelling  and  other  degenerative  changes  of  the  renal  epithelium, 
and,  the  renal  capsule  being  comparatively  inelastic,  compression  of 
the  renal  capillaries,  slowing  of  the  circulation,  and  consequent  oliguria 
result.  In  these  circumstances,  the  effect  of  heat  (as  opposed  to  cold) 
in  determining  blood  to  the  cutaneous  sm-face  and  reducing  renal 
blood  pressure  is  resorted  to  and  constitutes  the  basis  of  valuable  thera- 
peutic resources  (flannel  clothing,  hot  baths,  warm  climates,  etc.).  In 
these  cases  the  administration  of  large  amounts  of  water  to  flush  the 
kidneys  is  neither  wise  nor  efficacious,  since  before  the  kidneys  can 
functionate  properly  the  local  circulatory  conditions  and  the  renal  epi- 
thelium must  become  improved;  for  similar  reasons,  drugs  that  induce 
diiu-esis  by  increasing  renal  blood  pressure  are  directly  contra-indicated. 
The  relief  to  tension  is  in  part  at  least  the  rationale  of  decapsulation  in 
subacute  and  chronic  nephritis  with  oliguria.  Oliguria  results  in  all 
conditions  of  lowered  renal  blood  pressure,  as  in  chronic  passive  conges- 
tion, in  shock,  etc.;  excretion  ceases  if  the  pressure  is  reduced  to  40  mm. 
Hg.  The  polyuria  of  chronic  indurative  nephritis  is  due  largely  to 
increased  general  blood  pressure — which  is  a  manifestation  of  adaptation 
on  the  part  of  nature  to  compensate  for  changed  conditions,  and  it  should 
not,  therefore,  be  too  much  reduced,  since  reduction  may  lead  directly 
to  oliguria  and  uremia.  Polyuria  also  may  be  due  to  an  effort  on  the 
part  of  the  kidney  to  excrete  a  foreign  substance  such  as  sugar  (diabetes), 
or  to  excrete  the  normal  amount  of  normal  ingredients  when  the  kidneys 
become  reduced  in  capacity  (diabetes  insipidus). 

The  acidity  of  the  urine  is  due  to  acid  phosphates  and  organic  acids. 
Special  clinical  importance  attaches  to  /?-oxybutyric  acid  and  its  deriva- 


PATHOLOGICAL  PHYSIOLOGY  757 

tives  in  the  acidosis  of  diabetes  and  other  conditions.  The  nitrog- 
enous constituents  of  the  urine  make  up  about  16  grams  daily  on  an 
ordinary  diet;  about  85  per  cent,  is  urea,  1  to  3  per  cent,  uric  acid, 
2  to  5  per  cent,  ammonia  compounds,  and  the  remainder  purin  bases, 
creatinin,  hippuric  acid,  etc.  Of  special  chnical  importance  is  the  fact 
that  the  nitrogenous  excretion  in  health  is  proportionate  to  the  nitrog- 
enous intake;  that  it  is  futile  to  estimate  the  output  of  urea  (formed 
largely  in  the  liver  from  ammonia  compounds)  without  at  the  same 
time  estimating  the  total  nitrogenous  output  and  knowing  the  nitrog- 
enous intake  (the  protein  content  of  the  food);  and  that  although  the 
ratio  of  uric  acid  to  urea  is  usually  about  1  to  70,  it  varies  considerably 
in  health,  depending  upon  the  diet  and  other  factors.  The  ammonia 
output  has  come  to  be  recognized  as  a  valuable  measure  of  the  presence 
or  absence  of  acidosis,  and  is  of  much  clinical  importance  in  the  acid 
intoxication  of  diabetes,  pregnancy,  etc. 

Chlorides,  present  chiefly  as  sodium  chloride,  are  derived  from  the 
food,  and  in  health  the  output  is  proportionate  to  the  intake.  In  some 
cases  of  parenchymatous  nephritis  the  renal  epithelium  appears  to  be 
incapable  of  excreting  chlorides,  which  being  retained  constitute  at  least 
one  factor  in  the  causation  of  oedema.  The  phosphates  also  are  derived 
largely  from  the  food.  The  condition  spoken  of  as  phosphaturia  is  usually 
due  not  to  excessive  output,  but  to  lessened  acidity  of  the  urine  and  pre- 
cipitation of  earthy  phosphates;  rarely  there  may  be  an  excessive  output 
(so-called  phosphatic  diabetes)  in  neurasthenia,  tuberculosis,  diabetes, 
leukemia,  etc. ;  in  some  cases  it  seems  to  be  associated  with  disturbances 
of  the  calcium  metabolism. 

The  sulphates  result  from  decomposition  of  proteins,  and  occur  as 
inorganic  sulphates,  ethereal  (organic)  sulphates,  and  neutral  (unoxidized) 
sulphates.  The  ethereal  sulphates  result  in  part  from  metabolic  pro- 
cesses, and  in  part  from  the  union  of  sulphuric  acid  and  certain  aromatic 
products  of  intestinal  putrefaction  (phenol,  indoxyl,  skatoxyl);  to  some 
extent,  then,  they  are  a  measure  of  intestinal  putrefaction,  and  with 
reservation  may  be  thus  interpreted  clinically  (indicanuria). 

Oxalates  (chiefly  calcium)  are  derived  largely  from  vegetable  foods 
(spinach,  rhubarb),  but  in  part  from  metabolic  processes.  An  increase, 
spoken  of  as  oxaluria  (sometimes  spurious,  due  to  precipitation  in  con- 
sequence of  a  poverty  of  magnesium  salts),  is  sometimes  associated  with 
neurotic  disorders,  indigestion,  etc.;  and  the  salts  sometimes  constitute 
renal  calculi.  Urobilin  is  normally  present  in  small  amounts,  and  it  is 
increased  (urobilinuria)  in  cases  of  excessive  erythrocyte  destruction, 
(pernicious  anemia,  certain  forms  of  hemolytic  jaundice,  etc.). 

Abnormal  Constituents  in  the  Urine. — Under  varying  circum- 
stances the  urine  contains  a  large  number  of  substances  foreign  to  it  in 
health,  quantitatively  or  qualitatively;  of  these,  the  most  important  are 
albumin,  tube  casts,  blood,  and  pus — which  are  of  much  significance  in 
the  diagnosis  of  disease  of  tlie  kidney  and  the  urinary  tract;  furthermore, 
glycosuria  and  ketonuria  (major  phenomena  of  diabetes)  also  are  common ; 


758  DISEASES  OF  THE   URINARY  SYSTEM 

and  there  are  other  more  or  less  important  anomahes  of  urinary  excre- 
tion. 

Thiis^  the  urine  may  be  abnormally  colored.  Deep  yellowish  or  orange- 
colored  urine  may  be  due  to:  an  excess  of  urochrome  (the  normal 
urinary  pigment);  urobilin,  due  largely  to  the  action  of  intestinal 
bacteria  on  bilirubin,  and  found  in  conditions  of  excessive  hemolysis, 
pernicious  anemia,  hemolytic  jaundice  (sometimes  inaptly  called  urobilin 
jaundice)  constipation,  etc.;  uro-erythrin  (liver  disease,  fevers,  etc.); 
chrysophanic  acid  (rhubarb,  senna);  santonin,  etc.  Pinkish  or  reddish 
urine  may  be  due  to  oxyhemoglobin  (hemorrhage),  uro  erythrin  (pinkish 
uratic  sediment),  eosin,  rosanilin,  etc.  Greenish  urine  is  due  to  the  pres- 
ence of  bile  pigment  (biliverdin)  or  methylene  blue;  bluish  urine  is 
practically  always  due  to  methylene  blue.  Brown  or  black  urine  may 
be  due  to  methemaglobin  (hemorrhage — which  causes  smoky  urine; 
paroxysmal  hemoglobinuria— so-called  black-water  fever);  to  an  excess 
of  bile  pigment  (especially  biliverdin) ;  to  an  excess  of  indican  (blackness 
on  standing;  higher  oxidation  products  of  indol  and  not  indoxyl  sul- 
phate, which  is  colorless);  to  melanin  or  melanogen  (disseminated 
melanotic  tumors);  to  the  ingestion  of  carbolic  acid,  creosote,  salicyl 
compounds,  etc.;  to  hematoporphyrin,  which  causes  a  port-wine  or 
blackish  discoloration  of  the  urine  as  one  of  a  series  of  toxic  phenomena 
that  occur  especially  in  women  after  the  long-continued  use  of  sulphonal 
or  trional,  and  perhaps  under  other  circumstances  (lead  poisoning,  intes- 
tinal hemorrhage) ;  and  to  alkapton  (alkaptonuria,  a  brownish  or  blackish 
discoloration  of  the  urine  upon  exposure  to  the  air,  associated  with 
reduction  of  Fehling's  solution,  but  no  other  "sugar"  reaction,  no  fer- 
mentation, and  no  rotation  of  polarized  light) ;  and  ochronosis  (blackish 
pigmentation  of  the  cartilages),  which  is  a  congenital  vice  of  metabolism 
(incomplete  combustion  of  aromatic  derivatives  of  proteins) ,  resulting  in 
the  presence  in  the  urine  of  homogentisic  acid;  the  linen  may  be  stained 
black  by  the  urine,  and  ultimately  the  cartilages  of  the  ear,  the  sclerotica, 
and  even  the  skin  may  become  obviously  pigmented. 

Other  rare  urinary  anomalies  comprise  chyluria,  which  may  be  parasitic 
(true  chyle)  or  non-parasitic — opaque,  whitish,  opalescent,  milky  urine; 
lipuria  (fat  in  the  urine),  whicb  may  occur  after  an  excess  of  fatty  food, 
or  of  cod-liver  oil,  in  fat  embolism  after  fractures,  in  fatty  degeneration, 
phosphorus  poisoning,  prolonged  suppuration,  diabetes,  chronic  nephritis 
with  fatty  degeneration,  pyonephrosis,  spurious  chyluria,  etc.;  choluria, 
the  presence  of  bile  pigments  (bilirubin  and  biliverdin  in  cases  of  jaun- 
dice); cystinuria,  of  interest  because  rarely  it  may  lead  to  the  formation 
of  cystin  calculi;  fibrinuria,  the  formation  in  the  urine  of  a  jelly-like 
mass,  occasionally  associated  with  marked  albuminuria;  pneumaturia 
(the  presence  of  gas  in  the  urine),  which  may  result  from  trauma  or 
the  instrumental  introduction  of  gas  into  the  urinary  tract,  gas  from  the 
intestinal  tract  (vesico-enteric  fistula),  or  fermentation  of  urine  in  the 
bladder  by  gas-forming  organisms  (Bacillus  coli.  Bacillus  lactis  aerogenes. 
Bacillus    aerogenes    capsulatus) — usually    found   in   diabetic   subjects. 


PATHOLOGICAL  PHYSIOLOGY  759 

Uremia. — Uremia  is  a  form  of  auto-intoxication  that  occurs  in 
nephritis  and  in  certain  conditions  associated  with  anuria.  The  toxic 
agent  is  not  known.  Commonly  the  uremic  manifestations  are  ascribed . 
to  the  activity  of  retained  poisonous  metabohc  products  that  should  be 
and  in  health  are  eliminated  by  the  kidneys,  and  these  products  are  often 
assumed  to  be  nitrogenous  in  nature.  The  poison  is  not  urea,  uric  acid, 
potassium  or  sodium  salts,  creatinin,  etc.,  since  these  may  be  injected 
into  the  body  without  evil  consec|uences.  The  condition  has  been  attrib- 
uted also  to  an  acid  intoxication  (lessened  alkalinity  of  the  blood), 
to  urotoxins  (Bouchard),  to  toxemia  of  the  blood  (Hughes  and  Carter), 
to  oedema  of  the  brain  and  meninges  (Traube),  to  failure  or  perversion 
of  a  supposed  internal  secretion  of  the  kidneys;  to  nephrolysins,  etc. 
It  is  not  improbable  that  it  results  from  the  products  of  perverted  metab- 
olism or  from  non-detoxification  of  metabolic  products  normally  robbed 
of  the  poisonous  products  (by  the  liver,  for  instance).  The  cerebrospinal 
fluid  is  often  under  increased  pressure. 

Clinically  uremia  may  be  acute  or  chronic,  or  latent  (in  conditions 
of  obstruction  of  the  ureters  and  anuria).  Acute  uremia  may  occur 
in  any  type  of  nephritis,  but  it  is  especially  common  in  acute  and  chronic 
diffuse  non-indurative  nephritis;  it  is  often  preceded  by  chronic  mani- 
festations (headache,  restlessness,  dyspnoea,  insomnia,  etc.);  it  develops 
suddenly,  is  likely  to  last  only  a  short  time,  and  commonly  leads  to  death. 
Chronic  uremia  is  most  common  in  chronic  diffuse  indurative  nephritis; 
it  develops  insidiously,  is  mild  in  its  manifestations,  is  likely  to  last  a  long 
time,  may  disappear  and  recur,  but  is  likely  ultimately  to  lead  to  acute 
manifestations  and  death. 

The  major  symptoms  of  acute  uremia  are  nervous  in  nature  and  con- 
sist of  (o)  convulsions  (not  to  be  distinguished  from  those  of  epilepsy, 
except  probably  the  absence  of  the  initial  cry);  (6)  coma,  which,  aside 
from  that  which  attends  and  follows  the  convulsions,  may  come  on  insid- 
iously and  last  several  days  or  weeks,  and  lead  usually  to  death,  but 
sometimes  eventuates  in  recovery;  and  (c)  psychic  derangements  (melan- 
cholia, delusional  insanity,  mania,  etc.).  Hemiplegia  or  monoplegia 
sometimes  occurs,  and  may  be  due  solely  to  oedema  of  the  brain  and 
meninges.  Other  less  serious  and  more  chronic  nervous  manifestations 
comprise  headache,  heraicrania,  vertigo,  insomnia,  tinnitus  aurium,  am- 
aurosis, languor,  neurasthenic  phenomena,  muscular  pains  and  twitchings 
(especially  in  the  calves),  joint  pains,  etc.  Dyspnoea  (renal  asthenia)  is 
often  an  early  and  obtrusive  sign;  it  may  be  continuous  or  paroxysmal 
(developing  especially  at  night),  or  of  the  Cheyne-Stokes  type.  Nausea 
and  vomiting  (sometimes  uncontrollable)  are  common,  and  may  be  asso- 
ciated with  diarrhoea;  these  may  result  from  toxic  irritation  of  the  medul- 
lary centres  or  from  gastro-intestinal  irritation  provoked  by  the  excretion 
of  urea  into  the  stomach  and  its  decompositioji  into  ammonia.  Stomatitis, 
a  coated  tongue,  and  foul  breath  are  frecjueiit.  The  temperature  is 
usually  subnormal,  although  a  so-called  uremic  fever  has  been  described. 
Uremia  is  usually  easily  recognized,  but  in  the  event  of  coma  one  must 


760  DISEASES  OF  THE  URINARY  SYSTEM 

eliminate  alcoholism  (obvious  alcoholism,  alcoholic  habits,  less  deep 
coma),  opium  poisoning  (contracted  pupils,  infrequent  respirations,  no 
convulsions),  diabetic  coma  (ketonuria,  perhaps  glycosuria,  fruity  odor  to 
the  breath,  Kussmaul's  dyspnoea),  and  apoplexy  (sudden  onset  of  hemi- 
plegia, flapping  of  one  cheek,  conjugate  deviation  of  the  eyes,  perhaps 
unequal  pupils).  Apoplexy,  however,  is  common  in  chronic  nephritic 
subjects,  so  that  albumin  and  casts  in  the  urine  are  not  conclusive 
evidence  of  the  one  or  the  other  condition;  nor  do  they  exclude  diabetic 
coma,  since  at  least  one-half  of  the  diabetic  subjects  have  also  chronic 
nephritis. 

Cardiovascular  Changes  in  Nephritis. — The  cardiovascular 
changes  in  nephritis  are  of  extreme  interest  and  importance;  as  a  matter 
of  fact,  they  dominate  the  clinical  picture  of  the  disease  and  they  assume 
commanding  position  in  the  prognosis  and  in  the  treatment.  The 
lesions  are  widespread,  involving  the  heart,  the  large  and  the  small 
arteries,  the  capillaries,  sometimes  even  the  veins.  The  lesions  of  the 
heart  involve  the  muscle  and  find  their  expression  in  hypertrophy.  With 
this,  at  times,  there  is  associated  some  interstitial  myocarditis,  with 
increase  of  the  intermuscular  fibrous  trabeculse,  especially  in  the  neigh- 
borhood of  many  of  the  smaller  coronary  arteries,  which  frequently  are 
obliterated.  In  some  cases,  especially  late  in  the  course  of  the  disease, 
fatty  degeneration  of  the  heart  muscle  also  may  supervene.  Valvular 
lesions  are  extremely  uncommon.  Those  that  are  found  in  cases  of  renal 
disease  are  either  an  antecedent  condition,  or  they  result  from  mechanical 
causes,  from  dilatation  of  the  heart,  the  lesion  being  one  of  relative 
insufficiency.  The  hypertrophy  of  the  heart  is  predominantly  a  lesion  of 
the  left  ventricle.  In  the  majority  of  cases  the  left  ventricle  alone  is 
affected;  in  the  remainder  of  the  cases  both  ventricles  are  affected.  The 
right  ventricle  is  never  affected  alone.  Simple  hypertrophy  of  the 
left  ventricle  is  the  first  event;  later,  this  is  associated  with  some  dila- 
tation— eccentric  hypertrophy.  The  longer  the  nephritis  continues  (the 
longer  the  patient  lives),  the  more  certain  the  development  of  consecu- 
tive enlargement  of  the  right  ventricle,  the  increased  pressure  in  the  left 
ventricle,  coupled  with  degenerative  alterations  in  the  heart  muscle, 
leading  to  increased  pressure  in  the  right  ventricle.  Here  also  the  hyper- 
trophy is  of  the  eccentric  variety.  Predominating  dilatation  of  either 
or  both  ventricles  is  an  unusual  event  until  toward  the  termination  of 
life;  its  development  is  of  ominous  moment — it  usually  presages  an  early 
fatal  termination.  It  has  been  stated  by  Senator  and  others  that  the 
hypertrophy  of  the  primarily  contracted  kidney  is  of  the  simple  variety, 
whereas  that  associated  with  the  secondarily  contracted  kidney  and  with 
the  arteriosclerotic  kidney  is  of  the  eccentric  variety — hypertrophy  with 
dilatation.     But  this  statement  scarcely  permits  of  general  application. 

This  hypertrophy  of  the  heart  occurs  in  all  forms  of  nephritis,  but  not 
in  all  cases.  In  none  of  the  varieties,  however,  does  it  so  dominate  the 
clinical  picture  as  it  does  in  chronic  indurative  or  interstitial  nephritis. 
It  may  be  expected  from  the  time  of  the  contraction  or  atrophy  of  the 


PATHOLOGICAL  PHYSIOLOGY  761 

kidney,  be  it  of  the  primary  or  the  secondary  variety.  Thus  it  occurs 
early  in  the  primary  form,  but  its  occurrence  may  be  (but  usually  is  not) 
much  delayed  in  the  secondary  form.  It  may,  however,  occur  in  chronic 
diffuse  non-indurative  (or  parenchjTuatous)  nephritis,  and  it  is  observed 
in  some  cases  of  acute  nephritis,  particularly  in  some  of  the  cases  of 
acute  nephritis  following  the  infections.  In  some  of  the  chronic  cases 
in  which  it  should  be  expected,  for  some  more  or  less  inexplicable  reason 
it  may  not  occiu-,  at  all  events  not  to  a  noteworthy  degree.  These,  how- 
ever, are  the  unusual  cases.  The  absence  of  the  hypertrophy  may  be 
due  to  faulty  nutrition — the  heart  not  being  sufficiently  well  nourished 
to  enable  it  to  h}^ertrophy;  to  sclerosis  of  the  coronary  arteries;  to  the 
vicarious  action  of  one  of  the  other  emunctories  removing  those  excre- 
mentitious  products  ordinarily  eliminated  by  the  healthy  kidneys,  etc. 

The  changes  in  the  arteries  are  those  of  augmented  blood  pressure, 
and  arteriosclerosis  and  atheroma.  These  changes,  though  widespread, 
are  not  distributed  uniformly  throughout  the  body.  In  many  cases  they 
are  most  marked  in  the  kidneys;  in  a  few  cases  they  appear  to  be  almost 
confined  to  them.  In  many  cases  small  miliary  aneurysms  develop, 
especially  in  the  brain,  and  rupturing,  frequently  lead  to  the  fatal  ter- 
mination. 

The  cause  of  these  cardiovascular  alterations  has  not  been  thoroughly 
worked  out.  Considerable  discussion  still  obtains  with  reference  to 
whether  the  primary  alterations  are  in  the  arterioles  (stopcock  action  of 
Johnson)  or  in  the  capillaries  (the  arteriocapillary  fibrosis  of  Gull  and 
Sutton).  Doubtless,  the  conditions  differ  in  different  cases.  Thus, 
arteriosclerosis  itself  may  be  the  primary  event  (and  this  seems  to  be 
especially  common  in  this  country),  and  it  leads  to  both  the  kidney 
alterations  and  the  cardiac  hypertrophy.  In  this  instance  the  disease 
is  a  widespread  process,  and  its  etiology  is  the  etiology  of  arteriosclerosis. 
However,  in  many  cases  the  nephritis  is  the  primary  event,  and  leads 
to  the  cardiovascular  alterations.  Whether  these  are  mechanical  or 
chemical  in  nature  is  still  a  matter  of  discussion.  Augmented  blood 
pressure  is  undoubtedly  at  the  bottom  of  the  process,  but  the  old  view 
of  Traube  and  of  Cohnheim  that  this  resulted  from  an  effort  on  the  part 
of  the  cardiovascular  system  to  maintain  a  normal  or  adequate  flow  of 
blood  through  kidneys,  the  capillary  distribution  of  which  had  become 
reduced  by  interstitial  overgrowth,  has  been  largely  given  up.  It  has 
been  modified  to  some  extent  by  certain  observers,  who  point  out  that 
these  cardiovascular  lesions  occur  most  commonly  in  association  with 
disease  of  the  glomeruli,  and  that  the  function  of  the  glomeruli  seems  to 
be  that  of  filtration  dependent  upon  the  blood  pressure  (as  contrasted 
with  the  glandular  secretory  activity  of  the  renal  epithelium) ;  and  they 
suggest  that  when  the  glomeruli  become  more  or  less  inactive  in  conse- 
quence of  disease,  the  regulatory  mechanism  of  the  body  attempts  to 
compensate  therefor  (to  promote  glomerular  elimination)  by  increased 
blood  pressure — which  becomes  general.  On  the  other  hand,  it  has 
been  suggested  that  the  primary  increase  of  blood  pressure  is  chemical 


762  DISEASES  OF  THE   URINARY  SYSTEM 

in  origin,  is  due  to  the  angiotonic  properties  of  the  adrenal  body;  that 
the  condition  resuhs  from  hyperadrenahsm.  Alterations,  interpreted  by 
some  observers'  as  hyperplastic  in  nature,  have  been  found  in  the 
adrenals  in  nephritis  (although  it  has  not  yet  been  determined  whether 
they  are  the  cause  or  the  result),  and  a  pressor  substance  has  been  found 
in  the  disordered  kidneys.  Whether  this  is  adrenalin  or  a  substance 
allied  thereto,  and  whether  this  is  the  result  of  increased  formation  or 
of  retention  (reduced  elimination  by  diseased  kidneys),  has  not  been 
determined.  Perhaps  certain  enterogenic  or  other  poisons  not  detoxi- 
fied by  the  liver  may  be  at  the  bottom  of  the  process. 

The  Functional  Capacity  of  the  Kidneys. — The  most  obvious 
is  at  the  same  time  the  best  test  of  the  functional  capacity  of  the  kidneys 
— the  daily  amount  of  the  urine;  for  suppression  of  urine  is  a  certain 
sign  of  renal  inadequacy  (whether  the  primary  cause  be  resident  in  the 
kidneys  themselves  or  elsewhere,  such  as  the  cardiovascular  system).  In 
addition  to  oliguria  or  anuria,  albuminuria,  cylinduria,  and  uremia  are 
important  manifestations  of  functional  incapacity  of  the  kidneys;  these 
are  discussed  under  separate  headings. 

Other  tests  of  the  functional  capacity  of  the  kidneys  comprise:  (1) 
The  indigo-carmine  test.  This  consists  of  the  intramuscular  injection 
(gluteal  muscles)  of  20  c.c.  of  a  0.4  per  cent,  aqueous  solution  of  indigo- 
carmine,  and  ascertaining,  preferably  by  means  of  cystoscopy,  the  time 
of  beginning  excretion  (light  blue  color  to  the  urine)  and  the  time  of 
maximum  excretion  (dark  blue  color)  of  the  indigo-carmine.  Normally 
the  excretion  begins  within  twenty  minutes  (averaging  perhaps  fifteen) ; 
if  the  excretion  is  delayed  beyond  twenty  minutes,  certainly  if  beyond 
thirty  minutes,  serious  or  grave  disease  of  the  kidneys  is  almost  certain. 
This  test  is  especially  significant  of  surgical  diseases  of  the  kidney  or 
obstruction  of  the  ureter.  (2)  The  methylene  blue  test.  This  com- 
prises the  intramuscular  injection  of  1  c.c.  of  a  5  per  cent,  aqueous 
solution  of  methylene  blue;  the  collection  of  the  urine  after  the  lapse 
of  one-half  hour,  one  hour,  and  hourly  thereafter;  and  noting  the  time 
of  the  appeareance  of  a  bluish  tint  to  the  m-ine,  the  time  of  maximum 
coloration,  and  the  time  of  disappearance  of  the  coloring.  Normally  a 
slight  tint  may  be  noticed  in  the  first  specimen,  certainly  at  the  end 
of  one  hour;  the  maximum  coloration  occurs  at  the  end  of  three  or  fom' 
hours,  and  the  urine  is  free  of  coloring  at  the  end  of  thirty-six  to 
forty-eight  or  sixty  hours.  Delay  of  beginning  excretion  beyond  one 
hour  and  of  maximum  coloration  beyond  the  fourth  hour,  and  con- 
tinuation of  excretion,  as  may  occur  for  five  or  six  days,  is  indicative 
of  deficient  functional  capacity.  (3)  The  phloridzin  (glycosuric)  test. 
This  consists  of  the  intramuscular  injection  of  1  c.c.  of  a  0.5  per 
cent,  aqueous  solution  of  phloridzin,  and  the  collection  of  the  urine  as 
in  the  methylene  blue  test.  In  normal  subjects  glycosuria  may  be  de- 
tected at  the  end  of  one-half  to  one  hour,  and  it  disappears  at  the  end 
of  two  to  four  hours.  In  disordered  renal  epithelium  this  glycosuria 
may  be  delayed  or  may  not  occur  at  all.     (4)  Cryoscopy,  or  the  deter- 


ANURIA  763 

mining  of  the  freezing  point  of  the  urine,  is  a  test  of  its  molecular  con- 
centration, particularly  of  its  sodium  chloride  ions  and  protein  con- 
stituents. >s"ormally,  the  freezing  point  of  the  urine  varies  between 
— 1.3°  and — 2.3°  C;  in  diseased  states  the  freezing  point  is — 1°  or  less 
than — 1°  C.  (h}^osthenuria),  but  since  this  depends  upon  various 
factors  (sodium  chloride,  protein  constituents,  urates,  etc.)  it  loses 
clinical  value.  Comparison  of  the  freezing  point  of  the  urine  with 
that  of  the  blood,  which  normally  is  — 0.56°  C,  is  of  more  value.  (5) 
The  electrical  conductivity  of  the  urine.  This  varies  with  the  contained 
ions,  but  is  influenced  by  molecules  that  do  not  dissociate  (sugar,  etc), 
so  than  its  clinical  value  is  slight.  All  of  these  tests  are  of  more  value 
in  determining  the  relative  functional  capacity  of  the  two  kidneys  (sepa- 
rated urines)  than  the  absolute  functional  capacity  of  both  kidneys 
together,  and  they  are  especially  applicable  in  surgical  conditions  of 
the  kidneys  and  ureters. 

ANURIA. 

Anuria,  or  suppression  of  urine,  in  which  no  urine  enters  the  bladder, 
should  be  distinguished  from  retention  of  urine,  in  which  urine,  though 
present  in  the  bladder,  is  not  or  cannot  be  voided.  In  retention  (unless 
as  in  typhoid  fever,  for  instance,  the  sensibility  is  benumbed)  there  is 
likely  to  be  complaint  of  distress  referred  to  the  bladder,  although  in 
some  of  the  cases,  such  as  elderly  men  with  enlarged  prostates,  some 
overflow  of  urine  may  be  associated  with  extraordinary  retention  of 
residual  origin  altogether  unknown  to  the  patient;  in  any  event,  how- 
ever, examination  of  the  bladder  region  and  catheterization  will  reveal 
the  presence  or  absence  of  urine  in  the  bladder.  The  causes  of  reten- 
tion are  some  mechanical  obstruction  (urethral  stricture  or  stone, 
enlarged  prostate,  pregnant  uterus,  etc.)  or  some  functional  incapacity 
(paresis  from  overdistention,  functional  and  organic  diseases  of  the 
nervous  system,  etc.).     Anuria  may  be  obstructive  or  non-obstructive. 

Obstructive  Aniiria. — Obstructive  anuria  results  from  compression  of 
both  ureters,  as  by  a  pelvic  growth,  such  as  a  uterine  carcinoma,  for 
instance;  blocking  of  both  ureters  by  renal  calculi,  blood  clots,  tuber- 
culous material,  tumors,  twists  or  stricture,  etc.;  or  blocking  of  one  ureter 
in  cases  in  which  the  other  kidney  is  absent  or  functionless.  The  anuria 
in  these  cases,  which  are  sometimes  spoken  of  as  "latent  uremia,"  may 
persist  for  some  time  (one  or  two  weeks  or,  rarely,  longer)  and  the 
patient  suffer  comparatively  little  discomfort.  Uremia  (convulsions, 
coma,  or  psychoses)  and  oedema  are  quite  unusual.  The  treatment  is 
surgical. 

Non-obstructive  Anuria. — Non-obstructive  anuria  occurs:  (1)  In  acute 
toxic  degenerative  and  dift'use  nephritis,  such  as  occurs  in  the  infective 
diseases  (scarlet  fever,  yellow  fever,  cholera,  etc.)  and  in  different  poi- 
sonings (phosphorus,  lead,  cantharides,  etc.);  (2)  in  cardiovascular 
failure,  and  passive  congestion;  (3)  following  severe,  especially  abdom- 


764  DISEASES  OF  THE   URINARY  SYSTEM 

inal  injuries  and  operations  (sometimes  even  the  passing  of  a  catheter), 
particularly  in  persons  past  middle  life  whose  kidneys  and  bloodvessels 
are  somewhat  damaged;  and  (4)  as  a  manifestation  of  hysteria  (although 
hysterical  retention  and  deception  are  more  common).  Aside  from 
hysterical  anuria,  in  which,  as  in  obstructive  anuria,  there  is  usually 
a  remarkable  absence  of  symptoms,  non-obstructive  anuria  is  of  serious 
moment — being  one  of  the  manifestations  of  serious  degeneration  of  the 
kidney  or  nephritis.  The  treatment  is  that  appropriate  in  acute  diffuse 
nephritis. 

ALBUMINURIA. 

Albuminuria  is  a  term  used  to  denote  the  presence  in  the  urine  of 
different  protein  substances — ^serum  albumin,  serum  globulin,  nucleo- 
albumin,  albumose,  peptone,  fibrin,  and  hemoglobin.  "While  formerly 
regarded  as  diagnostic  of  Bright's  disease,  albuminuria  is  now  known  to 
be  dependent  upon  many  different  diseased  conditions.  Large  amounts 
of  albmnin  in  the  urine,  however,  practically  aWays  indicate  serious 
kidney  disease,  but  serious  disease  of  the  kidneys  may  exist  for  a  long 
time  with  little  or  no  albumin  in  the  m-ine.  In  the  majority  of  cases 
of  albuminuria  the  albumin  is  moderate  in  amount,  and  one  generally 
has  to  determine  whether  the  albumin  is  due  to  disease  of  the  kidneys,  to 
disease  of  some  other  organ,  or  to  both.  The  importance  and  significance 
of  albimiinuria  are  always  enhanced  by  the  associated  presence  of  tube 
casts,  but  both  albumin  and  casts  may  be  present  without  serious  disease 
of  the  kidneys,  and  serious  forms  of  Bright's  disease  may  exist  with 
at  least  temporary  absence  of  albimiin  and  casts  from  the  urine.  The 
differential  diagnosis  of  albuminuria,  therefore,  is  of  considerable 
importance.  The  following  forms  of  albuminuria  may  be  distinguished : 
(1)  Extrarenal,  spurious,  accidental,  or  factitious  albuminuria;  (2) 
so-called  functional,  physiological,  or  cyclic  albuminm-ia;  (3)  albuminuria 
without  noteworthy  alterations  in  the  kidneys;  and  (4)  albuminuria 
with  noteworthy  alterations  in  the  kidneys. 

Extrarenal,  Spurious,  Accidental,  or  Factitious  Albuminuria. — In  these 
cases  the  albuminuria  is  but  a  subsidiary  factor  and  entirely  dependent 
on  the  admixture  with  the  urine  of  different  albuminous  fluids — blood, 
pus,  chyle,  or  seminal  discharges.  Chyle  is  a  very  rare  constituent  of 
the  urine,  and  when  present  will  scarcely  fail  of  recognition.  Seminal 
discharges  in  the  urine  are  of  more  common  occurrence,  and  should  not 
escape  careful  observation.  The  greatest  interest  attaches  to  cases  of 
albuminuria  associated  with  blood  and  pus  in  the  urine — the  result  of 
inflammation  and  ulceration  of,  and  of  hemorrhage  from,  any  part  of  the 
genito-urinary  tract,  especially  the  renal  pelvis,  ureters,  bladder,  urethra, 
vagina,  uterus.  In  these  cases  the  amount  of  albumin  is  small — rarely 
more  than  1  part  per  1000  (Esbach's  method),  and  it  is  proportionate 
to  the  amount  of  blood  and  pus.  A  disproportionate  amount  of  albu- 
min should  always  excite  a  suspicion  of  the  co-existence  of  nephritis. 


ALBUMINURIA  765 

The  presence  of  tube  casts  in  the  urinary  sediment  is  of  the  great- 
est importance — their  persistence  being  clear  evidence  of  nephritis, 
and  indicating  that  at  least  a  part  of  the  albumin  in  the  urine  is  due 
to  circulatory  and  tissue  changes  in  the  kidneys.  One  must  avoid 
error  in  presuming  the  non-existence  of  nephritis  in  cases  in  which  a 
small  amount  of  albumin  and  casts  are  associated  with  a  few  leukocytes 
or  pus  corpuscles.  In  most  of  these  cases  the  albuminuria  is  due  in 
great  part  to  nephritis — a  few  leukocytes  or  pus  corpuscles  being  regular 
constituents  of  the  urine  in  Bright's  disease.  (For  additional  informa- 
tion, see  hematuria,  pyuria,  and  nephritis.) 

So-called  Functional,  Physiological,  Cyclic,  Intermittent,  Paroxysmal, 
Dietetic,  Postural  (Orthostatic),  and  Adolescent  Albuminuria. — ^The  occur- 
rence of  a  ''physiological"  albuminuria  is  now  generally  conceded.  It 
is  found  especially  in  young,  more  particularly  male,  subjects  under 
twenty-five  years  of  age.  It  is  usually  detected  accidentally,  as,  for 
instance,  at  examinations  for  life  insurance,  or  for  other  certificates  of 
health.'  In  some  cases  it  appears  to  be  constant,  and  it  lasts  for  a  relatively 
long  time;  in  other  cases  it  is  intermittent — occurring  at  stated  or  inde- 
terminate periods.  In  many  of  the  cases  the  presence  and  the  amount 
of  the  albumin  are  much  influenced  by  certain  circumstances — posture 
(whence  it  is  sometimes  absent  on  arising  in  the  morning  and  present 
later  in  the  day),  exercise,  emotional  and  other  excitement,  cold  baths, 
certain  articles  of  diet  (especially  proteins,  but  also  large  amounts 
of  ordinary  mixed  foods),  prolonged  anxiety,  college  and  university 
examinations,  etc.  In  diagnosticating  this  form  of  albuminuria  consider- 
able circumspection  must  be  exercised.  The  patient  should  be  a  young 
subject;  the  urine  should  be  normal  in  amount  (certainly  not  increased), 
normal  in  color,  and  normal  in  specific  gravity  (certainly  not  of  lessened 
specific  gravity);  the  amount  of  albumin  must  be  small — less  than  0.5 
per  1000  (Esbach);  the  urine  must  contain  no  other  abnormal  constit- 
uent; there  must  be  no  local  disease  of  the  genito-urinary  tract,  such  as 
gleet,  spermatorrhea,  leucorrhea,  etc.,  that  might  give  rise  to  spurious 
albuminuria;  every  bodily  organ  must  be  examined  and  found  to  be  in 
perfect  health — in  particular  there  must  be  no  hypertrophy  of  the  left 
ventricle  of  the  heart,  no  accentuation  of  the  aortic  second  sound,  and 
no  increased  arterial  tension;  nor  may  there  be  any  evidence  of  disorder 
of  the  heart,  lungs,  or  liver  that  might  occasion  congestion  of  the  kidneys; 
there  must  have  been  no  past,  nor  may  there  be  any  present,  oedema, 
uremic  manifestations,  or  retinal  changes;  and  at  the  most  there  must 
not  be  more  than  an  occasional  hyaline  cast.  Even  in  cases  that  meet 
these  requirements  much  caution  must  be  observed,  and  the  diagnosis 
must  not  be  made  until  the  patient  has  been  long  under  observation, 
until  both  the  morning  and  the  evening  urines  have  been  repeatedly 
examined,  and  until  tlie  al!)umin  is  found  to  vary  with  the  influences 
under  which  it  develops.  And  when  the  diagnosis  has  been  made  one 
should  stand  willing  to  renounce  it  immediately  on  the  development 
of  signs  of  disease  likely  to  be  attended  by  albuminuria.     Caution  is 


766  DISEASES   OF  THE   URINARY  SYSTEM 

always  necessary,  inasmuch  as  albumin  may  be  temporarily  absent, 
even  for  long  periods  in  certain  cases  and  at  certain  stages  of  chronic 
indurative  (or  interstitial)  nephritis,  whereas,  in  other  cases  it  may  be 
present  in  such  small  amounts  as  to  require  delicate  tests  for  its  detec- 
tion. More  than  a  small  amount  of  albumin  always  suggests  a  latent 
nephritis  that  for  the  time  being  may  reveal  itself  by  no  sign  other  than 
the  albuminuria.  The  caution  necessary  in  the  diagnosis  of  these  cases 
is  evident  from  the  statement  of  Senator,  who  believes  that  most  cases 
of  so-called  cyclic  or  functional  albuminuria  are  really  cases  of  latent 
nephritis,  and  that  no  case  of  albuminuria  may  be  regarded  as  functional 
or  physiological  if  the  albumin  exceeds  0.4  or  0.5  part  in  1000.  The 
diagnosis  of  functional  albuminuria  in  late  adult  life  had  best  be  dis- 
pensed with  entirely,  as  practically  without  exception  small  amounts  of 
albumin  in  the  urine  of  such  subjects  means  chronic  nephritis  (excluding 
cases  of  extrarenal  albuminuria). 

The  cause  of  this  functional  or  cyclic  albuminuria  is  not  well  understood. 
It  has  been  attributed  to  vascular  alterations  (congestion)  of  the  kidneys, 
and  to  disturbances  in  metabolism,  in  consequence  of  which  albumoses, 
excessive  in  quantity  or  abnormal  in  quality,  are  formed.  That  many 
of  these  cases  are  really  cases  of  physiological  albuminuria  may  well  be 
doubted.  Some  of  them  are  certainly  cases  of  spurious  albuminuria. 
In  most  cases  it  is  likely  that  the  glomerular  epithelium  suffers  some 
nutritional  disturbance.  In  some  cases  the  renal  epithelium  is  probably 
unduly  sensitive.  These  cases  may  be  confounded  with  the  rather  un- 
usual cases  in  which  following  an  acute  nephritis  in  early  childhood  a 
trace  of  albumin  persists  throughout  life,  but  the  patient  lives  to  a  good 
old  age  without  other  manifestations  of  nephritis  developing.  Such  per- 
sistent albuminuria,  of  course,  indicates  slight  alterations  in  the  renal 
epithelium,  and  in  case  careful  injuiry  is  not  made  into  the  antecedent 
history  of  the  patient  the  condition  may  be  regarded  as  "physiological" 
albuminuria. 

Albuminuria  without  Noteworthy  Alterations  in  the  Kidneys .^ — A  slight 
amount  of  albumin  may  be  found  in  the  urine  in  a  great  variety  of  morbid 
conditions  without  noteworthy  alterations  in  the  kidneys.  Thus  it  may 
be  found  in  different  blood  conditions,  such  as  the  anemias,  leukemia, 
purpura,  scurvy,  etc.;  in  certain  forms  of  intoxication,  such  as  lead 
poisoning,  mercurial  poisoning,  etc.;  in  conditions  associated  with  the 
presence  of  substances,  such  as  sugar  and  bile-pigment  in  the  blood; 
after  the  administration  of  anesthetics;  in  fever  conditions,  and  in  certain 
nervous  disorders — epilepsy,  apoplexy,  meningitis,  tetanus,  exophthalmic 
goitre,  injuries  to  the  head,  etc.  In  most  of  these  cases  the  albuminuria 
is  attributable  to  nutritional  disturbances  in  the  glomeruli  and  renal 
epithelium  induced  by  defective  blood  supply;  in  some  cases  to  the  result 
of  nervous  influences.  The  true  nature  of  these  cases  is  usually  readily 
recognized.  The  albuminuria  is  slight  and  temporary,  as  a  rule;  the 
primary  disorder  is  sufficiently  obvious,  and  there  is  no  other  manifesta- 
tion of  Bright's  disease.    It  is  important,  however,  to  point  out  that  the 


ALBUMOSURIA  767 

conditions  in  the  kidneys  found  in  some  of  the  intoxications  and  in 
fever  states  (toxic  degeneration  of  the  renal  epithehum)  merge  gradually 
into  the  well-defined  lesions  of  nephritis — that  there  is  no  sharp  divid- 
ing line  between  them. 

Albuminuria  with  Noteworthy  Alterations  in  the  Kidneys. — In  this  group 
are  included  the  cases  of  active  and  passive  congestion  of  the  kidneys, 
cases  of  toxic  degeneration  of  the  kidneys  (most  of  the  cases  of  febrile 
albuminuria),  the  kidney  of  pregnancy,  amyloid  degeneration  of  the 
kidneys,  the  acute  and  chronic  suppurative  and  non-suppurative  inflam- 
mations of  the  kidneys,  and  tumors  of  the  kidneys.  In  all  of  these  cases 
the  albuminuria  is  due  to  some  more  or  less  severe,  temporary  or  perma- 
nent, damage  to  the  kidneys,  and  the  albuminuria  acquires  its  clinical 
significance  and  diagnostic  importance  from  the  attendant  phenom- 
ena. In  acute  congestion  of  the  kidneys  the  albumin  is  small  in  amount, 
the  urine  is  decreased  in  quantity  and  frequently  more  or  less  hemor- 
rhagic, and  the  causative  factor  usually  can  be  determined.  In  most 
cases,  however,  acute  congestion  of  the  kidneys  represents  but  the  early 
stage  of  acute  nephritis,  from  which  it  is  scarcely  to  be  differentiated. 
In  chronic  congestion  the  albumin  varies  in  amount  in  different  cases. 
In  chronic  heart  and  lung  diseases  it  is  usually  small  in  amount,  but  in 
cases  of  chronic  congestion  due  to  obstruction  of  the  renal  veins  by  a 
tumor  or  ascites,  etc.,  the  amount  may  be  large.  The  diagnosis  of 
chronic  congestion  is  to  be  based  on  the  attendant  phenomena  and  not 
on  the  amount  of  albumin.  Toxic  or  febrile  albuminuria  is  an  interesting 
condition  that  merits  much  attention.  The  albumin  in  these  cases  is  due 
to  the  direct  action  of  some  toxin  on  the  renal  epithelium  rather  than  to  the 
fever,  though  this  may  be  a  contributing  factor;  in  the  one  case  the 
toxin  induces  marked  degeneration  of  the  renal  epithelium,  in  another 
case  it  leads  to  severer  lesions — to  an  acute  nephritis.  In  toxic  albumin- 
uria the  albumin  is  slight  or  moderate  in  amount  and  transitory,  dis- 
appearing with  the  intoxication  or  infection  that  gives  rise  to  it. 

ALBUMOSURIA. 

True  albumose  is  sometimes  found  in  the  urine — during  postpartum 
involution  of  the  uterus  (physiological),  during  fevers,  during  absorption 
of  pneumonic  exudates,  in  phosphorus  poisoning,  in  acute  yellow  atrophy 
of  the  liver,  and  in  other  conditions  of  autolysis — to  which  it  is  attrib- 
utable. True  peptonuria  has  occasionally  been  found  in  pneumonia, 
tuberculosis,  etc.  Globulin  is  occasionally  found  in  association  with  large 
amounts  of  albumin;  it  may  occur  alone. 

The  Bence-Jones  protein  (myelopathic  albumosuria;  Kahler's  dis- 
ease) is  a  protein  foreign  to  the  blood  in  health;  it  is  formed  in  multiple 
myeloma,  of  which  it  is  diagnostic;  and  it  may  be  excreted  by  normal 
kidneys  without  impairment  of  their  epithelium  (selective  action). 
It  is  distinguishable  from  ordinary  albuminuria  by  the  production  of 
cloudiness  in  the  urine  when  heated  to  50°  C,  by  a  flocculent  precipitate 


768  DISEASES  OF  THE   URINARY  SYSTEM 

between  50°  and  60°  C,  by  solution  of  the  precipitate  at  higher  temper- 
atures (especially  upon  the  addition  of  acetic  acid),  and  by  reprecipita- 
tion  upon  cooling. 

CYLINDRURIA. 

The  term  cylindruria  is  commonly  employed  to  designate  casts  of 
the  uriniferous  tubules  (cylinders,  tube  casts),  although  perhaps  other 
casts  might  be  included  within  the  scope  of  its  meaning;  these,  how- 
ever are  casts  of  the  renal  pelvis,  ureter,  urethra,  etc.,  and  since  they 
are  usually  made  up  of  blood,  they  are  referred  to  under  hematuria. 
Tube  casts  basically  are  made  up  of  coagulated  serum  or  a  serum- 
like substance  exuded  by  the  renal  epithelium  when  irritated,  or  perhaps 
they  result  from  the  interaction  of  serum  and  another  substance  elabo- 
rated or  liberated  by  disordered  renal  epithelium.  The  basic  (hyaline) 
cast  may  become  altered  or  attach  various  sorts  of  cells  and  debris, 
so  that  different  kinds  of  casts  may  be  distinguished — ^hyaline,  waxy, 
granular  (pale  and  dark),  and  cellular;  of  the  cellular  casts,  some- 
times (but  by  no  means  always)  the  type  of  cell  may  be  distinguished 
— epithelial,  leukocytic,  erythrocytic;  an  obvious  fatty  degeneration  of 
the  cells,  as  well  as  free  fat  droplets,  suggests  the  term  fatty  cast;  and 
some  casts  apparently  consist  wholly  of  leukocytes  or  erythrocytes 
without  the  basic  hyaline  material. 

Considerable  diagnostic  significance  attaches  to  the  presence  of  casts. 
They  suggest  mere  irritation  (hyaline  cast)  or  more  complete  destruction 
and  desquamation  of  the  renal  cells  (epithelial,  granular,  and  fatty  casts). 
A  few  hyaline  casts  may  occur  in  conditions  of  slight  nutritive  disturb- 
ance, such  as  occurs  in  congestion;  and  since  the  renal  epithelium  is  not 
markedly  disturbed  in  chronic  interstitial  nephritis,  few  casts  are  encoun- 
tered. Many,  especially  epithelial  and  granular,  casts  indicate  marked 
alteration  and  desquamation  of  the  renal  epithelium,  such  as  occur  in 
parenchymatous  nephritis.  Casts  and  albumin  may  and  usually  do  occur 
together,  but  either  may  occur  alone;  casts  alone  are  the  more  significant 
of  changes  in  the  renal  epithelium.  Few  casts  for  a  short  time  signify 
a  mere  transitory  disturbance;  the  continued  presence  of  even  a  few 
casts  means  chronic  nephritis;  many  cellular  (epithelial)  casts  mean 
serious  parenchymatous  involvement  of  the  renal  epithelium;  erythro- 
cytic casts,  an  acute  exacerbation;  and  a  lessening  number  of  cellular 
and  erythrocytic  casts,  a  subsiding  process,  etc. 

Too  much  importance  must  not  be  attached  to  a  few  hyaline  or  cellu- 
lar casts  in  a  single  specimen  of  urine;  they  are  common  in  transitory 
conditions,  such  as  anemia,  various  intoxications,  certain  infections,  etc., 
and  although  they  indicate  some  disturbance  in  the  renal  epithelium,  they 
subside  with  the  initiating  cause:  the  renal  condition  is  not  nephritis,  as 
is  too  often  supposed,  and  the  kidney  often  becomes  entirely  normal 
again.  Casts  should  not  be  mistaken  for  pseudocasts  or  cylindroids — 
long  hyaline  or  longitudinally  striated  objects  with  undulating  outline  and 
tapering  ends;  these  are  mucoid  in  nature  and  not  related  to  true  casts. 


PYURIA  769 


HEMATURIA. 

Blood  in  the  urine  may  come  from  any  part  of  the  genito-urinary  tract. 
Care  must  be  exercised  to  exclude  menstrual  blood  and  urine  stained 
with  logwood,  rhubarb,  etc.  Small  amounts  of  blood  in  the  urine  may 
escape  naked-eye  observation;  moderate  or  large  amounts  impart  a  dark 
brownish  or  smoky  color;  while  very  large  amounts  may  appear  as  bright 
or  dark  red  blood.  The  blood  may  be  recognized  by  microscopic, 
spectroscopic,  or  chemical  examination. 

Etiology. — Hematuria  may  be  due  to:  (1)  Disease  of  the  urethra — 
usually  traumatic  (catheterization,  bougieing,  passing  of  a  calculus,  etc.), 
of  which  there  is  a  history.  The  blood  is  pure  and  unmixed,  and  escap- 
ing at  any  time  may  stain  the  patient's  lifien.  (2)  Disease  of  the  pros- 
tate— benign  or  malignant  enlargement,  of  which  hematuria  is  some- 
times one  of  the  earliest  manifestations.  (3)  Disease  of  the  bladder — 
calculus,  tumor  (benign  or  malignant),  ulceration  (simple  or  tuber- 
culous), parasites,  foreign  bodies,  varicose  veins,  etc.  Blood  from  the 
bladder  is  usually  quite  apparent,  not  intimately  mixed  with  the  urine, 
often  irregularly  clotted,  and  may  escape  at  the  end  of  mictm-ition; 
bladder  epithelium  and  blood  corpuscles  are  detected  by  microscopic 
examination  (hemoglobinuria  does  not  occur  alone);  irrigating  the 
bladder  results  in  securing  a  blood-tinged  fluid;  and  the  local  symptoms 
are  referred  to  the  region  of  the  bladder.  (4)  Disease  of  the  kidneys — 
chronic  congestion  (heart  disease);  acute  and  chronic  nephritis;  infarc- 
tion; tumor  formation;  tuberculosis;  calculus;  parasitic  invasion;  etc. 
Blood  from  the  kidney  is  often  not  immediately  apparent  (the  urine  being 
smoky  only);  it  is  usually  intimately  mixed  with  the  urine  (although 
there  may  be  clots  partaking  of  the  shape  of  the  pelvis  or  the  ureter); 
blood  casts,  renal  and  pelvic  epithelium  are  usually  found  in  the  sedi- 
ment, and  blood  corpuscles  may  be  missed  (that  is,  hemoglobinuria  may 
occur  alone);  irrigating  the  bladder  results  in  securing  a  clear  fluid; 
and  local  symptoms  are  usually  referred  to  the  region  of  the  kidney  or 
the  testicles.  Cystoscopic  examination  and  catheterization  of  the  ureters 
also  may  be  of  value  in  differentiating  vesical  and  renal  hematuria. 
The  association  of  pus  and  blood  is  significant  of  disease  of  the  pelvis 
rather  than  of  the  renal  substance.  (5)  Certain  general  disorders,  such 
as  hemophilia,  scurvy,  leukemia,  and  certain  specific  infective  dis- 
eases, etc. 

PYURIA. 

Pyuria,  or  pus  in  the  urine,  may  be  due  to  suppuration  of  any  part 
of  the  genito-urinary  tract,  or  rarely  to  the  rupture  of  an  abscess  (pelvic, 
prostatic,  peri-appendicular,  etc.)  into  the  urinary  tract.  Pus  occasions  a 
general  cloudiness  of  the  urine,  and  a  whitish  or  cream-colored,  ropy, 
or  tenacious  sediment,  which  may  be  distinguished  from  a  somewhat 
49 


770  DISEASES  OF  THE   URINARY  SYSTEM 

similar  deposit  of  phosphates  by  the  fact  that  the  phosphates  are  whiter, 
less  dense,  and  are  decomposed  by  the  addition  of  an  acid.  Microscopic 
examination  completes  the  differentiation. 

Etiology. — Pyuria  may  be  due  to:  (1)  Disease  of  the  urethra — usually 
urethritis,  rarely  a  chancre.  The  pus  is  small  in  amount,  escapes  with 
the  urine  first  voided,  as  well  as  between  micturition,  and  is  associated 
with  painful  micturition,  other  signs  of  local  inflammation,  and  the 
presence  of  the  gonococcus.  (2)  Vaginitis,  in  which  in  addition  to 
evidences  of  local  inflammation,  vaginal  epithelium  and  possibly  the 
gonococcus  may  be  encountered.  (3)  Cystitis,  in  which  the  urine  may 
be  acid  when  voided  (Bacterium  coli  infections),  but  is  usually  or  soon 
becomes  alkaline  (Proteus  vulgaris,  streptococcic,  staphylococcic,  and 
other  infections),  and  is  associated  with  triple  phosphates,  bladder 
epithelium,  an  ammoniacal  odor,  and  other  evidences  of  decomposi- 
tion. (4)  Ureteritis,  which  is  difficult  (in  many  cases  impossible)  to 
differentiate  from  pyelitis,  except  by  evidences  of  local  inflammation. 
(5)  Pyelitis  and  pyelonephritis.  The  pus  is  usually  considerable  in 
amount  and  associated  with  renal  and  ■  pelvic  epithelium,  and  in 
pyelonephritis  may  escape  intermittently;  the  urine  is  usually  acid  in 
reaction  (calculous  disease.  Bacillus  tuberculosis  and  Bacterium  coli 
infections,  etc.),  but  if  the  pyelitis  is  secondary  to  cystitis  the  urine  may 
be  alkaline. 


ANOMALIES  OF  FORM  AND  POSITION  OF  THE  KIDNEY. 

The  kidneys  are  subject  to  several  malformations  and  malpositions 
of  clinical  interest.  One  or  both  kidneys  may  be  absent;  one  may  be 
hypoplastic  and  the  other  hyperplastic;  there  may  be  a  supernumerary 
kidney;  and  the  two  kidneys  may  be  fused — horseshoe  kidney,  disk- 
shaped  kidney. 

There  may  also  be  anomalous  ureters  (double  or  triple— unilateral 
or  bilateral),  and  anomalous  bloodvessels  (of  etiological  significance 
in  hydronephrosis).  These  anomalies  acquire  clinical  interest  in  con- 
nection with  contemplated  operations  on  the  kidney;  the  presence  and 
the  functional  capacity  of  its  fellow  should  always  be  determined  before 
an  operation  on  a  kidney  is  undertaken,  especially  an  operation  that 
may  comprise  removal  of  the  organ.  The  malpositions  of  the  kidney 
(movable  kidney,  floating  kidney,  nephroptosis)  are  discussed  in  con- 
nection with  visceroptosis  (page  685). 


CIRCULATORY  DISTURBANCES  OF  THE  KIDNEYS. 

Active  Congestion. — Active  (acute)  congestion  is  rare  without  con- 
current exudation;  that  is,  there  is  no  sharp  dividing  line  between  acute 
congestion  and  acute  nephritis.     Acute  congestion  has  been  attributed 


CIRCULATORY  DISTURBANCES  OF  THE  KIDNEYS  771 

to  sudden  contraction  of  the  peripheral  bloodvessels  induced  by  exposure 
to  cold,  and  to  increased  functional  activity,  such  as  may  occur  in  one 
kidney  if  the  ureter  of  its  fellow  be  blocked  by  calculus,  clot,  etc.,  or  if 
the  organ  itself  be  removed.  Otherwise  the  causes  of  acute  congestion 
are  the  causes  of  acute  nephritis.  The  lesions,  except  in  that  they  dis- 
appear with  removal  of  the  exciting  cause,  are  not  distinguishable  from 
those  of  the  mild  grades  of  acute  toxic  or  degenerative  nephritis. 

Passive  Congestion. — Passive  (chronic  or  mechanical)  congestion  of 
the  kidneys  is  usually  part  of  the  general  venous  stasis  that  accompanies 
chronic  cardiac  disease  (myocardial,  endocardial,  or  pericardial) ;  it  may 
occur  also  in  the  event  of  obstruction  to  the  return  circulation  from  the 
renal  veins  by  pressure  (tumor,  aortic  aneurysm,  pregnant  uterus,  ascites), 
angulation  (nephroptosis,  kyphosis,  etc.),  or  thrombosis  or  embolism  of 
the  renal  vein  or  veins  or  the  ascending  vena  cava.  The  kidney  is  enlarged 
and  firm;  the  capsule  strips  readily  and  reveals  distended  veins  and  a 
smooth,  dark  bluish-red  surface.  The  cortex  is  increased  in  thickness; 
the  pyramids  are  purplish.  In  the  course  of  time  the  organ  may  lessen 
in  size,  the  capsule  become  slightly  adherent,  and  the  surface  somewhat 
granular,  due  to  the  gradual  growth  and  subsequent  contraction  of  fibrous 
connective  tissue  and  consecutive  destruction  of  the  parenchyma  (the 
congested  and  contracted  kidney;  cyanotic  induration).  The  symptoms 
consist  of  oliguria  (retarded  circulation  of  the  blood  and  lessened  arterial 
pressure) — perhaps  200  c.c.  or  less  in  the  twenty-four  hours;  the  urine 
is  high  colored,  turbid,  of  increased  specific  gravity  (1022  to  1035), 
deposits  a  considerable  sediment  of  uric  acid  and  urates,  contains  a 
small  amount  of  albumin  (usually  less  than  2  parts  per  1000,  Esbach's 
test),  a  few  hyaline  (rarely  cellular)  casts,  and  a  few  leukocytes  and 
erythrocytes.  The  diagnosis  is  easy,  being  based  upon  a  recognition  of 
the  primary  disorder;  other  evidences  of  general  venous  stasis  (enlarge- 
ment of  the  liver  and  spleen,  oedema,  dropsy,  etc.),  or  a  local  factor 
obstructing  the  renal  return  flow ;  the  urinary  findings ;  and  fluctuation 
of  the  oliguria  and  albuminuria  with  the  functional  activity  of  the  car- 
diovascular system.  The  cyanosis  and  dropsy  contrast  strongly  with  the 
pallor  and  dropsy  of  nephritis.  The  prognosis  and  treatment  are  those 
of  the  primary  disorder. 

Thrombosis  and  Embolism. — Primary  thrombosis  is  very  rare; 
embolism  is  more  common,  and  is  due  usually  to  left-sided  endocar- 
ditis. The  lesions  consist  of  the  common  wedge-shaped  anemic  infarcts 
— which  may  be  simple  and  ultimately  replaced  by  a  contracted  scar, 
or  infected  and  give  rise  to  abscesses.  The  symptoms  often  are  not 
obtrusive;  but  the  diagnosis  may  sometimes  be  made  upon  the  sudden 
onset  of  severe  pain  in  the  region  of  the  kidney  (without  radiation  down 
the  ureters — which  distinguishes  it  from  renal  colic);  enlargement  and 
tenderness  of  the  kidney;  oliguria,  hematuria,  and  albuminuria  of  sudden 
onset  and  often  of  rapid  disappearance;  and  in  the  event  of  the  embolus 
being  infected,  chills,  fever,  sweats,  leukocytosis  (which,  however,  may 
be  already  present  in  consequence  of  the  primary  infection). 


772  DISEASES  OF  THE  URINARY  SYSTEM 


NEPHRITIS. 

The  following  varieties  of  inflammation  of  the  kidneys  may  be  dif- 
ferentiated : 

I.     Acute  nephritis. 

(a)  Acute  toxic  or  degenerative  nephritis.     (Cloudy  swelling 

or  parenchymatous  degeneration  of  the  kidney.) 

(b)  Acute  diffuse  nephritis.     (Acute  parenchymatous,  exuda- 

tive, catarrhal,  desquamative,  glomerular,  tubular,  or 
hemorrhagic  nephritis.) 

(c)  Acute  suppurative  nephritis. 

(d)  Acute  interstitial  non-suppurative  nephritis. 

(e)  The  kidney  of  pregnancy. 
II.     Chronic  nephritis. 

(a)  Chronic  diffuse  non-indurative  nephritis.     (Subacute  and 

chronic  parenchymatous,  exudative,  catarrhal,  desquama- 
tive, glomerular,  tubular,  or  hemorrhagic  nephritis;  the 
large  white  kidney;  the  large  red,  mottled,  or  variegated 
kidney.) 

(b)  Chronic  diffuse  indurative  nephritis. 

1.  Secondary  chronic  indurative  (or  interstitial)  nephritis. 

(Late  stage  of  chronic  parenchymatous  nephritis;  the 
small  white  kidney;  the  white  granular  kidney;  the 
secondarily  contracted  kidney.) 

2.  Primary  chronic  indurative  (or  interstitial)  nephritis. 

(The  red  granular  kidney;  the  gouty  kidney;  the  pri- 
marily contracted  kidney;  the  genuine  contracted 
kidney.) 

3.  Arteriosclerotic  nephritis.    (The  senile  kidney.) 
Strictly  speaking,  the  so-called  toxic  or  degenerative  nephritis  is  not 

a  true  inflammation;  but  it  is  due  to  factors  which  if  prolonged  or  of 
increased  virulence  result  in  inflammation,  it  is  often  associated  with 
more  or  less  active  congestion  and  slight  exudation,  and  it  is  the  impor- 
tant lesion  in  well-developed  acute  nephritis,  so  that  it  is  not  only  wise 
to  include  it  among  the  acute  nephritides,  but  practically  it  is  virtually 
impossible  to  exclude  it  therefrom :  it  represents  an  early  stage,  a  minor 
grade,  or  a  part  of  acute  nephritis.  Acute  suppurative  nephritis  will  be 
discussed  under  a  special  heading;  acute  interstitial  non-suppurative 
nephritis  is  largely  of  pathological,  of  little  clinical,  interest;  the  kidney 
of  pregnancy  is  a  peculiar  type  of  obvious  etiological  relationships. 

Practically,  therefore,  in  the  great  majority  of  acute  cases  the  physician 
has  to  deal  with  what  may  be  best  described  as  acute  diffuse  nephritis,  or 
simply  acute  nephritis ;  or  with  an  acute  exacerbation  of  cluronic  nephritis. 
The  chronic  nephritides  can  be  sharply  divided  into:  (1)  Those  that 
follow  subsidence  of  the  acute  process,  or  perhaps  begin  subacutely  or 
insidiously,  and  are  characterized  by  predominant,  but  not  exclusive 


ACUTE  DIFFUSE  NEPHRITIS  773 

changes  in  the  parenchyma  (chronic  diffuse  non-indurative,  or  paren- 
chymatoiiS;  nephritis) ;  and  (2)  those  in  which  the  chief  lesions  occur 
in  the  interstitial  tissue  (chronic  diffuse  indurative,  or  interstitial,  neph- 
ritis), but  in  which  the  renal  lesions,  diagnostically,  prognostically,  and 
therapeutically,  may  be  neither  primary  nor  of  the  greatest  importance 
(cardiovascular-renal  disease).  The  chronic  diffuse,  non-indurative,  or 
parenchymatous  nephritis  is  often  subject  to  acute  exacerbations,  and 
should  the  patient  survive  for  eighteen  months  or  more,  sclerotic  or 
cicatricial  lesions  may  develop,  and  a  form  of  so-called  mixed  nephritis 
(secondarily  contracted  kidney)  may  ensue. 


ACUTE  DIFFUSE  NEPHRITIS. 

(Acute  Parenchymatous  Nephritis;  Acute  Bright's  Disease.) 

Etiology. — ^Acute  nephritis  may  occur  at  any  age,  but  is  most  common 
before  the  fortieth  year  and  in  males  (excluding  the  kidney  of  pregnancy). 
Rarely  it  seems  to  follow  directly  upon  exposure  to  inclemencies  of  the 
weather,  especially  coldness  and  dampness  (said  to  cause  reflex  con- 
gestion of  the  kidneys,  to  favor  the  retention  of  excrementitious  sub- 
stances, to  produce  a  hemolysin  analogous  to  that  which  occurs  in 
certain  cases  of  paroxysmal  hemoglobinuria,  etc.);  these  cases  usually 
occur  in  alcoholic  subjects.  Otherwise,  acute  nephritis  is  due  to  autog- 
enous or  exogenous  infection  or  intoxication,  and  it  is  commonly  a 
secondary  process.  The  infectious  causes  comprise  the  infectious  dis- 
eases, especially  scarlatina,  diphtheria,  pneumonia,  typhoid  fever,  influ- 
enza, cholera,  yellow  fever,  smallpox,  the  pyococcic  infections,  etc.  In 
most  of  these  cases  the  renal  lesions  are  due  to  toxemia  and  the  excretion 
of  toxins,  rather  than  to  bacteremia;  the  bacteremia  of  septicopyemia  is 
likely  to  result  in  suppurative  lesions  (suppurative  nephritis).  The 
etiological  intoxications  comprise  (in  addition  to  the  toxemias  of  the 
infectious  processes) :  (1)  Autogenous  metabolic  poisons,  associated  with 
pregnancy,  anemia,  gout,  diabetes,  jaundice,  hemoglobinemia,  burns, 
diseases  of  the  skin  associated  with  lessening  of  the  cutaneous  functions, 
etc.;  and  (2)  exogenous  poisons,  such  as  spices,  alcohol,  ether,  chloro- 
form, turpentine,  cantharides,  salicyl  compounds,  carbolic  acid,  minerals, 
mineral  acids  and  salts,  etc.  In  anemic  and  mild  toxemic  states  degen- 
erative lesions  (toxic  degeneration  of  the  renal  epithelium)  are  common; 
in  severe  toxemias  and  in  bacteremias  degenerative  and  inflammatory 
lesions  are  likely  to  occur. 

Pathology. — In  mild  cases,  the  kidney  may  be  slightly  (if  at  all) 
increased  in  size,  and  somewhat  opaque  (toxic  degeneration  or  cloudy 
swelling);  in  more  severe  cases  it  is  perhaps  somewhat  congested.  In 
well-developed  acute  nephritis  it  is  increased  in  size,  the  capsule  is 
tense,  strips  readily,  leaving  a  smooth  surface — which  in  severe  cases 
is  dark  reddish  brown  in  color  (hyperemic  or  hemorrhagic  kidney) ;  in 
less  severe  casfes  and  in  the  subsiding  stages  of  severe  cases  it  is  pale 


774  DISEASES  OF  THE   URINARY  SYSTEM 

grayish  or  grayish  red  in  color  (anemic  kidney);  in  other  cases  it  ex- 
hibits a  combination  of  these  (mottled  or  variegated  kidney).  On  section 
the  organ  is  usually  soft,  opaque  (as  though  cooked),  oedematous,  friable, 
and  drips  blood;  the  cortex  is  swollen  and  the  normal  striations  obscured; 
the  pyramids  are  usually  much  congested.  The  toxins  sometimes 
exhibit  a  selective  action,  in  one  case  implicating  especially  the  epi- 
thelium of  the  glomeruli,  in  another  the  epithelium  of  the  convoluted 
tubules,  in  still  another  the  connective  tissues.  In  scarlatina,  for  instance, 
the  glomeruli  are  likely  to  be  especially  involved  (glomerulonephritis), 
and  may  appear  as  distinct,  minute,  pale  grayish  or  dark  reddish  (hemor- 
rhagic) points.  Microscopically,  the  lesions  may  be  confined  to  the 
parenchyma  (toxic  degeneration),  or  they  may  implicate  all  the  tissues 
(acute  diffuse  nephritis),  or  they  may  be  especially  conspicuous  in  the 
interstitial  tissue  (acute  interstitial  suppurative  or  non-suppurative 
nephritis).  The  parenchymatous  lesions  consist  of  cloudy  swelling 
(common  in  most  of  the  acute  infections);  fatty  degeneration  (common 
in  the  severe  infections,  in  certain  intoxications  such  as  phosphorus 
poisoning,  and  in  severe  anemias);  hydropsical  degeneration  and  com- 
plete necrosis  (which  occur  in  the  severest  infections,  such  as  cholera, 
and  in  severe  intoxications,  such  as  cantharidal  and  mercurial  poisoning, 
etc.).  In  addition,  in  the  event  of  inflammatory  lesions,  desquamation 
of  the  renal  epithelium  commonly  occurs  (desquamative  nephritis), 
and  may  be  excessive.  Here  and  there  the  lumen  of  the  tubules  or  of 
Bowman's  capsules  may  be  obstructed  or  distended  by  swollen  and 
desquamated  epithelium,  coagulated,  finely  granular  albumin,  fat 
granules,  erythrocytes,  leukocytes,  tube  casts,  and  detritus.  Special 
implication  of  the  tubules  or  of  the  glomeruli  suggests  the  terms  tubular 
and  glomerular  nephritis,  respectively.  The  interstitial  tissues  in  the 
merely  toxic  degenerative  cases  may  reveal  no  lesions  whatever;  in  the 
more  frank  or  severe  cases,  dilatation  and  overfilling  of  the  bloodvessels, 
swelling  and  oedema  of  the  intertubular  connective  tissue,  and  cellular 
exudation  and  proliferation  occur.  The  lesions,  as  a  rule,  are  focal 
rather  than  widespread,  and  are  most  marked  in  the  cortex.  In  some 
cases  hemorrhages  occur  into  the  tubules,  within  Bowman's  capsules, 
or  in  the  interstitial  tissue  (hemorrhagic  nephritis);  in  other  cases  the 
cellular  exudation  consists  largely  of  polynuclear  leukocytes  (suppu- 
rative nephritis),  and  in  other  cases  of  Unna's  large  mononuclear  plasma 
cells  (acute  interstitial  non-suppurative  nephritis). 

The  kidney  of  'pregnancy  (to  be  distinguished  from  nephritis  antece- 
dent to  the  pregnancy  and  from  an  ordinary  nephritis,  due  to  the  com- 
mon etiological  factors  developing  in  a  pregnant  woman)  develops 
especially  in  young  primiparte,  in  twin  pregnancies,  and  during  the  latter 
half  of  pregnancy.  Its  nature  is  not  well  understood,  although  it  is 
probably  toxic  in  origin,  the  consequence  of  the  maternal  kidneys  being 
obliged  to  serve  as  emunctories  for  both  the  mother  and  the  foetus;  it 
has  been  attributed  also  to  perversion  of  the  detoxifying  function  of  the 
liver  and  of  the  thyroid,  to  a  toxin  elaborated  by  the  syncytium  (syncy- 


ACUTE  DIFFUSE  NEPHRITIS  775 

tiolysins),  to  bacterial  infection  and  intoxication,  to  increased  intra- 
abdominal pressure  exerted  especially  on  the  renal  veins,  the  ureters,  or 
the  coeliac  ganglion  (occasioning  renal  anemia  in  consequence  of  reflex 
contraction  of  the  renal  arteries,  etc.).  The  kidney  varies  in  appear- 
ance in  different  cases;* it  may  not  be  distinguishable  from  the  more 
common  acute  diffuse  nephritis;  it  is  enlarged,  the  capsule  strips  readily, 
revealing  a  smooth,  pale  yellowish  or  mottled  surface.  The  microscopic 
lesions  are  largely  degenerative,  involving  the  parenchyma;  the  lesions 
(inflammatory)  in  the  interstitial  tissue  are  comparatively  slight. 

Symptoms. — Toxic  or  degenerative  nephritis  usually  runs  its  course 
without  noteworthy  symptoms;  the  general  manifestations  of  the  initi- 
ating infection  or  intoxication  may  be  not  in  the  least  disturbed,  and 
the  renal  condition  is  recognized  only  by  examining  the  urine — which 
exhibits  the  characteristics  of  so-called  febrile  urine.  It  is  lessened  in 
amount,  turbid,  of  high  color  and  increased  specific  gravity  (1022  to 
1030),  and  highly  acid;  it  contains  an  excess  of  solids  and  a  trace  or  a 
small  amount  of  albumin  (febrile  albuminuria),  and,  depending  upon  the 
concentration,  it  deposits  more  or  less  sediment  that  contains  a  few 
leukocytes  and  perhaps  a  few  hyaline  tube  casts.  With  the  subsidence 
of  the  causative  infection  or  toxic  process,  the  renal  conditions  and  the 
urine  usually  revert  to  the  normal;  in  severe  cases,  however  (cholera, 
cantharidal  and  mercurial  poisoning,  etc.),  anuria  may  develop  and  soon 
lead  to  a  fatal  issue. 

Acute  diffuse  nephritis  may  develop  insidiously  (as  in  the  infectious 
diseases)  or  suddenly  (as  after  a  debauch  and  exposure  to  coldness  and 
dampness,  severe  intoxications,  etc.);  in  either  event  its  existence  .is 
usually  revealed  by  oedema  or  changes  in  the  urine,  or  both;  rarely  by 
severe  uremia  (coma,  convulsions,  etc.).  (Edema  (due  probably  to  toxic 
alterations  of  the  endothelium  of  the  bloodvessels  and  capillaries,  as 
well  as  changes  in  the  chloride  metabolism,  sodium  chloride  retention) 
is  a  characteristic  sign,  and  although  not  invariably  present,  may  be 
detected  by  careful  examination  in  some  cases  in  which  it  is  thought  to  be 
absent.  It  may  develop  slowly,  the  patient  gradually  becoming  swollen 
and  pale;  or  it  may  come  on  suddenly  within  twenty-four  hours  of  the 
onset  of  the  disease  (especially  after  a  debauch,  in  scarlatina,  etc.). 
It  varies  much  in  different  cases;  it  usually  develops  coincidently  with, 
rarely  before,  the  oligiu-ia,  but  it  bears  no  relationship  to  the  amount 
of  urine  or  of  the  albuminuria.  Usually  it  develops  first  in  the  eyelids, 
then  in  the  face,  al)out  the  ankles,  in  the  hands,  legs,  scrotum,  and 
loose,  areolar,  and  dependent  portions  of  the  body;  finally,  it  may  become 
universal  (anasarca),  involving  even  the  serous  sacs  (which  rarely  may 
exhibit  collections  of  fluid  before  the  subcutaneous  tissues).  G^ldema 
of  the  meninges  may  occur  (and  may  cause  coma,  henn'plegia,  etc.); 
oedema  of  the  mucous  membranes,  except  perhaps  the  glottis,  palate, 
and  conjunctiva,  is  uncommon;  and  oedema  of  the  lungs  may  develop, 
especially  in  cases  proceeding  to  a  fatal  issue. 

Diminution  in  the  amount  of  urine  may  be  the  first  symptom  to  attract 


776  DISEASES  OF  THE  URINARY  SYSTEM 

attention;  the  daily  amount  may  be  300  c.c.  or  less;  in  some  cases  com- 
plete anuria  supervenes  and  may  lead  to  a  fatal  issue.  The  urine  is 
acid  in  reaction,  turbid,  highly  colored  (smoky,  rarely  bright  red,  from 
the  presence  of  more  or  less  blood),  and  of  increased  specific  gravity 
(1024  to  1030);  albuminuria  (the  albumin  of  the  blood  serum,  serum 
albumin,  and  globulin;  sometimes  also  nucleo-albumin)  is  constant — 0.3 
to  1  per  cent.  (5  to  10  grams)  daily;  the  total  output  of  urea  and  other 
nitrogenous  substances  is  lessened  (although  the  percentage  of  urea 
may  be  increased);  the  purin  bases  may  be  increased.  The  usually 
abundant  (sometimes  obviously  hemorrhagic)  sediment  consists  of 
erythrocytes  (and  blood  pigment),  leukocytes,  renal  and  vesical  epi- 
thelium, hyaline^  granular,  and  cellulai"  (epithelial,  leukocytic,  erythro- 
cytic) casts,  compound  granule  cells,  crystals  (especially  uric  acid  and 
oxalates),  cell  detritus,  bacteria  (not  always  extraneous  contamination), 
etc.  The  molecular  concentration  or  osmotic  pressure  of  the  urine  is 
usually  reduced  (hyposthenuria),  so  that  the  freezing  point  (cryoscopy) 
is  1°  or  less  than  1°  C.  (instead  of  the  normal  1.3°  to  2.3°  C.)  below  that 
of  distilled  water  (0°  C).  The  severity  of  the  urinary  changes  (amount 
of  albuminuria,  number  and  character  of  the  casts,  presence  or  absence 
of  blood,  etc.)  is  significant  of  the  severity  of  the  renal  changes. 

The  general  symptoms  are  not  characteristic;  local  symptoms  are 
often  in  abeyance,  although  rarely  there  may  be  lumbar  pain  or  tender- 
ness, frequent  micturition,  vesical  tenesmus,  etc.  If  the  disease  develops 
suddenly  (as  after  a  debauch)  or  in  children  there  may  be  fever  (101° 
to  103°  F.),  associated  or  not  with  chilhness,  nausea  and  vomiting, 
headache,  and,  in  children,  convulsions;  developing  during  the  course 
of  one  of  the  infectious  diseases  there  may  be  (but  not  necessarily) 
an  added  increment  of  fever.  Fever,  if  it  occurs,  may  last  for  several 
days  or  a  week.  The  pulse  is  usually  full  and  of  increased  tension, 
often  slowed  in  the  early,  and  perhaps  accelerated  in  the  later,  stages. 
Accentuation  of  the  aortic  second  sound  and  some  hypertrophy  of 
the  left  ventricle  may  develop  after  the  lapse  of  four  to  six  weeks;  per- 
haps earlier  in  children.  Epistaxis  is  a  suggestive  symptom  in  some 
cases.  Dyspnoea  (due  to  bronchitis,  bronchopneumonia,  oedema  of  the 
lungs,  hydrothorax,  hydropericardium)  may  occur,  especially  in  serious 
cases.  The  appetite  is  poor,  vomiting  may  ensue  (its  persistence  indi- 
cates the  early  advent  of  more  ominous  uremic  symptoms),  constipation 
may  be  present,  but  diarrhoea  is  not  unusual.  Loss  of  strength  and  flesh 
are  common,  but  emaciation  is  usually  concealed  by  oedema.  Uremia 
develops  and  is  progressive;  the  blood  is  hydremic  and  of  lessened 
specific  gravity,  and  shows  the  common  changes  of  secondary  anemia 
(oligocythemia  with  lowered  color  index — disproportionate  oligo- 
chromemia);  the  leukocytes  are  usually  normal,  but  there  may  be  a 
moderate  leukocytosis  (16,000  to  22,000),  especially  in  severe  cases 
of  acute  hemorrhagic  nephritis,  in  uremia,  and  in  complicating  in- 
fections. The  blood  becomes  toxic,  and  its  freezing  point  higher  than 
normally.      Severe  uremic  manifestations  (coma  or  convulsions)  may 


ACUTE  DIFFUSE  NEPHRITIS  777 

develop  at  any  time,  although  in  acute  nephritis,  as  a  rule,  they  occur 
only  when  there  is  marked  oliguria. 

Diagnosis. — ^The  diagnosis  may  be  suggested  by  the  history  of  the  case 
and  the  onset  of  oedema,  but  it  is  made  by  an  examination  of  the  urine. 
Frequent  examination  of  the  urine,  therefore,  should  be  made  in  all  cases 
in  which  the  likelihood  of  the  development  of  nephritis  is  even  remote, 
but  especially  in  infections,  intoxications,  coma,  convulsions,  and  preg- 
nancy. Wliether  the  renal  lesions  constitute  an  acute  nephritis  or  (as 
is  very  common)  an  acute  exacerbation  of  an  already  existing  subacute 
or  chronic  nephritis,  may  be  determined  in  part  by  the  history  of  the 
patient,  and  in  part  by  an  examination  of  the  urine,  especially  the  sedi- 
ment. 

Prognosis. — The  mild  degenerative  lesions  usually  subside  with  the 
initiating  infection  or  intoxication;  severe  lesions  (cholera,  yellow 
fever,  phosphorus  poisoning,  corrosive  sublimate  poisoning,  etc.) 
may  contribute  or  lead  more  directly  to  a  fatal  issue  (anuria,  uremia). 
Acute  diffuse  nephritis  of  mild  or  intermediate  grade  results  in  re- 
covery in  about  50  per  cent,  of  the  cases  within  four  to  six  weeks;  an 
additional  percentage  of  cases  pass  into  the  subacute  or  chronic  stage. 
The  prognosis  is  bad  in  the  event  of  extreme  anasarca,  marked  uremia 
that  does  not  respond  promptly  to  treatment  (recovery  may  ensue), 
and  complications  (secondary  infections,  oedema  of  the  lungs,  broncho- 
pneumonia, serous  membrane  transudates  and  inflammations,  etc.). 
The  kidney  of  pregnancy  may  lead  to  fatal  termination  at  almost  any 
time,  but  the  dangers  are  much  minimized  by  judicious  treatment, 
and  recovery  usually  follows  parturition. 

Treatment. — In  infections  the  likelihood  of  nephritis  developing  may 
be  prevented  by  the  avoidance  of  exposure  to  coldness  and  damp- 
ness; the  use  of  suitable  personal  and  bed-clothing;  the  non-use  of  irri- 
tating food  and  drink;  diluting  the  toxins  and  other  excrementitious 
substances  to  be  eliminated  by  the  kidneys;  and  promoting  the  functional 
activities  of  the  skin  and  intestines.  It  is  said  that  an  imminent  attack 
of  nephritis  manifested  by  hematuria  and  increased  arterial  tension 
may  be  averted  or  mitigated  by  an  active  cathartic — compound  jalap 
powder  or  a  saline  cathartic. 

When  acute  nephritis  has  developed,  we  must  secure  for  the  patient 
rest,  warmth,  and  a  suitable  diet;  the  rest  must  be  absolute  and  in 
bed  until  all  evidences  of  the  acute  manifestations  have  disappeared. 
He  should  rest  between  blankets  and  wear  light  flannels — the  absence 
of  sheets  lessens  the  likelihood  of  chill  and  the  flannels  promote  the 
functional  activity  of  the  skin.  The  diet  should  be  for  a  time  at  least 
as  non-nitrogenous  as  possible,  but  of  sufficient  caloric  value.  Milk  is 
the  most  suitable,  and  if  possible  should  constitute  the  sole  diet  for  four 
to  six  weeks;  it  may  be  diluted  one-third  with  lime  water  (which  serves 
to  decrease  the  acidity  of  the  urine)  or  with  plain  hot  water,  or  an  alka- 
line carbonated  water,  or  barley  water,  or  thin  oatmeal  gruel.  The  use  of 
bland  fluids  also  is  serviceable — pure  water  to  which  sodium  bicarbonate, 


778  DISEASES  OF  THE   URINARY  SYSTEM 

potassium  citrate,  or  sodium  benzoate  (5  to  10  grains,  0.3  to  0.6  gram 
to  the  ounce)  may  be  added;  weak  lemonade;  a  dram  of  cream  of 
tartar,  the  juice  of  a  lemon,  added  to  a  pint  of  boiling  water;  thin 
arrowroot,  etc. 

Local  depletive  measures  (dry  cups,  followed  by  hot  linseed  poultices 
or  other  forms  of  hot  moist  heat,  such  as  compresses,  or  the  Paquelin 
cautery)  sometimes  seem  to  relieve  the  engorgement  of  the  kidneys; 
they  are  especially  serviceable  in  cases  that  begin  with  local  distress, 
hematuria,  anuria,  etc. 

The  use  of  diaphoretics  and  purgatives,  by  promoting  the  functional 
activities  of  the  skin  and  the  intestines,  serve  to  secure  some  physio- 
logical rest  for  the  kidneys  and  to  avert  the  dangers  that  threaten  from 
the  accumulation  of  toxic  substances  in  the  blood.  Diaphoresis  is  best 
attained  by  the  use  of  hydrotherapy — the  hot-water  bath,  the  hot-air 
bath,  the  hot-vapor  bath,  or  the  hot  wet  pack,  repeated  daily  in  serious 
cases,  but  less  frequently  in  less  serious  cases  and  as  convalescence  becomes 
established.  The  sweating  thus  induced  may  be  increased  by  the  concur- 
rent administration  of  a  hot  drink  or  a  diaphoretic  mixture  (spirit  of 
nitrous  ether,  solution  of  ammonium  acetate,  etc.).  In  urgent  cases  pilo- 
carpine also  may  be  used — |  to  |  grain  (0.008  to  0.01  gram),  repeated 
perhaps  in  a  half-hour  if  necessary;  but  it  must  be  employed  with 
caution,  only  when  necessary,  and  it  must  be  avoided  in  children.  Free 
purgation  is  called  for  in  all  cases,  and  is  best  attained  by  the  use  of 
saline  cathartics,  compound  jalap  powder,  etc.  Calomel  should  be 
avoided,  in  the  early  stage  assuredly,  since  it  has  a  diuretic  action 
attained  by  provoking  renal  congestion.  Similarly,  all  stimulating 
diuretics  are  contra-indicated  in  the  early  stages.  Water  is  the  best 
diuretic;  it  flushes  the  kidneys,  facilitates  the  removal  of  the  products 
of  inflammation  and  desquamation,  lessens  the  acidity  of  the  urine,  and 
dilutes  the  toxins  in  the  blood  and  those  passing  through  the  kidneys. 
The  bland  alkaline  diuretics  already  mentioned  may  be  added  to  the 
water.  In  the  later  stages  the  more  stimulating  diuretics,  such  as 
digitalis,  strophanthus,  caffeine,  cocaine,  diuretin,  theobromine,  etc., 
may  be  serviceable. 

Special  symptoms  sometimes  demand  special  treatment.  Headache 
may  require  the  use  of  bromides.  Should  severe  uremic  manifestations 
(coma,  convulsions)  supervene,  venesection  should  be  performed,  and 
ten  to  twenty  ounces  of  blood  abstracted.  In  an  asthenic  subject  the 
volume  of  blood  removed  may  be  replaced  by  an  equal  volume  of  physio- 
logical saline  solution  (half  or  one-fourth  strength  in  the  event  of  oedema). 
Convulsions  not  thus  relieved  may  be  controlled  by  a  few  whiffs  of 
chloroform ;  by  chloral  (15  to  30  grains,  1  to  2  grams)  and  potassium 
bromide  (60  grains,  4  grams)  by  the  rectum ;  or  by  a  single  hypodermic 
injection  (j  grain,  0.015  gram)  of  morphine.  In  some  cases  lumbar 
puncture  has  been  efficacious  in  relieving  the  convulsions  and  the  coma; 
the  cerebrospinal  fluid  is  often  under  increased  pressure  in  these  cases. 
The  bowels  should  be  opened  immediately  and  freely,  by  an  enema  and 


ACUTE  SUPPURATIVE  NEPHRITIS  779 

by  the  use  of  croton  oil  (2  drops)  in  olive  oil  on  the  back  of  the  tongue, 
or  elaterium  (J  grain,  0.015  gram).  Profuse  sweating  also  should  be 
induced  by  a  hot  wet  pack  or  a  hot-vapor  bath.  Vomiting  and  diar- 
rhoea (uremic  phenomena)  often  subserve  a  useful  purpose  of  elimination, 
and  should  not  always  be  immediately  checked.  Vomiting,  if  exhausting, 
should  be  met  with  counterirritation  to  the  epigastrium,  and  bismuth, 
cerium  oxalate,  creosote,  carbolic  acid,  dilute  hydrocyanic  acid,  sips 
of  very  hot  water,  cracked  ice,  etc.  Anasarca  that  does  not  yield  to 
measures  already  mentioned  may  require  small  incisions  into  the  skin 
or  the  use  of  Southey's  tube;  often,  however,  it  can  be  markedly,  if  not 
altogether  relieved  by  the  use  of  a  salt-free  (or  salt-poor)  diet  (bread, 
meat,  potatoes,  eggs,  etc.,  cooked  and  eaten  without  salt).  Transudates 
in  the  serous  cavities  should  be  tapped.  Pulmonary  oedema,  broncho- 
pneumonia, and  other  complications  are  to  be  treated  on  general  prin- 
ciples. During  convalescence  care  should  be  taken  to  avoid  chill  and 
possible  relapse  (avoidance  of  exposure;  use  of  flannels,  etc.).  The 
diet  should  be  gradually  augmented;  first,  farinaceous  foods,  then  light 
vegetables,  non-acid  fruits,  meats,  etc.  Anemia  and  weakness  suggest 
the  use  of  iron  (liquor  ferri  et  ammonii  acetatis)  and  strychnine,  but 
iron  should  not  be  employed  unless  there  is  anemia,  nor  until  the  acute 
manifestations  have  subsided. 


ACUTE  SUPPURATIVE  NEPHRITIS. 

{Acute  Hematogenous  Infection  of  the  Kidney.) 

Etiology. — Infection  of  the  kidney  leading  to  suppuration  may  be  pro- 
voked by  staphylococci,  streptococci,  pneumococci,  gonococci,  colon 
bacilli,  typhoid  bacilli,  tubercle  bacilli,  etc.  Infection  may  occur  (1)  by 
way  of  the  blood  stream;  (2)  by  way  of  the  ureter — pyelonephritis 
(page  788);  or  (3)  by  contiguity  or  continuity  of  tissue — perinephritic 
abscess  (page  792).  The  hematogenous  infections  constitute  a  special 
form  of  nephritis.  The  condition  may  be  apparently  primary,  and 
of  traumatic  or  undiscoverable  cause;  or  it  may  be  secondary,  and 
follow  one  of  the  infectious  diseases  (typhoid  fever,  diphtheria,  etc.); 
septicopyemia  or  a  single  suppurative  focus  (furuncle,  phlegmon, 
osteomyelitis,  erysipelas,  etc.);  or  some  intestinal  infection,  especially 
in  children. 

Pathology. — The  lesions  consist  of  foci  of  suppuration  in  varying 
stages  of  development — from  mere  leukocytic  accumulations  to  well- 
marked  necroses  and  small,  usually  miliary  abscesses;  these  are  usually 
situated  in  the  cortex,  and  although  they  are  usually  bilateral,  they  are 
often  unilateral. 

Symptoms. — The  symptoms  consist  of  the  antecedent  disorder  (in- 
fectious disease,  localized  suppuration,  etc.),  to  which,  at  the  time  of 
infection  of  the  kidney,  sudden  increase  of  fever,  chills  or  chilliness, 
perhaps  sweating,  and  leukocytosis  are  added;  and  to  these  also  local- 


780  DISEASES  OF  THE   URINARY  SYSTEM 

izing  signs,  such  as  abdominal  pain,  tenderness  over  one  or  both  kidneys 
anteriorly,  and  tenderness  and  muscular  rigidity  at  one  or  both  costo- 
vertebral angles  posteriorly  (especially  significant  if  unilateral).  The 
urine,  as  a  rule,  is  somewhat  reduced  in  amount,  and  contains  albumin, 
pus,  blood,  and  casts.  In  some  severe  hyperacute  cases  the  onset  is 
sudden  and  severe,  prostration  is  marked,  fever  is  high  (104°  to  106°), 
and  the  general  picture  corresponds  with  that  of  general  septicopyemia 
and  obscures  the  local  phenomena  referable  to  the  kidney.  In  less  severe 
or  subacute  cases  there  are  more  or  less  protracted  chills,  fever,  sweats, 
leukocytosis,  and  unilateral  costovertebral  tenderness  and  muscular 
rigidity. 

Diagnosis. — The  diagnosis  is  often  uncertain,  but  may  often  be  made 
by  attention  to  the  etiological  factors,  the  local  signs,  the  urinary 
changes,  and  the  absence  of  any  vesical  or  renal  pelvic  condition  that 
might  cause  urogenous  infection  of  the  kidney  tissue  (cystopyelitis  and 
pyelonephritis). 

Prognosis. — ^The  prognosis  depends  upon  the  etiological  factors  and 
whether  the  condition  is  unilateral  or  bilateral. 

Treatment. — ^The  treatment,  in  general,  is  that  of  septicopyemia. 
The  local  lesions  may  be  favorably  influenced  by  bacterins  corresponding 
to  the  infection.  In  unilateral  infections  not  otherwise  remediable, 
resort  should  be  had  to  surgical  intervention. 


CHRONIC  DIFFUSE  NON-INDURATIVE  NEPHRITIS. 

{Subacute  and  Chronic  Parenchymatous  Nephritis;  Chronic  Bright' s  Disease.) 

Etiology. — Chronic  diffuse  non-indurative  (or  parenchymatous)  nephritis 
is  most  common  in  young  male  adults  between  the  ages  of  twenty  and 
forty  years;  but  it  is  not  rare  in  women,  and  in  children  especially  after 
scarlatina.  It  may  follow  acute  nephritis,  and  has  then  a  like  etiology 
and  pathogenesis.  Perhaps  in  most  cases  it  develops  insidiously,  sub- 
acutely,  or  chronically,  and  is  attributed  to  continued  or  repeated  expo- 
sure to  the  inclemencies  of  the  weather,  insanitary  surroundings,  over- 
indulgence in  alcohol,  or  infective  or  toxic  agents  insufficient  in  amount 
or  virulence  to  cause  acute  nephritis  (malaria,  tuberculosis,  syphilis, 
prolonged  suppuration,  in  which  event  it  may  be  associated  with  amyl- 
oidosis, etc.).  Although  the  course  is  chronic,  acute  exacerbations  are 
common;  indeed,  many  cases  of  so-called  acute  nephritis  are  likely 
acute  exacerbations  of  previously  unrecognized  subacute  or  chronic 
nephritis. 

Pathology. — The  lesions  are  not  essentially  different  from  those  of 
acute  nephritis,  except  in  the  addition  of  secondary  alterations,  the 
development  of  which  requires  time.  Two  types  of  kidneys  occur— the 
large  white  (more  properly  pale  or  yellow)  kidney,  and  the  large  red, 
mottled,  or  variegated  kidney.  Both  are  enlarged  (the  yellow  more 
so  than  the  red) ;  the  capsule  strips  readily,  revealing  a  smooth  surface — 


CHRONIC  DIFFUSE  NON-INDURATIVE  NEPHRITIS  781 

pale  yellowish,  or  mottled  grayish  yellow,  or  reddish  yellow,  in  the  one; 
and  grayish  red  or  mottled  (commonly  of  pale  and  dark  areas)  or  very . 
dark  reddish  brown  or  hemorrhagic,  in  the  other  (chronic  hemorrhagic 
nephritis).  The  cortex  is  swollen  and  pale,  mottled,  or  dark  red,  and 
hemorrhagic.  Should  the  patient  sm-vive  eighteen  months  or  more, 
the  lesions  of  indurative  nephritis  gradually  develop  (secondarily  con- 
tracted kidney).  Microscopically,  the  glomeruli  exhibit  proliferative  and 
degenerative  changes,  involving  the  epithelium  and  the  endothelium, 
similar  to  those  of  acute  nephritis ;  the  changes  in  the  tubular  epithelium 
are  especially  marked  in  the  convoluted  tubules,  and  are  similar  to 
those  of  acute  nephritis,  fatty  degeneration,  however,  being  conspicuous 
(fatty  degeneration  and  anemia  being  largely  responsible  for  the  pallor 
of  the  kidney).  The  changes  in  the  interstitial  tissue  are  similar  to  those 
of  acute  nephritis,  usually,  however,  less  active,  more  advanced;  in  some 
cases  there  is  considerable  hemorrhage  (acute  exacerbations;  chronic 
hemorrhagic  nephritis).  In  the  course  of  time  the  cellular  exudate 
becomes  converted  into  newly  formed  fibrous  connective  tissue,  which  by 
contracting  leads  to  atrophy  of  the  glomeruli  and  tubules  (secondarily 
contracted  kidney). 

Symptoms. — ^The  disease  may  develop  out  of  acute  nephritis — ^pallor, 
dropsy,  and  albuminuria  persisting.  Usually  it  develops  insidiously. 
The  patient  may  complain  of  gradual  failure  of  health,  loss  of  flesh  and 
strength,  headache,  pallor,  indigestion,  with  periodic  attacks  of  nausea 
and  vomiting,  etc.;  or  swelling  of  the  eyelids,  feet,  or  ankles;  or  cloudiness 
and  lessened  amount  of  urine  may  attract  his  attention;  or  albuminuria 
may  be  detected  accidentally  (examination  for  life  insurance,  etc.). 
As  in  acute  nephritis,  the  characteristic  signs  consist  of  oedema  (which 
rarely  may  be  absent)  and  of  changes  in  the  urine.  At  first  the  oedema 
is  usually  slight,  but  it  varies  much  in  different  cases;  it  partakes  of  the 
characteristics  already  mentioned  in  connection  with  acute  nephritis, 
and  having  disappeared  is  likely  to  recur.  The  urine  is  lessened  in 
amount  (usually  300  to  700  c.c),  acid  in  reaction,  turbid,  of  varying 
color  (depending  upon  the  concentration  and  the  amount  of  contained 
blood),  of  increased  specific  gravity  (1018  to  1025),  contains  considerable 
albumin  (1  to  3  per  cent.;  ^  to  |  by  bulk  after  the  heat  and  acid  test; 
15  to  30  grams  in  the  twenty-four  hours);  the  excretion  of  solids  is 
deficient;  the  sediment  is  usually  abundant,  and  consists  of:  erythrocytes 
and  leukocytes;  epithelium  from  the  uriniferous  tubules,  the  renal 
pelvis,  and  the  bladder;  hyaline,  granular,  and  cellular  (epithelial, 
fatty,  leukocytic,  and  sometimes  erythrocytic)  casts;  waxy  casts  (in 
associated  amyloid  disease);  compound  granular  cells,  fat  droplets, 
detritus,  bacteria,  etc.  The  general  symptoms  are  much  like  those 
mentioned  in  connection  with  acute  nephritis.  Debility  and  anemia 
are  usually  marked,  the  anemia  seemingly  bearing  some  relationship 
to  the  rapidity  of  the  renal  lesions.  Chronic  uremic  (especially  nervous 
and  gastro-intestinal)  symptoms  are  common  and  persistent,  although 
subject  to  remissions  and  exacerbations;  acute  uremia  is  less  common 


782  DISEASES  OF  THE   URINARY  SYSTEM 

than  in  acute  nephritis  and  chronic  indurative  nephritis.  The  blood 
pressure  is  usually  increased,  and  hypertrophy  of  the  heart  and 
arteriosclerosis  often  supervene.  Albuminuric  neuroretinitis  is  quite 
common. 

Diagnosis. — The  diagnosis  is  suggested  by  the  history  of  the  case, 
pallor,  and  oedema,  but  it  must  be  based  upon  an  examination  of  the 
urine.  Much  fat  (fatty  casts,  free  fat  droplets,  etc.)  suggests  the  pale 
kidney;  blood,  the  red  or  mottled  kidney — an  acute  exacerbation. 
The  amyloid  kidney  is  suggested  by  the  etiological  factors  of  amyloid 
disease,  enlargement  of  the  liver  and  spleen,  relatively  slight  oedema, 
relatively  few  casts  (and  these  hyaline,  waxy,  and  granular),  little  or 
no  hypertrophy  of  the  heart,  and  the  absence  of  uremia  and  of  neuro- 
retinitis. The  advent  of  secondary  renal  contraction  leads  to  symp- 
toms that  will  be  mentioned  under  chronic  indurative  nephritis. 

Prognosis. — ^The  duration  of  the  disorder  commonly  varies  from 
several  months  to  two  years  or  thereabouts;  remissions  and  exacer- 
bations are  common;  some  patients  gradually  developing  a  secondarily 
contracted  kidney  may  survive  for  a  number  of  years.  The  outlook 
however,  is  always  gloomy,  since  recovery  is  extremely  rare.  The  prog- 
nosis is  the  worse  the  greater  the  degree  and  persistence  of  albuminuria, 
oedema,  and  uremic  manifestations,  the  less  the  excretion  of  urinary  solids, 
and  the  more  marked  the  cardiovascular  changes,  the  neuroretinitis,  and 
other  complications. 

Treatment. — The  treatment,  hygienic,  dietetic,  and  medicinal,  is 
similar  to  that  of  acute  nephritis.  From  time  to  time  a  strict  milk  diet 
is  valuable.  In  other  cases  with  marked  oedema  benefit  accrues  from 
a  salt-poor  diet;  at  all  events,  as  little  salt  as  possible  should  be  given. 
The  oedema  may  also  be  favorably  influenced  and  perhaps  the  ten- 
dency to  uremic  manifestations  lessened  in  some  cases  by  Basham's 
mixture;  or  by  Trousseau's  diuretic  wine: 

IJ — Powdered  digitalis 1  dram  4  0 

Powdered  squill ^  dram  2  0 

Juniper  berries 5  drams        20  0 

Potassium  acetate 2  drams  8  0 

White  wine 6  oimces  200  0 — M. 

S. — One  tablespoonful  (15  c.c.)  3  or  4  times  daily. 

or  by  Grainger  Stewart's  mixture: 

I^ — Potassium  acetate 2  drams  SjO 

Infusion  of  digitalis 3  ounces  100,0 

Infusion  of  scoparius 3  ounces  lOOJO — M. 

S. — One  tablespoonful  (15  c.c.)  3  or  4  times  a  day. 

Strontium  lactate,  diuretin,  theobromine,  sparteine,  etc.,  may  render 
service  from  time  to  time.  Renal  decapsulation  has  been  practised  with 
good  results  in  some  cases.  The  treatment  of  urtemia  is  mentioned  on 
page  778. 


CHRONIC  DIFFUSE  INDURATIVE  NEPHRITIS  783 


CHRONIC  DIFFUSE  INDURATIVE  NEPHRITIS. 

(Chronic  Interstitial  Nephritis;  Arteriosclerotic  Kidney;  Chronic  Bright's  Disease;) 
Cardiovascular-rena I  Disease . ) 

Etiology. — Chronic  diffuse  indurative  (or  interstitial)  nephritis  may  be 
primary  or  secondary.  The  primary  condition  occurs  especially  after 
the  fortieth  year,  but  it  may  occur  even  in  children.  It  is  twice  as  com- 
mon in  men  as  in  women.  The  disease  is  largely  the  result  of  the 
exigencies  of  modern  life :  the  hurry  and  the  cares,  the  worries  and  the 
anxieties  of  modern  life,  the  nervous  tension  and  the  mental  strain  in- 
separable from  large  undertakings,  heavy  financial  responsibilities,  and 
high  society.  An  irregular  mode  of  life,  overeating  of  rich  and  highly 
seasoned  food,  excessive  indulgence  in  alcohol,  and  insufficient  muscular 
exercise  tend  to  increase  blood  pressure  and  to  pervert  metabolism,  the 
products  of  which  being  eliminated  by,  irritate  and  cause  progressive 
deterioration  of,  the  chief  emunctories,  the  kidneys.  In  some  cases  the 
disease  is  directly  attributable  to  certain  autogenous  and  exogenous 
poisons,  such  as  alcohol,  gout  (gouty  kidney),  lead,  etc.;  and  sometimes 
the  disease  seems  more  or  less  related  etiologically  to  certain  infections, 
such  as  syphilis,  malaria,  etc.  The  causes  of  the  disease  in  general  are 
those  of  arteriosclerosis,  which  is  apparent  in  the  separation  of  a  special 
type  of  the  disease  (arteriosclerotic  kidney)  believed  to  originate  in  the 
bloodvessels  rather  than  in  the  kidneys;  in  another  class  of  cases  the 
lesions  appear  to  be  merely  those  of  advancing  age  (senile  kidney). 
The  phenomena  in  most  cases  are  correctly  interpreted  by  recognizing 
that  the  disease  is  not  a  disease  of  the  kidneys  alone,  perhaps  not  even 
primarily,  but  a  disease  of  the  cardiovascular  system  and  the  kidneys 
(cardiovascular-renal  disease).  Secondary  chronic  diffuse  indurative 
nephritis  develops,  as  a  rule,  secondarily  to  the  large  white  kidney;  its 
etiology,  therefore,  is  that  of  the  antecedent  condition. 

Pathology. — In  the  primary  (and  the  arteriosclerotic)  process  the 
kidney  is  much  reduced  in  size  (both  together  may  weigh  less  than 
50  grams);  the  capsule  is  thickened  and  markedly  adherent,  and  when 
removed  reveals  a  dark  reddish  brown,  markedly  granular  surface, 
containing,  as  a  rule,  a  variable  number  of  small  cysts;  the  organ  is  firm 
hard,  and  dense;  the  cortex  is  much  reduced  in  thickness  (to  2  mm.). 
The  arteries  show  more  or  less  sclerosis.  Microscopically,  the  con- 
spicuous change  is  an  overgrowth  of  cicatricial  fibrous  connective 
tissue  with  associated  (consecutive)  atrophic  and  degenerative  changes 
in  the  parenchyma.  The  fibrosis  is  especially  marked  about  Bow- 
man's capsule  and  the  small  arteries — whence  it  spreads  to  the  adjoining 
tissues;  the  Malpighian  bodies  ultimately  may  be  represented  by 
a  functionless,  roundish,  hyaline  mass,  and  the  small  arteries  may 
become  completely  fibrosed  and  their  lumens  occluded.  Obstruction 
and  occlusion  of  uriniferous  tubules  give  rise  to  the  formation  of 
small  cysts.     In  the  arteriosclerotic  kidney  the  lesions  are  believed  to 


784  DISEASES  OF  THE   URINARY  SYSTEM 

originate  in  the  bloodvessels,  but  it  is  often  quite  impossible  to  dis- 
tinguish between  the  two  forms  of  the  disease — if  there  really  be  two 
forms.  The  secondarily  contracted  kidney  is  sometimes  slightly  en- 
larged, sometimes  normal,  and  sometimes  somewhat  reduced  in  size; 
it  is  firm  and  hard;  its  capsule  is  thickened  and  adherent,  and  when 
removed  reveals  a  granular  pale  yellowish  or  mottled  yellowish-red 
surface,  containing  a  variable  number  of  small  cysts;  the  cortex  is 
thinned.  Microscopically,  to  the  lesions  of  the  large  white  kidney  are 
added  overgrowth  and  cicatrization  of  connective  tissue,  more  or  less 
fibrosis  and  obliteration  of  the  glomeruli,  arteriosclerosis  and  obliter- 
ating endarteritis,  occluded  and  distended  uriniferous  tubules  (cysts), 
etc.  In  addition,  in  all  forms  of  chronic  indurative  nephritis  there 
is  more  or  less  widespread  arteriosclerosis,  and  hypertrophy,  and  later, 
dilatation  of  the  heart  (page  437) ;  and  perhaps  fibrosis  elsewhere  in  the 
body. 

Symptoms. — ^The  symptoms  of  primary  chronic  indurative  nephritis 
develop  as  insidiously  as  do  the  lesions  in  the  kidneys  and  the  cardio- 
vascular system.  The  disease  may  exist  for  years  entirely  devoid  of 
symptoms;  it  may  be  detected  accidentally  in  a  routine  examination 
of  the  urine  for  life  insurance  or  other  reason;  or  it  may  give  rise  to  an 
extremely  variable  set  of  initial  symptoms  that  are  likely  to  be  attrib- 
uted to  some  organ  other  than  the  kidneys.  Thus,  the  patient  may 
present  himself  to  his  physician  with  the  idea  that  he  is  suffering  with 
diabetes  on  account  of  the  large  amount  of  urine  that  he  voids;  or  he 
may  complain  of  dimness  of  vision,  the  consequence  of  albuminuric 
neuroretinitis;  or  of  one  of  the  many  manifestations  of  chronic  uremia, 
such  as  dyspnoea  or  asthma;  or  of  gastro-intestinal  derangements, 
such  as  gastric  catarrh,  gastric  hemorrhage,  or  diarrhoea;  or  of  headache, 
hemicrania,  tinnitus  aurium,  vertigo,  neurasthenia,  pains  in  the  muscles 
or  joints,  or  eczema;  or  palpitation  of  the  heart  and  precordial  distress; 
or,  the  patient  in  apparently  good  health,  may  suddenly  develop  a  severe 
and  even  fatal  attack  of  cardiac  failure,  or  he  may  pass  into  uremic 
coma  or  convulsions,  or  he  may  suffer  an  apoplexy  and  die. 

Variable  as  are  the  modes  of  onset,  the  diagnosis  of  the  disease  depends 
upon  an  examination  of  the  urine  and  of  the  cardiovascular  system.  The 
urine  is  increased  in  amount — 1800  to  4000  c.c.  daily — ^whence  the  common 
complaint  of  frequent  micturition  and  sometimes  of  increased  thirst; 
it  is  acid  in  reaction,  pale  in  color,  and  of  low  specific  gravity  (1002  to 
1015);  it  contains  a  slight  amount  of  albumin — usually  only  a  trace, 
and  at  times  no  albumin  at  all.  Albumin  may  be  absent  for  days  and 
even  weeks  at  a  time;  it  may  be  missed  in  the  early  morning  urine  and 
be  present  in  that  voided  later  in  the  day;  and  it  may  be  present  only 
after  exercise,  emotional  and  other  excitement,  or  after  eating,  especially 
after  eating  proteins.  The  urine  deposits  a  slight  flocculent  sediment 
that  contains  a  few,  sometimes  a  very  few  (often  very  narrow),  hyaline 
and  pale  granular  casts,  and  a  few  epithelial  cells,  mostly  from  the 
bladder.    The  solids  of  the  urine  are  usually  diminished. 


.  CHRONIC  DIFFUSE  INDURATIVE  NEPHRITIS  785 

The  characteristic  cardiovascular  signs  consist  of  increased  blood 
pressure  (an  early  and  valuable  sign),  arteriosclerosis,  accentuation 
of  the  aortic  second  sound,  and  hypertrophy  of  the  heart,  especially 
the  left  ventricle  (sometimes  obscured  by  co-existing  emphysema). 
Although  these  cardiovascular  signs  may  be  found  in  all  forms  of  Bright's 
disease  (but  not  in  all  cases),  in  none  of  the  forms  do  they  so  dominate 
the  clinical  picture  as  in  primary  chronic  interstitial  nephritis.  So  long 
as  the  nutrition  of  the  heart  is  well  maintained  there  may  be  no  symp- 
toms, although  for  months  or  years  dyspnoea  and  palpitation  of  the  heart 
may  be  provoked  by  exertion  or  excitement.  As  the  nutrition  of  the 
heart  begins  to  lag  behind  its  enlargement,  degeneration  and  dilatation 
ensue  and  symptoms  of  embarrassed  circulation  become  ascendent — 
cardiac  asthma,  congestion  and  oedema  of  the  lungs,  bronchitis,  gastro- 
intestinal disturbances,  generalized  oedema  and  effusions  within  the 
serous  cavities,  and  alterations  in  the  urine:  it  lessens  considerably  in 
amount  and  becomes  of  high  color  and  increased  specific  gravity; 
albumin  increases  in  amount  and  casts  become  more  numerous;  dark 
granular,  epithelial,  and  even  blood  casts  and  free  erythrocytes  may  be 
encountered.  The  symptoms  referable  to  the  heart  and  lungs,  at  first 
transitory  and  nocturnal,  become  permanent;  the  blood  pressure  lessens; 
the  aortic  second  sound  becomes  less  accentuated;  with  embarrassment 
of  the  right  heart  the  pulmonary  second  sound  becomes  at  first  accent- 
uated, and  later  fails;  signs  of  dilatation,  and  gallop  rhythm,  always  of 
serious  moment,  supervene;  and  if  relief  is  not  afforded,  death  ensues 
with  cardiac  failure  or  uremia,  or  both,  dominating  the  final  scene. 

In  some  cases  the  first  suggestive  symptom  may  be  oedema  of  the  lungs 
or  of  the  larynx;  the  dyspnoea  due  to  one  or  both  of  these  may  be 
augmented  by  hydrothorax;  Cheyne-Stokes  breathing  may  ensue,  and 
in  coma  the  patient  may  die.  Or  the  first  symptom  may  be  violent  head- 
ache— due  either  to  uremia,  cerebral  congestion,  or  cerebral  anemia. 
The  headaches  are  occasionally  relieved  by  epistaxis,  which  is  some- 
times frequent  and  sometimes  severe.  Drowsiness  and  other  nervous 
manifestations  of  chronic  uremia  may  be  associated  with  the  headache, 
and  frequently  presage  the  onset  of  severe,  acute,  and  fatal  uremia. 
In  some  cases  psychoses  are  prominent;  in  other  cases  neuralgias  or 
hemorrhages  into  the  brain  substance  or  into  the  meninges  may  occur. 
Hemorrhages  into  other  structures,  especially  the  stomach,  intestine, 
skin,  conjunctivae,  lungs,  etc.,  have  been  observed.  Severe  and  un- 
controllable vomiting  and  severe  and  exhausting  diarrhoea  are  not 
uncommon.  In  other  cases  the  disease  is  manifest  by  intolerable  itching, 
formication,  numbness  of  the  extremities;  in  still  other  cases,  by  urticaria. 
In  the  late  stages  more  or  less  widespread  erythematous,  or  bullous,  or 
desquamative  skin  lesions  may  occur.  Neuroretinitis  is  the  most 
important  symptom  on  the  part  of  the  special  senses;  at  times  tinnitus 
aurium,  possibly  associated  with  dizziness,  occurs;  less  frequently  deaf- 
ness or  diplopia  ensues. 

Secondary   chronic    interstitial    nephritis    (the   small   white   kidney) 
50 


786  DISEASES  OF  THE   URINARY  SYSTEM 

is  usually  only  with  difficulty  differentiated  from  its  antecedent  stage 
(the  large  white  kidney).  Presumptive  evidence  of  secondary  contrac- 
tion of  the  kidney,  however,  is  afforded  by  long  duration  of  the  disease 
(more  than  a  year),  lessening  of  dropsy,  lessening  of  albuminuria, 
increase  in  the  daily  excretion  of  the  urine,  and  decrease  in  the  specific 
gravity,  and  the  development  and  progression  of  the  cardiovascular 
signs  of  chronic  interstitial  nephritis. 

Diagnosis. — As  long  as  cardiac  compensation  is  maintained,  the 
diagnosis  of  chronic  indurative  nephritis  is  evident  from  the  results  of 
an  inquiry  into  the  antecedents  of  the  patient,  the  special  etiological 
factors  in  the  case,  the  course  of  the  disease,  the  different  clinical  manifes- 
tations, and  an  examination  of  the  urine  and  of  the  cardiovascular 
apparatus.  The  diagnostic  importance  of  the  cardiovascular  alterations 
cannot  be  overestimated.  They  are  among  the  earliest  clinical 
manifestations  of  the  disease,  and  they  may  be  detected  even  in  the 
absence  of  positive  signs  of  kidney  disease  on  the  part  of  the  urine. 

It  is  usually  a  matter  of  extreme  difficulty  to  distinguish  clinically 
between  primary  chronic  interstitial  nephritis  and  the  arteriosclerotic 
kidney;  in  some  cases  it  is  impossible,  in  most  cases  it  is  unnecessary. 
Usually  the  arteriosclerotic  kidney  exists  for  a  long  time  without  albu- 
minuria, or  with  but  the  slightest  trace  of  albumin  in  the  urine.  The 
disease  may  be  suspected  in  elderly  persons,  with  hypertrophy  of  the 
heart,  increased  arterial  tension,  and  marked  atheroma  of  the  superficial 
arteries.  Occurring  as  a  manifestation  of  senility,  it  is  usually  of  relative 
unimportance  as  contrasted  with  the  co-existing  emphysema,  dementia, 
marasmus,  etc. 

When  the  heart  begins  to  fail  in  chronic  interstitial  nephritis,  diag- 
nostic difficulties  arise.  The  clinical  picture  in  these  cases  much  re- 
sembles that  of  a  disorder  primarily  cardiac  and  secondarily  renal.  The 
presence  of  murmurs  is  not  conclusive  evidence,  since  they  may  be  due 
to  dilatation  as  well  as  to  valvular  disease.  Diastolic  murmurs,  however, 
suggest  a  primary  cardiac  disorder,  whereas  albuminuric  neuroretinitis 
suggests  a  primary  renal  disorder.  In  some  cases  the  diagnosis,  for  a  time 
at  least,  is  impossible;  in  other  cases  it  may  be  made  by  a  careful  analysis 
and  balancing  of  all  the  features  of  the  case,  by  a  knowledge  of  the  past 
history  of  the  patient,  and  by  the  results  of  administering  digitalis  and 
other  heart  tonics.  Following  the  administration  of  digitalis,  should  the 
patient  improve  materially,  the  urine  increase  in  amount,  and  albumin 
and  casts  finally  disappear  from  the  urine,  the  condition  has  been  defi- 
nitely determined  to  have  been  primarily  cardiac  with  secondary  renal 
congestion.  If,  however,  with  improvement  in  the  condition  of  the  heart, 
albumin  and  casts  do  not  disappear  from  the  urine,  one  may  be  confident 
of  the  existence  of  nephritis,  a  conviction  that  may  be  confirmed  by 
examining  the  cardiovascular  apparatus  now  that  compensation  has 
been  restored.  It  is  scarcely  likely  that  chronic  indurative  nephritis 
will  be  confounded  with  the  so-called  functional,  physiological,  cyclic, 
intermittent,  paroxysmal,  or  adolescent  albuminuria. 


CHRONIC  DIFFUSE  INDURATIVE  NEPHRITIS  787 

Prognosis. — In  general  the  prognosis  depends  upon  the  integrity  of 
the  cardiovascular  apparatus.  The  disease  may  run  a  course  entirely 
latent  and  lead  to  sudden  death  by  apoplexy,  acute  uremia,  etc.  Ordi- 
narily, however,  the  course  is  from  ten  to  twenty  years,  depending  upon 
the  habits  and  mode  of  life.  When  the  circulation  becomes  embarrassed 
the  prognosis  is  bad;  lessening  in  the  amount  of  urine,  especially  if 
associated  with  headache,  often  presages  the  speedy  onset  of  acute  uremia. 

Treatment. — In  the  early  stages  of  the  disease,  appreciating  our  in- 
ability to  cure  our  patient,  we  should  be  alert  to  the  dangers  that  threaten 
him  (rupture  of  small  arteries,  especially  of  the  brain,  uremia,  cardiac 
failure).  He  must  be  cautioned  not  to  expose  himself  to  the  inclemencies 
of  the  weather,  to  avoid  all  excessive  muscular  exercise  and  all  mental 
worry;  he  must  have  his  bowels  open  at  least  once  daily  (alkaline  mineral 
waters,  saline  cathartics,  occasional  blue  mass  pill,  etc.);  and  he  must 
favor  the  action  of  the  skin  so  as  to  relieve  the  subnormal  cardiovascular- 
renal  system;  warm  or  hot  baths  are  serviceable,  but  they  are  contra- 
indicated  if  they  cause  unpleasant  throbbings  (increasing  blood  pressure). 
The  diet  is  of  the  utmost  importance,  the  duration  of  life  probably 
depending  more  upon  discretion  in  eating  and  drinking  than  upon  any 
other  factor.  In  many  cases  an  exclusive  milk  diet  for  a  time  (four  to 
six  weeks)  is  desirable;  and  it  may  be  repeated  from  time  to  time.  In 
general  the  diet  should  be  sufficiently  varied  to  be  attractive,  it  should 
be  free  from  irritating  qualities  and  readily  assimilable,  and  the  nitrog- 
enous constituents  should  be  relatively  reduced.  The  meat  allowance 
should  not  exceed  100  grams  daily;  a  diet  of  ample  fuel  value  should  be 
constructed  by  adding  a  sufficiency  of  fats  and  carbohydrates;  an  excess  of 
meat  is  said  to  favor  the  development  of  uremia;  red  and  white  meats 
are  of  equal  value,  and  may  be  allowed  in  accordance  with  the  patient's 
desires,  x^s  a  rule,  alcohol  should  be  prohibited,  although  in  some  cases 
a  little  of  the  lighter  wines  appears  to  do  no  harm.  In  many  cases  the 
foregoing  produces  not  only  amelioration  of  the  symptoms,  but  perhaps 
also  arrest  of  the  lesions;  if  so,  other  measures  are  not  required. 

When  the  circulation  becomes  embarrassed  medication  is  called  for — 
the  most  serviceable  remedies  being  nitroglycerin  and  caffeine.  Nitro- 
glycerin lowers  the  arterial  tension  and  enables  the  heart  still  capable 
of  performing  its  work  to  do  so  unhampered  by  excessive  resistance  in 
the  arterial  tree;  it  is  said  also  to  favor  reduction  in  the  amount  of  albu- 
min excreted,  but  this  action  is  doubtful  and  certainly  immaterial. 
This  dose  may  be  increased  until  the  desired  result  is  obtained.  It  is 
not  necessary  that  the  drug  be  given  to  the  extent  of  producing  unpleas- 
ant symptoms;  sufficient  reduction  in  the  arterial  tension  is  usually 
produced  without  this.  Nor  is  great  reduction  in  the  arterial  tension 
desirable;  indeed,  it  is  directly  contra-indicated,  since  a  reduction 
even  to  that  of  the  normal  tension  is  fraught  with  danger  of  serous 
effusions,  and  of  uremia  (on  account  of  reduction  in  the  amount  of 
urine  excreted).  The  nitroglycerin  should  be  given  for  four  to 
six  weeks  and  then  discontinued  for  a  week  or  ten  days,  unless  the 


788  DISEASES  OF  THE   URINARY  SYSTEM 

condition  of  the  patient  should  render  an  earlier  return  to  its  use  neces- 
sary. The  nitrite  of  potassium  or  of  sodium  or  erythrol  tetranitrate 
may  be  substituted  for  the  nitroglycerin,  but  they  are  less  efficacious. 
Inasmuch  as  the  nitrites  interfere  somewhat  with  the  oxygenating  powers 
of  the  blood,  their  continuous  administration  should  not  be  persisted  in  too 
long.  Iodide  of  potassium  or  of  sodium  in  small  doses,  mercuric  bichlor- 
ide, and  chloride  of  gold  and  sodium  are  still  advocated;  in  some  cases 
good  results  appear  to  attend  their  prolonged  use.  It  is  difficult,  how- 
ever, to  estimate  the  amount  of  good  that  with  justice  may  be  attributed 
to  their  use.  In  the  absence  of  serious  cardiac  debility,  cardiac  stimu- 
lants, such  as  digitalis  and  strophanthus,  should  not  be  given.  Nor 
is  the  routine  administration  of  iron  to  be  countenanced.  Anemia  is 
rarely  marked,  and  any  virtues  that  iron  may  possess  are  outweighed 
by  certain  ill  effects,  such  as  its  tendency  to  constipate,  to  produce  head- 
aches, etc.  However,  should  anemia  become  marked,  iron  may  be  given 
in  small  doses.  Quinine,  strychnine,  and  arsenic  are  often  of  service 
in  this  stage  of  the  disease,  as  well  as  earlier.  Renal  decapsulation  is 
sometimes  of  service. 

When  marked  cardiac  debility  and  manifest  failure  of  compensation 
develop  (generalized  oedema,  effusions  in  the  several  serous  cavities,  dimi- 
nution in  the  amount  of  urine,  increase  in  the  amount  of  albumin,  etc.), 
digitalis  and  other  cardiac  stimulants  should  be  given.  In  general, 
the  treatment  of  this  stage  of  the  disease  does  not  differ  from  that  already 
recommended  in  connection  with  acute  and  chronic  non-indurative 
nephritis,  and  from  that  commonly  practised  in  cases  of  lack  of  cardiac 
compensation.  Impending  uremia,  manifest  by  headache,  restlessness, 
foul  breath,  coated  tongue,  vertigo,  etc.,  may  be  warded  off  by  nitro- 
glycerin and  caffeine,  saline  cathartics,  alkaline  diuretics,  large  amounts 
of  water,  hydrotherapeutic  measures,  and  restriction  of  the  diet  to  milk. 
In  some  cases  digitalis  is  urgently  called  for.  The  treatment  of  acute 
uremia  developing  in  the  course  of  chronic  indurative  nephritis  does 
not  diflfer  from  that  already  mentioned  (page  778). 


CYSTITIS;  URETERITIS;  PYELITIS;  PYELONEPHRITIS;  PYELO- 

NEPHROSIS. 

Etiology. — Inflammation  of  the  bladder,  the  ureter,  and  the  renal 
pelvis  may  occur  singly  or  in  combination ;  the  inflammatory  phenomena 
may  ascend  from  a  part  of  the  urinary  tract  low  down  to  that  high  up, 
or  they  may  descend;  and  they  may  be  acute  or  chronic.  Although  many 
bacteria  have  been  described  in  these  urinary  infections,  the  most 
important  are  the  typhoid  and  colon  bacilli  (acute  and  chronic  infec- 
tions), gonococci,  staphylococci,  streptococci,  and  pneumococci  (acute 
infections),  the  tubercle  bacillus  (chronic  infections),  and  perhaps  also 
certain  anaerobic  organisms.  Ascending  (urogenous)  infections  of 
the  bladder  are  usually  preceded  by  urethritis  (or  vaginitis),  commonly 


CYSTITIS  789 

ofonococcic:  thev  mav  result  from  the  introduction  into  the  bladder  of 
infected  foreign  bodies  (catheters,  etc.);  or  they  may  be  due  to  the  transit 
of  infectious  agents  (commonly  the  colon  bacilli  or  the  pyococci)  from 
the  rectum  or  other  pelvic  viscus  directly  to  the  bladder  (transparietal 
route).  Thence  the  ureters,  the  renal  pelves,  and  the  kidneys  themselves 
may  become  infected,  commonly  by  progressive  ascending  infection  of 
the  mucosa;  rarely  by  the  transit  of  the  infectious  agent  through  the 
blood  stream  or  the  lymph  stream.  Descending  infections — the  con- 
sequence of  the  elimination  of  bacteria  by  the  kidneys  (therefore  hema- 
togenous infections) — occur  under  circumstances  similar  to  those  that 
induce  suppurative  nephritis  (page  779);  they  are  usually  due  to  the 
typhoid  bacillus,  the  colon  bacillus,  proteus  vulgaris,  the  pyococci,  etc. 
Pyelitis  may  be  the  initial  lesion,  but  in  some  cases  the  bacteria  pass 
through,  apparently  without  injuring,  the  pelvis,  and  may  first  set  up  a 
cystitis.  As  is  well  known,  the  mucosa  of  the  urinary  tract  is  remarkably 
resistant  to  the  influence  of  bacteria  eliminated  with  the  urine.  Appar- 
ently healthy  kidneys  may  excrete  bacteria  (as  in  many  infections, 
notably  typhoid  fever),  and  these  may  be  discharged  from  the  body, 
without  damage  to  the  urinary  tract.  Certain  predisposing  factors 
seem  operative  in  many  cases,  and  may  determine  the  primary  local 
infection — such  as  trauma,  arteriosclerosis,  diabetes,  a  calculus  (in  the 
renal  pelvis  or  the  bladder),  enlarged  prostate,  urethral  stricture, 
ammoniacal  decomposition  of  the  urine,  a  pelvic  tumor,  a  pregnant 
uterus,  the  excretion  of  irritating  drugs,  etc. 

Pathology. — The  lesions  may  be  catarrhal,  suppurative,  or  ulcerative; 
unilateral  or  bilateral;  and  acute  or  chronic.  In  the  catarrhal  process 
there  is  swelling,  oedema,  and  congestion  of  the  mucosa,  with  the  exces- 
sive formation  of  mucus;  in  aggravated  cases  considerable  mucopus 
or  almost  pure  pus  is  formed,  and  there  is  more  or  less  desquamation 
and  superficial  erosion  of  the  epithelium  and  foci  of  hemorrhage;  or 
more  or  less  widespread  and  deep  ulceration  may  occur.  In  the  chronic 
cases  there  is,  in  addition,  more  or  less  thickening  and  pigmentation. 
Rarely  fibrinous  exudations  or  gangrene  ensue.  There  is,  as  a  rule,  more 
or  less  decomposition  of  the  urine  with  the  precipitation  of  urates  and 
phosphates.  Wlien  the  infection  extends  from  the  renal  pelvis  to  the 
kidney  substance  (urogenous  pyelonephritis)  yellowish  purulent  streaks 
are  found  extending  from  the  papillse  into  the  medulla  and  the  cortex, 
and  small  miliary  abscess  throughout  the  kidney,  but  most  numerous 
in  the  cortex  just  beneath  the  surface  and  arranged  often  in  groups. 
In  the  event  of  obstruction  in  the  renal  pelvis,  the  ureter,  bladder, 
or  urethra,  with  consequent  increased  intrapelvic  (renal)  pressure,  the 
pelvis  and  calices  become  distended,  the  renal  tissue  more  or  less  de- 
stroyed, and  the  kidney  ultimately  converted  into  an  intercommuni- 
cating, many-chambered  pus  sac  (pyonephrosis)  lined  by  the  remains 
of  the  pelvic  mucosa;  should  this  become  very  large,  veiy  little  kidney 
tissue  may  be  demonstrable  (degeneration,  atrophy,  and  replacement 
by  connective  tissue). 


790  DISEASES  OF  THE  URINARY  SYSTEM 

Symptoms. — ^The  symptoms  vary  with  the  site  and  progression  of  the 
lesions;  in  some  cases,  especially  in  children,  there  may  be  no  symptoms 
whatever  referable  to  the  urinary  tract. 

Acute  cystitis,  as  a  rule,  is  manifested  by  pain  in  the  region  of  the 
bladder  developing  spontaneously,  augmented  by  urination,  and  radiat- 
ing to  the  urethra;  strangury  and  vesical  tenesmus;  and  local  tender- 
ness. Occasionally,  in  consequence  of  sphincter  spasm  or  urethral 
obstruction  by  a  plug  of  mucus,  there  may  be  retention  (ischuria). 
The  general  phenomena  consist  of  fever,  perhaps  chill  or  chilliness 
(at  the  beginnmg  of  acute  cases),  leukocytosis,  headache,  malaise, 
etc.  In  subacute  and  chronic  cystitis  the  local  and  general  phenomena 
are  less  marked  and  may  be  quite  in  abeyance.  The  urine  when  voided 
may  be  acid  or  alkaline  depending  upon  the  infecting  organism:  acid  in 
colon-bacillus  infections,  and  alkaline  in  infections  by  urea-decomposing 
organisms.  Furthermore,  the  urine  contains  more  or  less  mucus,  pus, 
erythrocytes,  albumin  (proportionate  to  the  pus  and  blood),  bladder 
epithelium,  perhaps  particles  of  necrotic  bladder  mucosa,  many  bacteria, 
and  in  the  event  of  alkaline  decomposition  (urea-decomposing  organisms), 
triple  phosphates,  ammonium  urate,  etc.  Cystoscopic  inspection  of 
the  bladder  reveals  the  inflammatory  lesions;  in  the  chronic  process — 
often  tuberculous  ulcers.  The  thickening  that  develops  in  chronic 
cases  may  be  palpable — above  the  pubes;  or  bimanually — vaginal 
(or  rectal)  and  suprapubic.  Acute  cystitis  lasts  for  several  days  to  several 
weeks,  and  may  then  subside  entirely,  or  go  on  to  the  chronic  stage; 
this  may  continue  for  months  or  years,  and  ultimately  lead  to  ascending 
infection  of  the  urinary  tract. 

Ureteritis  is  rarely  if  ever  an  independent  affection;  usually  it  is  part 
of,  or  associated  with,  cystitis  and  pyelitis.  Local  pain,  tenderness, 
and  palpable  thickness  along  the  course  of  the  ureter  can  sometimes  be 
made  out,  and  cystoscopic  examination  of  the  bladder  often  reveals 
excessive  inflammatory  phenomena  at  the  mouths  of,  and  perhaps 
some  distance  into,  the  ureters. 

Pyelitis  and  pyelonephritis  are  manifested,  as  a  rule,  by  impairment 
of  the  general  health,  by  more  or  less  obtrusive  symptoms  of  septi- 
copyemia, and  by  certain  local  signs.  In  the  milder  cases  (subacute 
or  chronic  urogenous  pyelitis  or  pyelonephritis)  fever  may  be  mild 
(99°  to  100°)  but  more  or  less  continuous;  there  may  be  a  tendency  to 
ready  sweating;  slight  leukocytosis  is  likely  to  be  present;  anemia  de- 
velops and  progresses.  In  some  cases,  suddenly  chills,  fever,  and  sweats 
supervene  and  the  leukocytosis  increases;  the  fever  may  reach  a  high 
grade  (104°  or  more),  continue  for  several  days  or  a  week  or  more,  and 
gradually  subside  to  the  previous  grade.  At  varying  intervals,  such  an 
attack  may  recur  (recurring  t}^e).  In  addition  there  may  be  local  pain 
(often  spontaneous  and  colicky)  and  tenderness  in  the  region  of  the  kid- 
ney (or  kidneys),  frequent  micturition,  and  in  the  event  of  pyelonephrosis 
a  variable-sized,  tender,  fluctuating  mass  in  the  region  of  the  kidney. 


CYSTITIS  791 

The  urine  contains  mucus,  pus,  erythrocytes,  albumin  (proportionate 
to  the  pus  and  blood),  fibrinous  plugs,  caudate  epithelium  from  the 
renal  pelvis  (not  always  recognizable)  and  other  epithelium,  and  crystals, 
often  corresponding  to  a  calculus  in  the  renal  pelvis,  but  otherwise 
varying  with  the  alkalinity  or  acidity  of  the  urine.  The  amount  of  urine 
varies  much  in  some  cases,  being  often  reduced  and  then  suddenly 
increased — associated  with  release  of  an  obstruction  and  discharge 
of  accumulated  urine,  lessening  in  size  of  the  palpable  fluctuating 
tumor,  and  subsidence  of  the  general  manifestations  of  toxemia.  In 
chronic  cases  there  may  be  presistent  polyuria  (usually  due  to  secondary 
chronic  interstitial  nephritis). 

Diagnosis. — ^The  diagnosis  of  infection  of  the  urinary  tract  is  easy 
in  the  great  majority  of  cases;  but  some  difficulty  may  be  experienced 
in  determining  the  seat  and  extent.  Cystitis  is  readily  recognized  by 
vesical  pain  and  tenesmus,  strangury,  and  the  condition  of  the  urine; 
and  outspoken  pyelitis  by  pyuria  (especially  intermittent  pyuria),  pain, 
tenderness,  and  a  fluctuating  mass  in  the  region  of  the  kidney.  In  many 
cases,  however,  these  are  not  obtrusive,  and  the  diagnosis  depends 
upon  the  differential  interpretation  of  pyuria;  this  is  especially  the  case 
in  marked  toxemias  or  infections  which  are  common  in  children,  during 
pregnancy  and  the  puerperium,  etc. — whence  the  importance  of  examin- 
ing the  urine  in  all  obscure  febrile  conditions,  particularly  those  without 
any  localizing  symptoms.  In  some  cases,  special  importance  attaches 
to  an  antecedent  enlarged  prostate,  urethral  stricture,  etc.  Pressure 
on  the  kidney  and  massage  in  the  direction  of  the  ureter  may  lead  to  the 
discharge  of  pus  into  the  bladder — which  may  be  observed  by  means 
of  a  cystoscope.  Effort  should  always  be  made  to  determine  the  nature 
of  the  infection;  the  tubercle  bacilli  may  be  recovered  in  many  cases 
not  thought  to  be  tuberculous.  More  albuminuria  than  can  be  explained 
by  the  pus  and  blood  suggests  concurrent  nephritis. 

Prognosis. — The  prognosis  depends  upon  the  nature  of  the  infection — 
tuberculous  or  non-tuberculous,  and  whether  simple  or  associated  with 
a  calculus.  In  acute  cases  the  prognosis,  as  a  rule,  is  good;  chronic 
cases  may  last  for  years. 

Treatment. — Efforts  should  be  made  to  prevent  the  infection — by 
the  use  of  clean  catheters,  etc. ;  by  prompt  and  efficient  treatment  of 
gonorrhoea,  vaginitis,  cystitis,  etc;  and  when  the  urinary  tract  is  damaged, 
by  avoiding  irritating  drugs  that  must  be  eliminated  by  the  kidney; 
etc.  The  developed  infection  should  be  met  by  l)laiul  fluids  (milk,  water, 
mineral  waters)  to  flush  the  urinary  tract,  and  urinary  antiseptics,  such 
as  hexamethylenamin,  salol,  sandal  oil,  etc.  In  urinary  acidity  (colon 
bacillus  infections),  potassium  acetate  and  citrate  and  sodium  benzoate 
are  of  much  service.  Autogenous  vaccines  corresponding  to  tlie  infecting 
organism  are  of  much  value  in  many,  especially,  protracted  cases. 
Local  warm  applications  afford  relief  in  cystitis.  In  protracted  cystitis 
irrigations  with  mild  antiseptics  should  be  used;  or  persisting  ulcerations 


792  DISEASES  OF  THE   URINARY  SYSTEM 

(usually  tuberculous)  may  require  the  local  application  (through  the 
cystoscope)  of  lactic  acid,  etc.  Urethral  strictures,  enlarged  prostate, 
vesical  and  renal  calculi,  etc. ,  should  be  treated  surgically.  Pyelonephritis 
and  pyonephrosis  also  usually  require  surgical  intervention. 


PERINEPHRITIS  AND  PARANEPHRITIS. 

(Periiiephritic  Abscess.) 

Etiology. — Inflammation  of  the  fil^rous  capsule  of  the  kidney  (peri- 
nephritis) and  of  the  surrounding  fibro-adipose  tissue  (paranephritis) 
may  be  due  to  trauma;  to  extension  of  inflammation  from  the  kidney 
(pyelitis,  pyelonephritis,  pyelonephrosis),  from  the  intestine  (especially 
appendicitis  and  ulcerative  processes  involving  the  colon),  from  the 
vertebrae  (tuberculosis),  pleura  (empyema),  etc.;  and  occasionally 
it  follows  infections,  septicopyemia,  etc.,  the  process  being  embolic. 
The  disorder  is  most  common  in  male  adults. 

Pathology.- — In  some  cases  the  lesions  are  those  of  more  or  less  vrell- 
marked  inflammation  with  considerable  inflammatory  oedema;  the 
process  may  subside.  Usually,  however,  the  lesions  progress  to  suppu- 
ration, the  kidney  being  more  or  less  surrounded  with  pus,  sometimes 
embedded  in  a  large  abscess  cavity;  the  pus  may  have  a  fecal  odor 
(intestinal  origin).  The  abscess  may  burrow  downward  along  the 
psoas  muscle  and  appear  in  the  groin,  or  upward  into  the  pleura  and 
lungs,  and  perhaps  be  evacuated  through  a  bronchus ;  or  it  may  perforate 
the  intestine,  the  peritoneum,  the  vagina,  etc.  Rarely  there  is  a  chronic 
indurative  perinephritis,  thickening  and  induration  of  the  perirenal 
fibro-adipose  tissue,  and  compression  of  the  kidney  (which  produces 
no  significant  symptoms). 

Symptoms. — In  the  absence  of  suppuration  there  are  no  unequivocal 
symptoms.  The  phenomena  of  abscess  formation  may  be  insidious 
or  abrupt  in  onset.  In  the  course  of  one  of  the  aforementioned  etiological 
disorders,  deep-seated  pain  develops  in  the  renal  region;  the  pain  may 
radiate  to  the  thigh  or  the  testicle  (which  may  be  retracted),  or  be  referred 
to  or  near  the  hip-joint;  the  thigh  may  be  favored  or  flexed  (irritation 
of  the  psoas  muscle),  and  the  spine  may  be  immobile  from  contraction 
of  the  erector  spinee  and  other  muscles  of  the  affected  side.  On  palpa- 
tion there  may  be  swelling  of  the  lumbar  region,  with  perhaps  oedema 
of  the  skin  (especially  significant);  or  distinct  deep-seated  fluctuation 
may  be  elicited.  The  general  signs  of  suppuration,  chills,  fever,  sweats, 
and  leukocytosis,  are  usually  present;  the  urine  may  be  clear,  or  reveal 
the  evidence  of  a  concomitant  (antecedent  or  sequential)  pyelitis  or 
pyelonephritis. 

Diagnosis. — ^The  diagnosis,  as  a  rule,  is  comparatively  easy — ^by  attention 
to  the  antecedent  etiological  factors  and  the  evidences  of  suppuration. 

Prognosis. — ^The  prognosis  depends  upon  the  primary  cause,  the 
amount  of  damage  done,  and  the  amenability  of  the  condition  to  opera- 


HYDRONEPHROSIS  793 

tion.  Cure  may  be  effected  in  some  cases  by  prompt  evacuation  of  the 
abscess,  but  in  some  cases  prolonged  suppuration  and  consecutive 
amyloid  disease,  etc.,  ensue. 

Treatment. — The  treatment  is  essentially  surgical. 

HYDRONEPHROSIS. 

Etiology. — Hydronephrosis,  a  saccular  dilatation  of  the  renal  pelvis 
and  calices,  associated  with  the  accumulation  of  a  urinary  fluid,  may 
be  congenital  or  acquired,  and  unilateral  or  bilateral.  The  congenital 
cases  (bilateral  in  65  per  cent,  of  the  cases)  are  due  to  atresia  of  the  ureter 
near  the  renopelvic  junction,  to  congenitally  displaced  kidneys,  or  to 
anomalous  renal  bloodvessels  compressing  the  upper  part  of  the  ureter. 
The  acquired  cases  are  due  to  traumatic  and  inflammatory  strictures ; 
partial  or  complete  obstruction  by  a  calculus,  or  fibrinous,  or  other  plug; 
to  displacement  of  the  kidney,  and  angulation  or  twisting  of  the  ureter; 
or  to  tumors  or  other  lesions  compressing  the  pelvis  or  the  ureter  from 
without,  or  the  ureter  at  its  entrance  into  the  bladder. 

Pathology. — ^The  saccular  distention  varies  considerably  in  different 
cases,  and  it  may  be  complete  or  incomplete,  or  intermittent.  The  larger 
distentions  occur  when  the  obstruction  is  of  slow  development,  incom- 
plete, and  intermittent  rather  than  when  rapid  and  complete;  sudden 
and  considerable  intrapelvic  pressure  soon  overcomes  the  renal  blood 
pressure  and  inhibits  the  excretion  of  urine,  whereas  slow  increase  and 
intermittent  reduction  of  the  intrapelvic  pressure  permits  of  more 
abundant  secretion  of  urine.  The  kidney  and  the  pelvis  and  perhaps 
the  ureter  are  more  or  less  enlarged,  irregular,  saccular;  the  renal  papillae 
are  flattened,  the  calices  distended,  the  renal  tissue  atrophic  and 
sclerosed.  In  many  cases  the  kidney  and  the  pelvis  form  a  distinct 
cystic  tumor  with  more  or  less  thinned  walls. 

Symptoms. — The  symptoms  vary  with  the  antecedent  and  associated 
conditions;  in  some  cases  they  are  inconsequential.  In  uncomplicated 
cases,  such  as  are  common  in  young  adults,  the  symptoms  consist  of 
periodic  attacks  of  sudden  severe  abdominal  pain  usually  localized  to 
the  region  of  the  kidney  (upper  right  or  left  abdominal  quadrant  and 
the  costovertebral  angle  posteriorly)  and  not  radiating  down  the  ureter, 
as  a  rule;  these  attacks  are  often  associated  with  nausea  and  vomiting. 
Often  a  more  or  less  large,  firm,  or  cystic  tumor  may  be  palpable  in  the 
region  of  the  kidney — which  characteristically  varies  in  size  from  time 
to  time  (change  in  posture,  etc.),  decrease  in  size  being  associated  with 
an  increase  in  the  amount  of  urine  (intermittent  hydronephrosis).  The 
changes  in  the  urine  are  variable,  and  depend  more  upon  associated 
conditions  (inflammations,  tumors,  calculi,  etc.)  than  upon  the  hydro- 
nephrosis itself.  The  intermittent  passage  of  a  large  amount  of  clear, 
pale  urine  of  low  specific  gravity  is  indicative  of  the  intermittent  type 
of  the  disorder.  In  the  bilateral  disorder,  which  is  usually  more  or  less 
permanent,  the  amount  of  urine  may  be  below  normal. 


794  DISEASES  OF  THE   VPdXARY  SYSTEM 

Diagnosis. — ^The  diagnosis  in  uncomplicated  cases  is  usually  easy. 
Other  forms  of  renal  and  other  retroperitoneal  tumors  must  be  excluded. 
Pyonephrosis  may  be  excluded  by  the  absence  of  evidence  of  septico- 
pyemia, and  of  pus  from  the  urine  (although  some  pus  cells  may  be 
found  microscopically  in  many  cases  of  hydronephrosis).  The  acute 
attacks  of  pain  simulate  appendicitis,  cholelithiasis,  and  renal  calculus; 
ordinarily  little  difficulty  should  be  experienced  in  excluding  these. 

Prognosis. — The  prognosis  depends  entirely  upon  the  underlying 
condition  and  its  amenability  to  treatment. 

Treatment. — The  treatment  is  essentially  surgical,  although  if  the 
condition  occasions  little  or  no  distress,  operation  need  not  be  insisted 
upon.  Division  of  anomalous  bloodvessels  where  they  cross  and  obstruct 
the  ureteropelvic  junction  suffices  in  some  cases  to  cure  the  condition; 
in  other  cases  plastic  operations  on  the  ureter  and  pelvis,  nephrotomy, 
anchoring  a  displaced  kidney,  etc.,  may  be  necessary;  or  complicating 
calculi,  tumors,  etc.,  must  be  removed. 


NEPHROLITHIASIS. 

(Re'iud  Calculus.) 

Etiology. — Renal  calculi  are  most  common  in  adult  life  (thirtieth  to 
sixtieth  year);  and  in  males  (75  per  cent,  of  the  cases).  Their  forma- 
tion is  said  to  be  favored  by  a  sedentary  life  and  by  habits  in  eating  and 
drinking  that  favor  the  development  of  gout.  Bacterial  mfection  is 
an  active  factor  in  many  cases. 

Pathology. — Primarily  urinary  calculi  are  renal  in  origin  m  the  very 
great  majority  of  cases;  but  secondary  accretions  may  occur  m  the  renal 
pelvis,  in  the  ureter,  or  in  the  bladder,  and  calculous  deposits  may 
occur  in  and  about  divers  inflammatory  and  necrotic  processes  in  the 
urinary  tract — ^whence  a  distinction  is  sometimes  made  between  primary 
and  secondary  calculi.  Furthermore,  calculi  may  be  solitary  or  multiple, 
and  unilateral  or  bilateral  (20  to  25  per  cent,  of  the  cases).  According 
to   size   one   may  distinguish:   (1)  PLcnal   sand,   fine,   gritty  particles; 

(2)  gravel,  concretions  up  to  1  to  2  mm.  m  diameter;  and  (3)  calculi 
(or  stones),  varying  in  size  from  that  of  a  pea  or  bean  to  large  dendi'itic 
or  coral-shaped  formations  that  fill  out  even  a  dilated  renal  pelvis  and 
the  calices.  Chemically  the  calculi  may  be  composed  of:  (1)  Uric  acid 
and  urates — the  most  common  (two-thirds  of  the  cases).  Sand  and 
gravel  almost  always  consist  of  uric  acid  and  urates;  often  also  the 
small  solitary  or  the  larger  dendritic  stones.  These  are  hard,  reddish 
in  color,  have  a  smooth  surface,  and  on  section  are  dense  and  stratified; 
and  they  occur  in  acid  urine.  (2)  Calcium  oxalate  (mulberry  calculi,  the 
second  in  point  of  frecjuency),  hard,  gray  or  dark  in  color,  and  witli  a 
rough  surface,  or  studded  with  spines;  they  also  occur  in  acid  urine. 

(3)  Phosphates  (^calcium  and  ammonio-magnesium),  small,  grayish 
in  color,  and  soft;  they  are  uncommon,  and  occur  in  alkaline  urine; 


NEPHROLITHIASIS  795 

phosphates  may  form  a  coating  of  other  calculi.  (4)  Certain  rarer  forms, 
such  as  calcium  carbonate,  xanthin,  cystin,  indigo,  and  urostealiths 
(fatty  calculi,  which  originate  usually  in  the  bladder).  Precipitation 
of  the  urinary  salts  may  occur  in  the  kidney  substance — so-called  renal 
infarcts,  of  which  the  following  varieties  may  be  distinguished:  (1) 
Uric-acid  (urate)  infarcts,  which  occur  in  the  newborn  and  in  gouty  sub- 
jects, usually  at  the  apices  of  the  pyramids;  (2)  calcium  (phosphate  and 
carbonate,  perhaps  also  oxalate),  whitish  opaque  streaks,  found  especially 
in  the  pyramids  in  senility,  metallic  poisoning,  etc.;  (3)  pigmentary 
infarcts — derivatives  of  hemoglobin,  biliary  pigment,  etc. 

Calculi  induce  various  lesions  in  the  urinary  tract.  In  some  (aseptic) 
cases  there  may  be  few  if  any  lesions  beyond  the  mere  presence  of  the 
calculus;  in  other  (also  aseptic)  cases  there  may  be  more  or  less  hydro- 
nephrosis or  chronic  interstitial  connective-tissue  overgrowth  with  con- 
traction and  atrophy  of  the  renal  parenchyma.  In  infected  cases  there 
is  an  associated  pyelitis,  pyelonephritis,  pyonephrosis,  or  perinephritic  or 
paranephritic  abscess.  In  unilateral  aseptic  cases  there  may  be  more 
or  less  hypertrophy  of  the  opposite  kidney;  in  infected  cases  there  is 
often  a  descending-ascending  infection  of  the  bladder  and  the  other 
kidney. 

The  mode  of  formation  of  renal  calculi  is  not  thoroughly  understood. 
Roberts  believes  that  the  main  factors  in  the  formation  of  uric  acid 
salts  are  high  urinary  acidity  (which  favors  the  deposition  of  uric  acid), 
excess  of  uric  acid,  and  deficiency  of  salines  and  of  pigments.  Ebstein  has 
proved  that  urinary  calculi  are  not  simple  conglomerations  of  crystalline 
deposits,  but  that  they  possess  an  organic  framework,  the  product  of 
pathological  processes  in  the  urinary  tract,  in  which  the  crystalline 
deposits  are  embedded  and  held  together.  Schade,  pointing  out  the 
fundamental  error  of  believing  that  the  urinary  constituents  exist  in  simple 
watery  solution,  emphasizes  the  importance  of  the  colloids  in  maintaining 
solution;  lie  states  that  when  the  crystalloids  go  out  of  solution  they 
take  with  them  colloids  (pigment,  etc.)  and  form  concretions  with  a 
complex  colloidal  stroma,  to  which  is  due  the  well-known  insolubility 
of  the  calculus  as  compared  with  a  simple  crystalline  mass  of  the  same 
chemical  nature.  The  special  colloid  is  believed  to  be  fibrin  or  fibrinogen, 
a  product  of  inflammation;  which  facts,  in  connection  with  the  frequency 
of  infection  of  the  urinary  tract  and  the  finding  of  bacteria  in  many 
urinary  calculi  suggest  that  urinary  calculi,  in  part  at  least,  are  infectious 
or  inflammatory  in  origin  (analogous  to  biliary  calcifli);  in  part  there 
is  perhaps  an  excess  in  the  urine  of  the  crystalloids  in  question  or  a 
lessened  ability  of  the  urine  to  hold  them  in  solution. 

Symptoms.— Nephrolithiasis  may  be  entirely  latent;  a  large  dendritic 
calculus  may  constitute  an  accidental  necropsy  finding;  or  sand  or 
gravel  may  be  passed  from  time  to  time  for  years  with  little  or  no  note- 
worthy discomfort;  or  oliguria  or  anuria  may  suddenly  develop  from 
ureteral  obstruction;  or  such  may  be  the  destruction  of  renal  tissue 
that  uremia  may  come  on  without  obtrusive  antecedent  symptoms. 


796  DISEASES  OF  THE   URINARY  SYSTEM 

In  the  majority  of  cases,  however,  the  disorder  is  manifest  by  renal 
pain,  hematuria,  pyuria,  and  other  evidences  of  pyehtis  or  pyelonephritis. 
The  pain  may  be  dull  and  aching  in  character  in  the  region  of  the  kid- 
ney, and  more  or  less  continuous,  although  aggravated  by  violent  exer- 
cise (jumping,  etc.) ;  or  it  may  be  that  spoken  of  as  renal  colic — sudden 
severe  cutting  or  stabbing  pain  in  the  region  of  one  kidney  radiating 
down  the  ureter  to  the  bladder,  testicle  (which  may  become  retracted), 
urethra,  labia,  or  thigh;  rarely  to  the  opposite  kidney  or  upward  or 
about  the  chest.  The  severe  pain  is  usually  associated  with  strangury, 
reflex  nausea,  vomiting,  and  more  or  less  shock  (pallor,  sweating,  and 
feeble  rapid  pulse);  and  in  children  perhaps  convulsions.  The  pain 
may  last  a  few  moments  and  then  intermit  or  remit;  or  it  may  recur 
paroxysmally  for  several  hours,  the  patient  perhaps  meanwhile  being 
conscious  of  the  transit  of  the  calculus  through  the  ureter.  Finally, 
it  may  pass  into  the  bladder  and  be  discharged  with  the  urine  (with  or 
without  a  painful  paroxysm) ;  or  it  may  remain  in  the  bladder  and  form 
the  nucleus  of  a  urinary  calculus.  Some  dull  aching  usually  remains 
for  some  time  after  the  colic;  and  the  colic  may  recur  from  time  to  time. 
Hematuria  is  very  common;  it  occurs  during  and  after  an  attack  of  colic, 
but  it  is  usually  present  also  in  the  absence  of  colic.  Pyuria  occurs  in 
the  event  of  pyelitis  and  pyelonephritis  (which  are  common).  There 
is  also  albuminuria  (proportionate  to  the  pus  and  blood),  crystals  of 
uric  acid,  calcium  oxalate,  etc.  (that  sometimes  indicate  the  chemical 
constitution  of  the  calculus);  and  sometimes  also  casts  (concomitant 
nephritis).  Anuria  is  sometimes  observed;  it  may  be  due  to  bilateral 
calculi;  to  obstruction  of  one  ureter  and  disease  (atrophy)  or  reflex  sup- 
pression of  the  function  of  the  opposite  kidney;  or  to  urethral  obstruction. 
In  some  cases,  when  the  ureter  is  completely  blocked  and  the  opposite 
kidney  healthy,  the  urine  voided  (excreted  by  the  healthy  kidney)  may 
be  entirely  normal.  Occasionally  there  is  fever  and  other  septicopyemic 
manifestations  of  pyelitis  and  pyelonephritis;  in  some  cases  there  are 
recurrent  attacks  which  recall  Charcot's  biliary  intermittent  fever  (of 
cholelithiasis).  The  kidney  may  be  tender  to  palpation,  or  enlarged 
(hydronephrosis,  pyonephrosis).  An  impacted  stone  may  be  palpable 
along  the  course  of  the  ureter  (abdominal  or  vaginal  or  rectal  palpation). 
An  a;-ray  examination  m^y  reveal  the  presence,  size,  shape,  and  location 
of  the  stone  or  stones  (uric-acid  calculi  give  a  faint  shadow;  oxalate  and 
phosphate  calculi,  more  marked  shadows).  Cystoscopic  examination 
and  examination  of  the  separated  urines  may  reveal  whether  one  or 
both  sides  are  diseased. 

A  calculus  in  the  bladder  gives  rise  to  pain,  especially  at  the  end  of 
urination,  to  sudden  stoppage  of  the  urinary  stream,  and  to  its  re- 
establishment  upon  change  of  posture  (from  the  erect  to  the  recumbent) ; 
and  to  hematuria,  pyuria,  and  other  evidences  of  cystitis.  It  may 
be  detected  by  bimanual  and  cystoscopic  examination  of  the  bladder. 

Diagnosis. — The  diagnosis  of  renal  calculus  is  obvious  in  the  event  of 
renal  colic,  enlargement  and  tenderness  of  the  kidney,  hematuria,  pyuria, 


CYSTS  OF  THE  KIDNEY  797 

positive  results  of  an  rr-ray  examination,  and  the  detection  of  gravel 
or  sand;  but  a  negative  radiogram  by  no  means  excludes  a  stone.  One 
must  exclude  other  causes  of  pyelitis  and  pyelonephritis,  renal  tumors, 
tuberculosis  of  the  urinary  tract,  essential  renal  hematuria;  and  renal 
colic  must  be  distinguished  from  intestinal  and  gallstone  colic,  appendi- 
citis, Dietl's  crises,  etc. 

Prognosis. — ^The  course  is  chronic  and  seldom  (but  sometimes)  results 
in  spontaneous  cure  after  the  passage  of  the  then  existing  calculi.  The 
likely  complications  (pyelitis,  pyelonephritis)  and  the  likelihood  of 
recurrence  render  the  prognosis  doubtful. 

Treatment. — Perhaps  the  dietetic  regulations  recommended  in  con- 
nection with  gout  may  tend  to  prevent  the  formation  of  renal  calculi. 
The  treatment  of  renal  colic  is  similar  to  that  of  gallstone  colic — 
rest;  morphine,  atropine,  and  perhaps  nitroglycerin  hypodermicly; 
inhalation  of  chloroform,  if  necessary,  until  the  morphine  produces  its 
effect;  a  hot  foot  bath,  and  hot  applications  locally.  Inversion  of  the 
patient  or  the  lateral  posture  sometimes  serves  to  dislodge  an  impacted 
stone,  and  reverse  massage  may  lead  to  the  same  result.  Between 
attacks  the  patient  should  avoid  sudden  exertions.  He  should  keep  up 
a  goodly  excretion  of  urine  by  drinking  large  amounts  of  water;  and  in 
the  event  of  uric  acid  calculi,  he  should  reduce  the  urinary  acidity  with 
potassium  citrate,  acetate,  or  bicarbonate,  etc.  (or  the  alkaline  mineral 
waters  if  desired);  in  the  event  of  alkaline  urine  and  phosphatic  calculi, 
hexamethylenamin,  salol,  and  other  urinary  antiseptics  should  be  given. 
It  seems  quite  impossible  to  dissolve  calculi  in  the  urinary  tract,  so  that 
it  is  more  than  doubtful  that  lithium  salts,  piperazin,  and  other  so-called 
uric-acid  solvents  have  any  such  action  in  the  body.  In  the  event  of 
repeated  renal  colic,  pyelitis,  anuria,  etc.,  operation  should  be  resorted 
to;  and  with  a  full  knowledge  of  the  condition,  operation  should  not  be 
too  long  delayed :  sooner  or  later  the  renal  tissue  becomes  destroyed  and 
operation  cannot  restore  it. 

CYSTS  OF  THE  KIDNEY. 

Various  sorts  of  cysts  are  encountered  in  the  kidneys:  (1)  Small 
multiple  cysts  common  in  chronic  indurative  nephritis  and  attributed 
to  obstruction  and  consequent  dilatation  of  renal  tubules  or  Bowman's 
capsules;  (2)  a  large,  often  solitary  cyst,  sometimes  found  projecting 
from  the  cortex  of  an  otherwise  healthy  kidney,  containing  clear  watery 
or  colloid  fluid,  and  attributable  also  to  obstruction  of  the  tubules  (perhaps 
a  foetal  defect);  (3)  parasitic  (echinococcic)  cysts,  which  cause  enlarge- 
ment of  the  kidney,  fluctuation,  hematuria,  pyuria,  and,  should  the  cyst 
rupture  into  the  renal  pelvis,  vesicles,  booklets,  or  membrane  in  the  urine 
(the  passage  of  which  may  occasion  renal  colic);  and  (4)  so-called  con- 
genital cystic  kidneys. 

Congenital  cystic  kidneys  may  be  observed  at  birth  (obstructing 
labor)  or  in  later  life;  many  cases  first  come  to  observation  in  adult 


798  DISEASES  OF  THE   URINARY  SYSTEM 

life,  and  especially  in  men.  The  kidney  may  attain  an  enormous  size, 
being  made  up  of  numerous  cysts,  varying  in  size,  as  a  rule,  from  2  to 
20  mm.  in  diameter,  and  containing  urinous,  colloid,  or  hemorrhagic 
fluid ;  often  little  if  any  renal  tissue  can  be  detected  even  microscopically. 
The  condition  is  bilateral,  although  one  kidney  may  be  larger  than  the 
other,  and  perhaps  enlarge  before  the  other.  The  nature  of  the  disorder 
is  not  definitely  determined;  it  seems,  however,  to  be  a  congenital  defect 
of  development  (rather  than  retention  cysts  or  cystic  tumor  formation, 
as  has  been  suggested),  since  it  is  often  associated  with  other  anomalies  of 
development),  cystic  disease  of  the  liver,  imperforate  anus,  malformation 
of  the  heart,  etc.).  The  condition  may  remain  latent  until  adult  life, 
or,  as  seems  to  have  occurred  in  some  cases,  slow  progressive  growth 
occurs  from  early  life.  In  some  cases  there  are  the  cardiovascular  changes 
of  chronic  indurative  nephritis. 

Symptoms. — In  some  cases  the  enlarged  kidneys  interfere  with  parturi- 
tion. In  the  cases  that  develop  in  later  life  there  are :  gradual  enlargement 
of  both  kidneys  (although  one  may  precede),  which  may  form  visible 
and  palpable  (perhaps  cystic)  tumor  masses;  hematuria — chronic  and 
remittent  and  induced  by  palpating  the  kidneys;  and  the  gradual  de- 
velopment of  the  urinary  and  cardiovascular  changes  of  chronic  indura- 
tive nephritis,  and  of  chronic  uremia;  sometimes  the  sudden  onset  of 
acute  uremia.  Modern  tests  reveal  lessening  of  the  functional  capacity 
of  one  or  both  kidneys. 

Diagnosis. — The  diagnosis  can  be  readily  made  in  the  event  of  palpably 
enlarged  kidneys,  hematuria,  and  the  urinary  and  cardiovascular  changes 
of  chronic  indurative  nephritis. 

Prognosis. — ^The  ultimate  outlook  is  hopeless,  although  the  subject 
may  live  many  years  (as  in  chronic  indurative  nephritis). 

Treatment. — ^The  treatment  is  that  of  chronic  indurative  nephritis. 
Operation  may  be  undertaken  in  the  rare  unilateral  cases  in  which  the 
other  kidney  is  of  good  functional  capacity  (modern  tests),  and  in  the 
event  of  suppuration;  but  the  mortality  is  high  and  the  outlook  not 
reassuring. 

TUMORS  OF  THE  KIDNEY. 

Tumors  of  the  kidney  may  be  benign  or  malignant,  primary  or  second- 
ary. The  benign  growths  comprise  fibroma,  lipoma,  angioma,  and 
adenoma,  and  are  of  little  clinical  interest.  The  primary  malignant 
growths  comprise  hypernephroma,  sarcoma,  and  carcinoma.  The  hy- 
pernephroma, a  tumor  derived  from  misplaced  adrenal  tissue,  is  the 
most  common  tumor  in  adults,  and  includes  most  of  the  so-called 
adenomas,  carcinomas,  sarcomas,  endotheliomas,  and  peritheliomas  oc- 
curring in  adult  life.  It  may  be  small  and  an  accidental  finding  at  the 
necropsy,  or  it  may  attain  the  dimension  of  a  man's  head.  In  its  early 
growth  it  is  usually  encapsulated  against  the  renal  substance;  but  later 
the  capsule  becomes  invaded  and  penetrated,  and  the  renal  veins  are 


TUMORS  OF  THE  BLADDER  799 

likely  to  be  implicated — ^whence  metastases  occur  by  way  of  the  blood- 
vessels, to  the  lungs,  bones,  etc.  Sarcoma  is  the  common  tumor  in 
infants  and  children,  and  may  attain  a  very  large  size;  it  may  be  of 
the  common  types,  but  especially  when  occurring  very  early  in  life 
a  rhabdomyoma,  or  a  so-called  congenital  adenosarcoma,  etc.  Secondary 
tumors  may  occur  by  hematogenous  or  lymphogenous  metastases  or  by 
growth  by  contiguity  of  tissue. 

Symptoms. — ^The  significant  symptoms  consist  of  pain,  hematuria, 
a  palpable  tumor,  and  progressive  anemia,  cachexia,  and  emaciation. 
The  pain  may  be  slight,  perhaps  absent,  or  very  severe;  sometimes  it  is 
colicky  (passage  of  blood  clots  down  the  ureter).  Hematuria  may  be 
mild  or  severe,  continuous  or  intermittent;  it  is  present  sometimes  dur- 
ing the  course  of  50  to  90  per  cent,  of  the  cases,  but  in  the  early  stages 
of  hypernephromas  it  is  usually  wanting  because  of  the  encapsulation 
of  the  growth  and  its  virtual  separation  from  the  kidney  tissue.  Sooner 
or  later  a  tumor  becomes  palpable  in  the  renal  region  retroperitoneally 
(behind  the  intestines  and  projecting  into  the  flank  or  lumbar  region); 
it  varies  in  size,  is  soft  or  firm,  and  often  nodular.  In  addition  to  blood, 
fluid  or  clotted  (casts  of  the  renal  pelvis  or  ureter),  the  urine  may  contain 
bits  of  tumor  tissue.  Metastasis,  especially  in  adults,  to  the  lungs  or 
bones  may  be  observed  in  some  cases ;  or  growth  of  the  tumor  may  lead 
to  thrombosis  of  the  inferior  vena  cava  and  oedema  of  the  legs,  varicocele 
(compression  of  the  spermatic  vein),  or  to  compression  and  obstruction 
of  the  intestines,  etc. 

Diagnosis. — ^The  dig^gnosis  virtually  is  that  of  a  retroperitoneal  growth, 
in  which  event  hematuria  suggests  its  renal  origin;  progressive  anemia 
and  cachexia  exclude  other  enlargements  of  the  kidney  (hydronephrosis, 
cystic  disease),  and  the  absence  of  fever  and  other  evidences  of  septico- 
pyemia excluded  pyelonephrosis.  Sarcoma  of  the  retroperitoneum 
(Lobstein's  cancer)  must  be  excluded.  Occasionally  also  tumors  of  the 
spleen  or  the  liver  must  be  differentiated. 

Prognosis. — ^The  prognosis  depends  entirely  upon  the  possibility  of 
removal  of  the  growth. 

Treatment. — The  treatment  is  wholly  surgical — removal  of  the  tumor. 


TUMORS  OF  THE  BLADDER. 

Tumors  of  the  bladder  comprise  especially  papilloma  and  car- 
cinoma; fibroma  and  sarcoma  are  rare.  The  major  sympioms  of 
papilloma  or  carcinoma  consist  of  local  pain,  disturbances  in  urination, 
hematuria,  cystitis,  and  gradually  developing  anemia  and  cachexia. 
Sometimes  the  disorder  is  not  suspected  until  a  small  bit  of  tumor  tissue 
is  discharged  with  the  urine,  whereupon  microscopic  examination  reveals 
the  true  nature  of  the  disease.  In  any  case  the  diagnos'i's  may  be  readily 
made  by  cystoscopic  examination.     The  treatment  is  wholly  surgical. 


SECTION  X. 
DISEASES  OF  THE  NERVOUS  SYSTEM. 


Pathological  Physiology. — ^Tlie  nervous  system,  composed  of  two  parts, 
the  cerebrospinal  and  the  sympathetic,  is  the  chief  regulating  and  gov- 
erning mechanism  of  the  organism.  It  is  designed  to  exercise  an  orderly 
control  over  all  the  functions  of  the  body — motor,  sensory,  secretory, 
vasomotor,  and  trophic;  voluntary  and  involuntary;  conscious  and  un- 
conscious. The  integrity  of  the  nervous  system  is  essential  to  the  proper 
execution  of  purposeful  acts;  to  muscular  activity  and  coordination;  to 
the  reception  of  sensory  impressions  and  the  reaction  thereto,  as  in  reflex 
action,  for  instance;  to  the  normal  functioning  of  the  special  sense  organs, 
and  of  the  various  glands;  to  proper  growth  and  trophic  influence;  and 
to  the  normal  activity  of  the  cardiovascular,  respiratory,  digestive,  uri- 
nary, cutaneous,  and  reproductive  organs.  Disorder  of  the  nervous 
system  thus  becomes  manifest  not  only  in  morbid  phenomena  referable 
directly  to  the  system  itself,  but  also  in  many  varied  disorders  referable 
to  the  different  systems  of  organs — which  have  already  been  discussed. 

In  the  final  analysis  the  nervous  system  is  made  up  of  a  complex  of 
neurons;  that  is,  of  certain  ultimate  anatomical  and  physiological  units, 
each  of  which  consists  of  a  cell  body,  provided  with  a  number  of  usually 
short,  branching  processes,  so-called  dendrons  (dendrites),  and  a  single, 
usually  long,  branch  or  process,  the  axon,  axis  cylinder,  or  nerve  fiber. 
The  axons  of  the  cerebrospinal  system  soon  after  leaving  the  cell  body 
become  ensheathed  with  myelin  and  neurilemma  (sheath  of  Schwann), 
both  of  which  are  lost  near  the  termination  of  the  axon;  these  medullary 
sheaths  are  absent  in  the  sympathetic  nervous  system.  The  neurons  are 
in  physiological  relationship  or  communication  by  means  of  so-called 
collateral  branches  or  the  terminal  arborization  of  the  axon  of  one 
neuron  and  the  dendrons  of  another  neuron.  The  prevailing  conception 
is  that  there  is  no  anatomical  connection  between  physiologically  related 
neurons,  that  the  relationship  is  one  of  contact  only — contiguity,  but 
not  continuity,  of  structure;  but  it  is  not  impossible  that  the  ultimate 
divisions  of  the  terminal  arborization  of  the  axons  actually  enter  the 
dendrons  of  another  neuron  (by  means  of  so-called  neurofibrils). 

Neurons  are  classified  as:  (1)  Primary  neurons,  which  comprise  those 
the  cell  body  of  which  is  situated  in  the  central  nervous  system  or  ganglia, 
51 


802  DISEASES  OF  THE  NERVOUS  SYSTEM 

and  the  axon  of  which  extends  to  the  periphery  (skin,  a  muscle,  a  gland, 
a  sense  organ,  etc.);  and  (2)  secondary  (or  association)  neurons,  which 
comprise  those  the  cell  body  of  which  is  situated  in  the  central  nervous 
system  and  the  axons  of  which  do  not  extend  to  the  periphery,  but  serve 
as  a  means  of  communication  between  different  parts  of  the  nervous  sys- 
tem; that  is,  the  axon  communicates  with  the  dendrons  of  another 
neuron  (primary  or  secondary).  Neurons  also  are  classified,  according 
to  their  function,  into  motor,  sensory,  secretory,  and  trophic;  and  a 
number  of  neurons,  usually  related  functionally,  are  collected  and  held 
together  by  neuroglia  and  other  connective  tissue,  and  thus  make  up  the 
different  peripheral  nerves,  the  nerve  tracts  of  the  spinal  cord  and  brain, 
and  the  elements  of  the  sympathetic  system.  Extensive  communications 
exist  between  the  cerebrospinal  and  the  sympathetic  systems — by  way  of 
the  spinal  roots  and  nerves  with  the  spinal  cord,  and  by  way  of  the  vagus 
(chiefly)  with  the  brain.  The  sympathetic  system  is  largely  concerned 
with  regulating  the  cardiovascular  system  and  the  vegetative  functions; 
its  activities  are  automatic  and  unconscious,  although  it  is  somewhat 
under  the  influence  of  the  cerebrospinal  system,  and  it  may  be  deranged 
by  emotional  and  other  states;  but  we  know  comparatively  little  of  the 
pathology  of  its  disorders. 

All  disease  of  the  nervous  system  is  attributed  to  some  disorder  of  the 
neuron.  This  may  be  supposedly  functional  in  nature  and  temporary 
(functional  disorders),  or  it  may  be  organic,  more  or  less  destructive  in 
nature,  and  susceptible  of  partial  or  complete  repair  (organic  disease). 
The  important  facts  are  that  when  diseased  the  neuron  is  disordered 
(degenerates)  as  a  whole;  that  many  diseases  of  the  nervous  system  tend 
to  involve  certain  collections  of  neurons  physiologically  homologous  (so- 
called  system  diseases);  and  that  a  knowledge  of  the  anatomical  and 
physiological  relationships  of  these  collections  of  neurons  facilitates  a  com- 
prehension of  their  diseases  and  permits  a  ready  localization  of  the  lesion. 

Motor  Neurons. — Motor  impulses  are  conveyed  from  the  cerebral 
cortex  to  the  periphery  by  the  motor  neurons,  of  which  there  are  two  sets, 
the  upper  and  the  lower.  The  upper  motor  neuron  (the  motor  tract) 
begins  w^ith  the  cell  bodies  in  the  motor  area  of  the  cerebral  cortex; 
thence  the  axons  pass  through  the  corona  radiata,  the  internal  capsule,  the 
crus,  the  pons,  the  medulla,  and  the  spinal  cord.  In  the  pons  and 
medulla  most  of  the  axons  decussate,  some  to  go  to  the  nuclei  of  the  motor 
cranial  nerves,  the  others  to  course  down  the  opposite  side  of  the  spinal 
cord,  as  the  crossed  pyramidal  tract,  and  finally  to  break  up  into  terminal 
arborizations  about  the  cells  of  the  anterior  cornua  (the  cell  bodies  of  the 
lower  motor  neuron);  the  axons  that  do  not  decussate  in  the  medulla 
descend  in  the  spinal  cord  as  the  direct  pyramidal  tract,  but  finally  also 
decussate  to  the  opposite  side  by  way  of  the  anterior  commissure.  The 
lower  motor  neuron  begins  with  the  cell  bodies  in  the  anterior  cornua  of 
the  spinal  cord;  thence  the  axons,  by  way  of  the  anterior  (ventral)  spinal 
roots  become  collected  into  the  spinal  nerves,  and  ultimately  reach  the 
muscles  to  which  they  transmit  motor  impulses. 


PLATE    I 


Areas  of  Anaesthesia  upon  the   Body  after  Lesions  in  the  Various 
Segments  of  the  Spinal  Cord. 

The  segments  of  the  cord  are  numbered:  C  I  to  VIII,  D  I  to  XII,  L  1  to  V,  S  1  to  5 
and  these  numbers  are  placed  on  the  region  of  the  skin  supplied  by  the  sensory'  nerves  of 
the  corresponding  segment. 


PATHOLOGICAL  PHYSIOLOGY  803 

Motor  impulses  must  pass  through  both  of  these  neurons;  and  disease 
of  one  or  the  other  or  both  results  in  loss  of  voluntary  muscular  power. 
There  are,  however,  differences  in  the  other  results  of  disease  of  the  two 
motor  neurons,  which  are  due  to  the  fact  that  the  upper  neuron  exercises 
an  inhibiting  influence  on  the  lower,  and  that  the  lower  serves  to  main- 
tain the  nutrition  of  the  muscles  with  which  it  is  connected.  In  general, 
therefore,  disease  of  the  upper  motor  neuron  results  in  loss  of  voluntary 
muscular  power,  rigidity  and  spasticity  of  the  muscles,  and  eventual 
contractures  (the  muscles  of  flexion  and  adduction  overcoming  those  of 
extension  and  abduction);  increase  of  the  deep  reflexes,  as  well  as  the 
Babinski  plantar  reflex  (extension  of  the  great  toe) ;  little  if  any  muscular 
wasting,  and  that  only  from  disuse;  and  no  noteworthy  changes  in  the 
electrical  reactions  of  the  nerves  or  muscles.  This  is  well  exemplified 
in  lateral  sclerosis  (spastic  paraplegia)  and  in  combined  lateral  and  pos- 
terior sclerosis  (ataxic  paraplegia).  On  the  other  hand,  disease  of  the 
lower  motor  neuron  results  in  loss  of  voluntary  muscular  power,  flac- 
cidity,  and  wasting  of  the  muscles;  ultimate  contractures,  due  largely 
to  the  action  of  unopposed  non-paralyzed  muscles;  loss  of  deep  reflexes; 
and  often  the  response  to  electrical  stimulation  known  as  the  reactions  of 
degeneration.  This  is  well  exemplified  in  epidemic  poliomyelitis  (in- 
fantile paralysis),  progressive  spinal  muscular  atrophy,  progressive  bul- 
bar paralysis,  etc.  In  some  cases  both  motor  neurons  may  be  diseased, 
as  in  amyotrophic  lateral  sclerosis. 

Sensory  Neuron. — ^Sensory  impressions  are  conveyed  from  the 
periphery  to  the  nerve  centres  by  the  sensory  neurons.  The  cell  bodies 
of  these  are  situated  in  the  ganglia  of  the  posterior  spinal  roots  and  in  the 
homologous  ganglia  of  the  sensory  cranial  nerves,  as  well  as  in  the  sym- 
pathetic nervous  system.  The  sensory  impression  is  received  by  certain 
fine  nerve  filaments  in  the  skin  or  tactile  corpuscles  and  conveyed  by  a 
sensory  nerve  or  bundle  (through  or  past  the  cell  body)  to  the  spinal 
cord.  Herein  the  axon  bifurcates,  one  portion  ascending  in  the  posterior 
columns,  the  other  descending  a  short  distance. 

The  peripheral  nerves  carry  three  systems  of  sensory  fibers:  (1)  The 
protopathic  system,  which  transmits  sensations  of  pain  and  of  extremes 
of  temperature  (above  45°  C.  and  below  20°  C.) ;  (2)  the  epicritic  system, 
which  transmits  sensations  of  light,  touch,  of  cutaneous  localization,  and 
of  slight  temperature  variations;  and  (3)  the  deep  sensibility  system, 
which  transmits  sensations  of  pressure  and  of  movements  of  the  joints, 
muscles,  and  tendons — so-called  muscle  sense  (the  ability  to  distinguish 
difterence  in  weight  of  objects  of  similar  size),  as  well  as  the  stereognostic 
sense  (the  ability  to  recognize  the  shape  of  objects),  and  the  ability  to 
recognize  with  the  eyes  closed  the  position  into  which  the  limbs  may  be 
passively  placed.  The  unit  of  the  protopathic  system  is  in  the  posterior 
spinal  roots,  that  of  the  epicritic  system  in  the  peripheral  nerves;  so  that 
the  areas  of  sensory  disturbances  are  difl'erent  in  disease  of  the  periph- 
eral nerves  (Fig.  15)  from  what  they  are  in  disease  of  the  spinal  roots  or 
segments  (Plate  I).     Furthermore,  after  injury  to  a  peripheral  nerve,  for 


Fig.   15 


,chUar 


gSg   ;1 


Ui/pogastrie 

\  I>orsalis 
'     Penis  of 


Inf.  ScemorrJioidal 

ofPtKlic 

Superficial  Perineal  of\ 

Pudic  and  InfeHor 

Pudendal  of  small 

Sciatic 


The  distribution  of  the  sensory  nerves  in  the  skin.  The  areas  of  the  skin  supplied  by  the 
cutaneous  nerves  are  shown  in  finely  dotted  outline.  The  circles  on  the  trunk  show  areas  occa- 
sionally anesthetic  in  hysteria.  The  lines  across  the  limbs  at  the  ankle,  knee,  thigh,  wrist, 
elbow,  and  shoulder  show  the  upper  limits  of  anesthesia  in  multiple  neuritis  of  varying  degrees 
of  severity.     (After  Flower.) 


PLATE   II 


XIII 


The  Cervical  and  Sacral  Enlargements  of  the  Spinal  Cord  in  Cross-section. 

(Starr.) 

Showing  the  various  neurons  in  the  gray  matter,  the  direction  of  their  axons,  and  the 
varieties  of  fibers  in  the  different  columns  of  the  cord.  Blue,  motor  neurons  ;  red,  sensory- 
neurons  ;  purple,  association  neurons  and  axons. 

I.  Anr.  median  column.  II.  Anterolateral  column.  III.  Gowers'  anterolateral  ascending  column. 
I\'.  Marginal  column.  V.  Lateral  pyramidal  column.  VI.  Direct  cerebellar  column.  Nil.  Lissauer's 
tract.  ^'III.  lO.xt.  portion  of  column  of  Burdacli.  IX.  Root  z<ine  of  the  cohnnn  of  lUirdacli.  X. 
Descending  comma-shaped  bundle  of  Schultze.  XI.  Po.st.  co»nmi,ssural  tract.  XII.  t'olumn  of  Coll. 
XIII.   Septomarginal  tract. 


PATHOLOGICAL  PHYSIOLOGY  805 

instance,  the  different  forms  of  anesthesia  are  not  ahke  in  distribution, 
,and  during  recovery  the  sensibihty  to  pain  returns  before  that  of  mere 
touch;  that  is,  sensation  for  touch  and  pain  is  subserved  by  different 
fibers.  If  a  peripheral  nerve  represents  largely  a  single  posterior  spinal 
root,  the  area  of  analgesia  is  likely  to  be  well  defined;  but  if  the  peripheral 
nerve  contains  fibers  from  several  posterior  spinal  roots,  the  disturbances 
of  protopathic  sensibility  are  likely  not  to  be  well  demarcated.  After  all 
the  cutaneous  sensory  fibers  have  been  destroyed,  the  deep  sensibility  of 
the  part  may  still  be  preserved. 

Sensory  impressions  are  transmitted  in  the  spinal  cord  by  the  following 
tracts  (Plate  II) :  (1)  The  posterior  columns — the  postero-internal  column 
of  Goll,  and  the  postero-external  column  of  Burdach.  The  fibers  of  these 
columns  are  a  continuation  of  those  of  the  posterior  roots;  they  ascend, 
giving  off  collateral  branches  which  penetrate  the  gray  matter  of  the  cord, 
and  they  terminate  in  the  homolateral  nucleus  gracilis  and  nucleus  cune- 
atus  of  the  medulla;  thence  another  set  of  fibers  proceeds,  soon  decus- 
sates, and  ends  in  the  thalamus  of  the  opposite  side;  from  this,  in  turn, 
another  set  of  fibers  proceeds  to  the  sensory  area  of  the  cerebral  cortex. 
These  fibers  are  chiefly  concerned  in  transmitting  impulses  of  cutaneous 
tactile  sensibility  (light  touch)  and  localization,  and  of  deep  sensibility, 
especially  muscular  and  limb  position;  lesions  of  these  fibers  give  rise 
to  ataxia.  A  few  fibers  cross  soon  after  they  enter  the  cord,  ascend  in 
contralateral  ascending  anterior  column,  and  finally  terminate  in  the 
thalamus.  These  fibers  also  transmit  impulses  for  tactile  sensibility,  and 
may  escape  involvement  in  cases  of  Brown-Sequard  paralysis.  The 
posterior  columns  also  contain  fibers  concerned  in  the  transmission  of 
painful  impressions;  soon  after  entering  the  cord  they  terminate  about 
cells  in  the  gray  matter,  whence  other  axons  proceed,  decussate,  and 
ascend  in  the  opposite  anterolateral  tract.  (2)  The  anterolateral  tract 
of  Gowers.  This  comprises  the  aforementioned  fibers  for  pain,  as  well 
as  others  concerned  in  transmitting  temperature  impulses;  these  ulti- 
mately, in  large  part,  reach  the  cerebellum,  by  way  of  the  superior  ped- 
icle), but  some  of  them  proceed  to  the  homolateral  thalamus.  (3)  The 
direct  (dorsolateral)  cerebellar  tract  of  Flechsig.  Some  of  the  fibers 
entering  the  cord  by  way  of  the  posterior  roots,  proceed  to  cells  in  Clark's 
columns  (at  the  base  of  the  posterior  cornua);  thence  axons  proceed, 
ascend  as  the  direct  cerebellar  tract,  and  end  in  the  cerebellum.  These 
fibers  convey  impulses  of  deep  sensibility  (muscles,  joints,  tendons,  etc.), 
and  disorder  of  them  results  in  ataxia. 

Reflexes. — The  contraction  of  a  muscle  or  set  of  muscles  that  fol- 
lows a  sensory  impulse  is  known  as  a  reflex  act;  its  occurrence  is  depend- 
ent upon  the  integrity  of  the  so-called  reflex  arc.  This  is  composed  of 
(a)  an  afferent  (sensory)  nerve,  along  which  the  impulse  passes,  enters 
the  spinal  cord  by  way  of  the  posterior  roots,  and  reaches  (6)  the 
so-called  centre,  the  motor  cells  of  the  anterior  cornua;  from  these,  in 
response  to  the  stimulus,  an  impulse  passes  out  along  (c)  an  efferent 
(motor)  nerve,  and,  reaching  a  muscle,  causes  it  to  contract.     Reflexes 


806  DISEASES  OF  THE  NERVOUS  SYSTEM 

may  occur  in  the  event  of  integrity  of  a  single  segment  of  the  spinal  cord; 
but,  although  independent  of,  they  are  much  modified  by,  the  higher 
centres  in  the  brain.  In  disease  they  may  be  lessened  (or  abolished)  or 
exaggerated.  Lessening  or  absence  of  the  reflexes  implies  a  lesion  in 
either  the  sensory  nerve,  in  which  event  it  is  associated  with  anesthesia; 
or  in  the  motor  cells  in  the  anterior  cornua,  or  in  the  motor  nerve,  in 
which  event  it  is  associated  with  paralysis,  flaccidity,  and  wasting  of  the 
muscles;  or  in  the  sensory  reflex  fibers  within  the  spinal  cord,  in  which 
event  the  reflexes  being  diminished  or  absent,  without  associated  sensory 
(anesthetic)  or  motor  (paralytic)  phenomena  referable  to  a  nerve  trunk, 
means  a  lesion  of  the  spinal  cord.  Of  these,  the  most  important  are 
locomotor  ataxia,  paretic  dementia  (with  associated  posterior  sclerosis), 
acute  and  chronic  anterior  poliomyelitis,  syringomyelia,  diffuse  and 
transverse  myelitis,  as  well  as  hemorrhage  and  tumors  (which  abolish 
reflexes  at  the  level  of  the  lesion),  and  multiple  sclerosis  (which  also  may 
abolish  a  reflex  if  a  sclerotic  patch  involves  the  reflex  arc).  Exaggeration 
of  the  reflexes  occurs  in  consequence  of  lessening  or  abolition  of  the  in- 
hibiting influence  of  impulses  normally  passing  from  the  brain  by  way  of 
the  motor  tracts  in  the  lateral  columns  of  the  spinal  cord;  the  exaggera- 
tion may  progress  to  the  condition  known  as  clonus,  which  comprises  a 
series  of  rapidly  recurring  contractions  of  a  muscle,  provoked  by  sudden 
marked  tension  on  the  tendon  of  the  muscle.  Exaggerated  reflexes  are 
indicative  of  disease  of  the  lateral  columns  of  the  spinal  cord,  and  are 
found  especially  in  lateral  sclerosis  (spastic  paraplegia),  below  the  lesion 
in  cases  of  descending  degeneration  of  the  pyramidal  tracts,  in  the  early 
stages  of  amyotrophic  lateral  sclerosis  (later  they  become  lost  in  the 
arms),  in  conditions  of  slight  pressure  impeding  the  passage  of  inhibiting 
impulses  down  the  cord  (as  in  the  early  stage  of  caries  of  the  vertebrae, 
tumors,  etc.,  causing  slight  compression),  and  in  functional  disorders, 
such  as  hysteria  and  neurasthenia.  In  cases  of  complete  severance  of 
the  cord,  however,  the  reflexes  are  abolished  below  the  lesion. 

There  are  three  principal  classes  of  reflexes:  (1)  The  deep  or  tendon 
reflexes,  which  result  from  tapping  a  tendon  near  its  insertion,  whence 
contraction  of  the  muscle  ensues.  The  most  important  are  the  knee- 
jerk  (patella  tendon  reflex),  the  Achilles  tendon  reflex,  the  biceps,  the 
triceps,  the  supinator  longus,  the  plantar  (flexion)  tendon  reflex,  etc. 
Special  diagnostic  importance  attaches  to  the  knee-jerk:  it  may  be 
diminished  or  lost  in  disturbance  of  the  reflex  arc  interfering  with  the 
transmission  of  impulses,  such  as  disease  of  the  muscles,  nerves  (neu- 
ritis), posterior  roots  (tabes  dorsalis),  or  anterior  roots,  and  disorders  of 
the  lumbar  cord  (second,  third,  and  fourth  lumbar  roots)  which  destroy 
the  centre  (acute  and  chronic  poliomyelitis,  etc.).  In  some  cases,  occa- 
sionally, but  only  for  a  very  short  time,  the  knee-jerks  may  also  be  lost — 
from  irritation  or  stimulation  of  the  inhibiting  influence  of  the  pyramidal 
fibers — in  cerebral  hemorrhage,  meningitis,  compression  of  the  cord  from 
fracture-dislocation,  etc.  The  knee-jerks  may  be  exaggerated  in  conse- 
quence of  lessening  or  abolition  of  the  inhibiting  influence  of  the  pyram- 


PATHOLOGICAL  PHYSIOLOGY  807 

idal  tract  above  the  lumbar  region,  such  as  occurs  in  lateral  sclerosis 
(spastic  paraplegia),  transverse  myelitis,  compression  from  fracture- 
dislocation  or  other  causes  (except  in  cases  of  complete  severance  of  the 
cord,  in  which  event  the  reflexes  below  the  lesion  are  abolished);  exag- 
geration of  the  knee-jerk  occurs  also  in  functional  disorders,  such  as 
hysteria  and  neurasthenia.  Under  like  conditions,  exaggeration  of  the 
Achilles  tendon  reflex — that  is,  ankle  clonus — may  ensue,  and  the  so- 
called  Babinski  phenomenon  (or  sign)  may  be  elicited;  this,  which  con- 
sists of  extension  (sometimes  called  dorsal  flexion)  of  the  great  toe  upon 
stimulating  the  sole  of  the  foot,  is  proof  of  disease  of  the  upper  motor 
neuron.  (2)  The  superficial  or  cutaneous  reflexes,  which  are  elicited 
by  stroking  or  irritating  the  skin.  The  most  important  are  the  epigastric 
reflex — contraction  of  the  muscles  of  the  epigastrium  upon  stroking  the 
lower  part  of  the  thorax;  the  cremasteric  reflex — retraction  of  the  testicle 
and  scrotum  upon  stroking  the  inner  aspect  of  the  thigh;  the  gluteal 
reflex — contraction  of  the  gluteus  muscle  (dimpling  in  the  gluteal 
fold)  on  stroking  the  buttock;  and  the  abdominal,  scapular,  palatal, 
pharyngeal,  and  conjunctival  reflexes.  Most  of  these  reflexes  are 
believed  to  be  due  to  contraction  of  involuntary  muscular  fibers  beneath 
the  skin  near  the  point  of  irritation.  The  presence  of  these  superficial 
reflexes  implies  integrity  of  the  reflex  arc,  whence  they  may  serve  to  deter- 
mine the  level  of  disease  of  the  spinal  cord.  In  general  they  are  dimin- 
ished or  absent  in  diseases  in  which  the  deep  or  tendon  reflexes  are  exag- 
gerated. (3)  Visceral  reflexes,  of  which  the  most  important  are:  (a) 
pharyngeal  and  laryngeal  reflexes,  which,  when  lessened  or  abolished, 
result  in  difficulty  in  swallowing  and  coughing,  and  may  lead  to  regurgi- 
tation of  food  through  the  nose,  or  to  aspiration  pneumonia  or  asphyxia- 
tion; (h)  visceral  and  rectal  reflexes.  Disease  of  the  spinal  cord  above 
the  centre  for  the  bladder  and  the  rectum  (fourth  and  fifth  sacral  segments) 
results  in  loss  of  control  by  higher  centres,  so  that  the  bladder  must 
depend  upon  its  reflex  activity;  usually  it  becomes  overdistended  and 
finally  overflow  from  distention  ensues.  If  the  spinal  centres  are  de- 
stroyed retention  of  urine  is  usually  impossible,  and  there  is  continuous 
incontinence.  The  result  of  involvement  of  the  rectal  centre  is  consti- 
pation and  involuntary  evacuation  of  the  feces. 

Electrical  Reactions. — Normally  the  application  of  a  faradic  (in- 
terrupted) or  galvanic  (constant)  current  to  a  nerve  or  muscle  results  in 
contraction  of  the  muscle,  especially  when  the  current  is  applied  to  the 
so-called  motor  points.  On  the  use  of  the  galvanic  current,  contractions 
occur  only  when  the  contact  is  made  or  broken;  and  normally  the 
cathodal  (negative  pole)  closing  contraction  (CCC)  is  greater  than  the 
anodal  (positive  pole)  closing  contraction  (ACC).  In  lesions  of  the  lower 
motor  neuron,  usually  within  four  or  five  days,  the  so-called  reactions  of 
degeneration  develop.  The  nerve  shows  a  gradual  loss  of  excitability  to 
both  the  faradic  and  the  galvanic  currents,  and  finally  fails  to  respond  at 
all,  that  is,  there  is  no  muscular  contraction  upon  applying  the  current 
to  the  nerve.     The  muscle  at  first  responds  feebly  and  slowly  to  the 


808  DISEASES  OF  THE  NERVES 

faradic  current,  but  soon  ceases  to  respond;  on  the  other  hand,  the 
muscle  may  be  for  some  thne  unduly  sensitive  to  the  galvanic  current, 
that  is,  it  may  respond  to  a  weaker  current  than  in  health;  but  the  char- 
acteristic reactions  of  degeneration  consist  in  a  slow,  wave-like  contrac- 
tion to  the  galvanic  current  (instead  of  instant  and  quick  response,  as  in 
health),  and  in  the  anode-closing  contraction  being  greater  than  the 
cathode-closing  contraction.  This  last  is  sometimes  not  present  (partial 
reaction  of  degeneration).  In  severe  cases  all  response  to  even  the  gal- 
vanic current  may  become  lost.  A  gradual  increase  in  galvanic  irrita- 
bility in  cases  in  which  it  has  been  absent  or  slight  is  of  good  prognostic 
significance,  indicating  regeneration. 


DISEASES  OF  THE  NERVES. 


NEURALGIA. 

Neuralgia  is  a  term  used  to  describe  recurring  or  persistent  pain  in  a 
peripheral  nerve  and  its  area  of  distribution.  Strictly  speaking,  the  pain 
is  unassociated  with  demonstrable  lesions  in  the  nerve  trunk  or  its  centres, 
but  the  pain  of  definite  neuritis  is  also  often  spoken  of  as  neuralgia. 

Etiology. — Neuralgia  occurs  especially  in  neuropathic  individuals  or 
families,  and  is  more  common  in  women  than  in  men.  It  is  commonly 
provoked  by  anemia  and  general  nervous  debility;  but  it  may  follow 
"  taking  cold,"  or  be  due  to  infections,  such  as  malaria,  typhoid  fever, 
rheumatism,  etc.;  to  intoxications,  such  as  intestinal  auto-intoxication, 
Bright's  disease,  gout,  etc. ;  or  to  reflex  irritation,  such  as  carious  teeth, 
eyestrain,  etc. 

Pathology. — Neuralgia  fer  se  is  not  associated  with  demonstrable  ana- 
tomical lesions.  The  pain  is  very  likely  due  to  irritation  or  oversuscep- 
tibility  of  the  sensory  neuron. 

Symptoms. — The  chief  symptom  is  pain.  Although  this  may  be  more 
or  less  constant,  it  is  characteristically  intermittent,  recurring  from  time 
to  time  (seconds,  minutes,  or  longer  intervals)  in  paroxysms  of  sharp, 
stabbing,  lightning-like  aching  or  boring  pain,  which  is  limited  to  the 
area  of  distribution  of  a  nerve  or  group  of  nerves.  '  Usually  there  is  also 
hyperesthesia  over  this  area,  and  painful  or  tender  spots  along  the  course 
of  the  nerve;  and  there  may  be  vasomotor  alterations,  such  as  pallor  or 
flushing,  excessive  sweating,  erythema,  or  oedema,  and  trophic  changes, 
such  as  blanching  and  falling  of  the  hair.  Reflex  spasms  of  the  muscles 
in  the  painful  area  sometimes  supervene,  as  in  trigeminal  neuralgia. 
The  attack  may  last  several  minutes,  several  hours,  or  a  day  or  more,  and 
recur  at  regular  or  irregular  intervals. 

Trigeminal  neuralgia  (trifacial  neuralgia;  tic  douloureux),  a  very 
common  disorder,  may  be  symptomatic  of  carious  teeth,  eyestrain,  nasal 


NEURALGIA  809 

disease,  brain  tumor,  etc.,  or  it  may  occur  as  an  apparently  primary  dis- 
order of  unknown  cause.  The  pain,  which  is  often  extremely  severe, 
may  be  limited  to  any  one  of  the  three  great  divisions  of  the  nerve  (the 
ophthalmic,  the  superior  and  the  inferior  maxillary),  but  it  may  involve 
all  three;  it  is  rarely,  if  ever,  bilateral.  Cutaneous  hyperesthesia  is 
usually  present,  painful  or  tender  spots  are  commonly  found  where 
the  nerve  emerges  from  the  foramina,  and  the  eyebrows  and  the  hair 
are  likely  to  become  gray  or  fall  out.  The  paroxysms  may  be  set  up 
by  various  sorts  of  stimuli,  such  as  a  draught  of  cold  air,  touching  the 
hyperesthetic  area,  the  movements  of  chewing,  speaking,  etc. ;  they  tend 
to  increase  in  severity  and  the  intervals  to  lessen;  and  associated  spasm 
of  the  facial  muscles  may  supervene  (facial  spasm). 

Cervicooccipital  neuralgia  occurs  in  the  back  of  the  head,  in  the  area  of 
distribution  of  the  first  four  cervical  nerves;  it  may  be  confined  to  the 
posterior  branches.  There  is  often  a  tender  spot  midway  between  the 
mastoid  process  and  the  first  cervical  vertebra  where  the  great  occipital 
nerves  emerge,  between  the  trapezius  and  the  sternomastoid  muscle, 
and  above  the  parietal  eminence.  The  scalp  is  usually  markedly  hyper- 
esthetic. 

Cervicohrachial  neuralgia  occurs  in  the  shoulder  and  arm,  in  the  area  of 
distribution  of  the  four  lowest  cervical  and  the  first  thoracic  nerves 
(brachial  plexus).  Tender  spots  may  be  found  at  the  posterior  border  of 
the  deltoid  muscle  (circumflex  nerve),  over  the  musculospiral  nerve  near 
the  outer  condyle  of  the  humerus,  over  the  ulnar  nerve  in  the  groove 
between  the  inner  condyle  and  the  olecranon  process,  and  over  the  ulnar 
and  the  radial  nerves  at  the  wrist. 

Phrenic  neuralgia  sometimes  follows  pleurisy  or  pericarditis,  and  only 
very  rarely  occurs  as  a  primary  disorder.  The  pain  occurs  at  the  lower 
part  of  the  chest,  in  the  neighborhood  of  the  attachment  of  the  diaphragm, 
and  is  aggravated  by  deep  inspiration,  coughing,  sneezing,  and  other 
sudden  or  violent  movements  of  the  diaphragm. 

Intercostal  neuralgia  is  very  common.  The  pain  follows  the  course  of 
the  intercostal  nerves,  and  is  often  continuous,  though  subject  to  acute 
exacerbations.  Painful  spots  are  common  near  the  vertebrae,  where  the 
posterior  branches  emerge;  in  the  midaxilla,  where  the  lateral  branches 
reach  the  surface;  and  toward  the  anterior  midline,  where  the  anterior 
branches  reach  the  surface.  The  most  intractable  intercostal  neuralgia 
(as  well  as  other  neuralgias)  may  follow  herpes  zoster. 

Lumbar  neuralgia  occurs  in  the  area  of  distribution  of  the  sensory 
fibers  of  the  sacral  plexus,  and  is  most  common  along  the  crest  of  the 
ilium,  in  the  inguinal  region,  and  in  the  genitalia  (scrotum  and  labia). 

Coccygodijnia,  a  neuralgia  of  the  coccygeal  plexus,  is  common  in 
women.  The  pain  may  be  more  or  less  constant  and  intractable,  and  is 
usually  aggravated,  or  at  least  induced,  by  the  sitting  posture. 

Sciatica  may  be  a  neuralgia,  although  it  may  result  also  from  neuritis, 
pressure  of  tumors,  enlarged  lymph  nodes,  sacro-iliac  disease,  etc.  The 
pain,  which  is  often  severe,  may  extend  throughout  the  course  of  the 


810  DISEASES  OF  THE  NERVES 

nerve  and  into  its  branches  in  the  leg.  Hyperesthesia  is  usually  present, 
and  painful  spots  may  be  found  at  the  sciatic  notch,  in  the  popliteal  space, 
and  at  the  outer  edge  of  the  fibula.  There  is  usually  pain  and  difficulty  in 
walking,  and  the  common  attitude  in  standing  and  walking  (throwing  the 
weight  on  the  unaffected  side)  may  lead  to  lateral  curvature  of  the  spine. 

Meralgia  jpcu'cesthetica  is  a  neuralgia  (or  neuritis)  of  the  external 
cutaneous  nerve  that  gives  rise  to  painful  paresthetic  phenomena  on  the 
outer  side  of  the  thigh,  and  sometimes  also  some  anesthesia. 

Plantar  neuralgia  may  occur  in  the  tips  of  the  toes,  or  it  may  be  more 
widespread.     It  is  rather  common  in  typhoid  fever. 

Painful  heel  (pododynia)  may  be  a  pure  neuralgia,  but  in  some  cases 
it  results  from  definite  exostoses  and  infiltrations  of  the  plantar  fascia. 
They  are  not  uncommon  after  gonococcic  infection,  and  may  be  demon- 
strated by  the  ic-rays.     Pains  in  the  feet  also  are  often  due  to  flat  foot. 

Metatarsalgia,  Morton's  painful  affection  of  the  foot,  is  usually  attrib- 
uted to  compression  of  the  metatarsal  nerve  (usually  about  the  fourth 
metatarsal  phalangeal  joint). 

Visceral  neuralgias  are  sometimes  described,  such  as  cardialgia,  gas- 
tralgia,  hepatalgia,  nephralgia,  etc.,  but  these  painful  affections  usually 
have  an  anatomical  basis. 

Diagnosis. — Neuralgia  should  be  distinguished  from  definite  neuritis. 
In  neuralgia  there  is  no  discoverable  cause  for  the  pain;  the  pain  is  usu- 
ally unilateral,  corresponds  with  the  area  of  distribution  of  a  nerve,  and 
is  characteristically  paroxysmal  and  intermittent;  there  is  no  noteworthy 
anesthesia  (rather  hyperesthesia),  no  muscular  wasting,  and  no  reactions 
of  degeneration;  in  neuritis  there  is  early  and  usually  marked  tender- 
ness along  the  nerve  trunks.  The  pains  of  tabes  dorsalis,  of  gummas, 
and  of  inflammation  of  the  meninges  should  not  be  mistaken  for  neuralgia. 

Prognosis. — The  neuralgias  of  general  ill  health  and  anemic  states 
usually  disappear  with  the  causative  factors.  Trigeminal  neuralgia, 
sciatica,  and  the  pain  following  herpes  zoster,  etc.,  may  continue,  for  a 
long  time — sometimes  indefinitely. 

Treatment. — Possible  causative  factors  must  be  searched  for,  such  as 
carious  teeth,  refractive  errors,  nasal  disease,  pressure  of  tumors,  anemia, 
nervous  exhaustion,  gout,  etc.,  and,  when  found,  these  must  be  appro- 
priately treated.  Iron  and  arsenic  are  useful  in  any  event;  in  some 
cases  also  phosphorus,  cod-liver  oil,  and  strychnine.  Quinine  is  of  value 
in  cases  definitely  malarial,  and  perhaps  in  some  other  cases,  for  its  bitter 
tonic  properties.  The  iodides  sometimes  render  service  in  chronic  cases 
and  in  those  associated  with  arteriosclerosis,  gout,  etc.  Alkalies,  such  as 
sodium  benzoate,  ammonium  chloride,  etc.,  gelsemium,  and  cannabis 
indica  also  have  been  recommended,  as  well  as  injections  of  alcohol  into 
the  nerve.  Otherwise,  the  treatment  is  largely  that  of  pain:  hot  applica- 
tions, freezing  the  skin  (ether  or  rigoline  spray),  the  Paquelin  cautery, 
blistering,  the  application  of  equal  parts  of  camphor,  chloral,  and  menthol, 
and  galvanism  locally;  and  the  internal  use  of  the  coal-tar  analgesics 
(acetphenetidin,  acetanilide,  etc.).     These,  as  well   as   preparations  of 


NEURITIS  811 

opium,  should  be  used  with  the  greatest  caution,  since  the  common 
intractabihty  of  neuralgia  is  likely  to  lead  to  the  formation  of  a  drug 
habit.  In  many  cases  surgical  treatment  must  eventually  be  resorted 
to — resection  of  the  nerve  (or  of  the  Gasserian  ganglion  in  trigeminal 
neuralgia). 

NEURITIS. 

Etiology. — Neuritis  may  be  acute  or  chronic,  and  it  may  involve  one 
or  many  nerves — mononeuritis  or  multiple  neuritis.  Single  or  mono- 
neuritis may  be  due  to  traumatism,  to  the  action  of  cold,  or  to  extension 
of  inflammation  from  adjacent  parts,  as  facial  neuritis  in  middle-ear 
disease  and  caries  of  the  temporal  bone.  Multiple  neuritis  may  be  due 
to  infections  (diphtheria,  typhoid  fever,  pyococcic  infections,  leprosy, 
etc.),  and  those  factors  associated  with  "catching  cold"  and  exposure 
(acute  febrile  polyneuritis);  exogenous  intoxications,  such  as  alcohol, 
lead,  arsenic,  and  mercury,  and  that  associated  with  beri-beri;  endog- 
enous intoxications  associated  with  gout,  diabetes,  nephritis,  intestinal 
auto-intoxications,  etc. ;  anemic  and  cachectic  states. 

Pathology. — In  general  the  lesions  are  those  of  inflammation  (conges- 
tion, oedema,  and  cellular  infiltration),  fragmentation  of  the  myelin 
sheaths,  and  parenchymatous  swelling  and  ultimate  fatty  and  granular 
degeneration  of  the  nerve  fibers.  The  lesions  may  be  superficial,  chiefly 
perineural,  or  they  may  penetrate  to  the  deeper  parts — so-called  inter- 
stitial neuritis.  In  some  cases  (so-called  parenchymatous  neuritis)  the 
axons  are  chiefly  involved,  showing  degenerative  changes  alike  to  those 
that  follow  isolation  of  the  axon  from  the  cell  body.  The  cell  bodies  also 
may  reveal  changes  showing  that  the  etiological  factor  tends  to  involve 
the  entire  lower  motor  neuron. 

Symptoms. — Since  most  of  the  peripheral  nerves  carry  motor,  sensorv, 
and  trophic  fibers,  the  symptoms  of  neuritis  may  be  also  motor,  sensorv, 
and  trophic.  In  single  or  mononeuritis  the  chief  complaint  is  usually 
of  pain  in  the  course  of  the  nerve  and  in  its  area  of  distribution.  In 
addition  there  is  usually  hyperesthesia  and  perhaps  hyperalgesia  or 
paresthesia  of  the  overlying  skin;  in  some  cases  also  patches  of  hypesthesia 
or  anesthesia,  or  sometimes  erythema  or  oedema.  Furthermore,  there  is 
loss  of  power  of  the  muscles,  which  soon  become  flabby,  wasted,  and 
tender  (especially  on  motion  or  pressure),  and  reveal  fibrillary  twitchings 
and  the  reactions  of  degeneration.  The  reflexes  become  lessened  and 
may  disappear.  The  involved  nerve,  if  accessible  to  palpation,  is  found 
swollen  and  tender.  In  protracted  cases,  in  addition  to  the  foregoing, 
more  or  less  marked  trophic  changes  occur:  the  skin  becomes  thin, 
smooth,  red,  and  shiny  or  glossy;  the  tips  of  the  fingers  become  pointed 
(from  atrophy  also  of  the  subcutaneous  tissues) ;  the  nails  and  the  hair 
grow  irregularly;  and  the  joints  may  become  stifl"  and  immobile. 

In  multijde  neuritis,  since  the  poison  is  carried  by  the  blood,  the  lesions 
are   widespread   and   usually    symmetrically   bilateral.     In    the   acute 


812  DISEASES  OF  THE  NERVES 

febrile  (infectious  or  toxic?)  cases  the  onset,  following  cold  or  exposure, 
may  be  sudden,  and  attended  by  a  chill  or  chilliness,  fever  (103°  to  104°), 
pains  and  tenderness  of  the  limbs,  and  loss  of  muscular  power.  The 
other  symptoms  mentioned  under  mononeuritis  develop,  but  are  wide- 
spread, and  the  patient  is  usually  totally  incapacitated. 

The  alcoholic  (the  most  common)  cases  usually  begin  with  paresthesia 
(tingling  or  numbness)  and  hyperesthesia,  especially  in  the  legs,  and  these 
may  be  associated  with  tenderness  of  the  calf  muscles.  Soon  weakness  of 
the  muscles  of  the  legs,  especially  of  the  anterior  tibial  group,  develops; 
this  leads  to  ''foot-drop"  and  to  a  characteristic  high-steppage  gait. 
There  is  also  atrophy  of  the  muscles,  loss  of  the  knee-jerk  and  the  plantar 
reflex,  the  reactions  of  degeneration,  incoordination  (loss  of  muscle  sense), 
and  other  phenomena  mentioned  under  mononeuritis.  In  advanced  cases 
walking  finally  becomes  impossible  (complete  paralysis),  and  areas  of 
anesthesia  (stocking-and-glove,  or  cuff  forms)  supplant  the  hyperesthesia. 
The  arms  maybe  involved,  but  less  commonly  and  less  severely.  Although 
the  cranial  nerves  usually  escape,  vision  may  become  impaired,  optic 
neuritis  may  occur,  and  involvement  of  the  phrenic  nerve  (paralysis  of  the 
diaphragm)  or  of  the  vagus  nerve  (tachycardia)  may  ensue.  Mental 
phenomena  are  not  uncommon  in  aggravated  cases,  such  as  loss  of  mem- 
ory, hallucinations,  mental  deterioration,  and  delirium.  Some  chronic 
alcoholic  subjects  exhibit  the  combination  of  multiple  peripheral  neuritis, 
loss  of  memory,  and  pseudoreminiscences  (false  notions  as  to  time, 
place,  and  actualities) — a  condition  spoken  of  as  Korsakoff's  psychosis. 

The  arsenical  cases  much  resemble  the  alcoholic;  the  legs  are  usually 
involved  first,  but  the  arms  may  become  implicated  later,  and  there  is 
usually  also  a  brownish  pigmentation  of  the  skin.  In  the  cases  due  to 
lead  the  extensors  of  the  wrist  and  hand  are  most  likely  to  become  in- 
volved (wrist-drop),  and  the  other  symptoms  mentioned  on  page  295 
develop.  In  the  diphtheritic  cases  the  muscles  of  the  palate  are  com- 
monly involved  and  lead  to  regurgitation  of  food  through  the  nose;  but 
the  external  muscles  of  the  eye  may  become  affected  or  the  disorder 
may  become  widespread. 

Diagnosis. — ^The  diagnosis  is  usually  apparent  from  the  mentioned 
symptoms.  The  neural  distribution  of  the  motor  and  sensory  symp- 
toms, tenderness  of  the  nerve  trunks  and  the  muscles,  the  bilateral 
symmetry  of  the  phenomena  in  the  multiple  neuritis  cases,  and  the 
absence  of  involvement  of  the  sphincters  of  the  bladder  and  the  rectum 
and  of  the  Argyll  Robertson  pupil  usually  serve  to  exclude  spinal-cord 
disease. 

Prognosis. — ^The  outlook  in  general  is  good,  gradual  improvement 
occurring  in  most  cases  after  the  lapse  of  several  weeks  or  months.  Re- 
covery, however,  may  not  be  complete,  and  death  may  ensue  from  com- 
plications, such  as  bronchopneumonia. 

Treatment. — ^The  causative  factor  must  first  be  entirely  eliminated — 
especially  alcohol,  arsenic,  lead,  gastro-intestinal  autotoxemia,  etc.  Rest 
and  good  nutritious  food  are  essential  in  all  cases,  and  care  must  be 


HERPES  ZOSTER  813 

exercised  that  deformities  do  not  ensue.  The  initial  pains  may  be  re- 
lieved by  local  applications,  such  as  hot  fomentations,  saturated  solu- 
tions of  magnesium  sulphate,  liniments  containing  chloroform,  bella- 
donna, etc.,  and  by  the  internal  use  of  salicyl  preparations  or  small 
doses  of  acetphenatidin  and  other  coal-t&r  derivatives.  After  the  acute 
manifestations  have  subsided,  resort  should  be  had  to  massage,  passive 
movements,  and  galvanism  to  maintain  the  nutrition  of  the  muscles,  and 
the'  patient  should  be  encouraged  to  attempt  voluntary  movements. 
Strychnine  in  large  doses  is  useful  in  many  cases,  and  iron,  quinine,  cod- 
liver  oil,  and  other  tonics  in  the  anemic  cases. 


HERPES  ZOSTER. 

Herpes  zoster  is  an  acute,  probably  specific,  infectious  inflammation 
and  degeneration  of  the  ganglia  of  the  posterior  spinal  roots  and  of  the 
homologous  ganglia  of  the  sensory  cranial  nerves,  characterized  clinically 
by  fever,  and  by  pain,  erythema,  and  an  herpetic  eruption  in  the  area  of 
distribution  of  one  or  more  of  these  roots. 

Etiology. — Head  and  Campbell  seem  to  have  proved  that  herpes 
zoster  is  an  acute  specific  infectious  disease,  involving  especially  the  pos- 
terior spinal  roots  and  ganglia,  but  the  infectious  agent  has  not  been  deter- 
mined. The  disorder  also  sometimes  develops  secondarily  to  tubercu- 
losis of  the  vertebrse,  meningitis,  etc. 

Pathology. — ^The  chief  lesions  consist  of  inflammatory  foci,  with  ne- 
croses and  hemorrhages  involving  the  affected  ganglion  and  its  sheath. 
Many  ganglion  cells  are  destroyed,  and  in  consequence  their  axons  and 
dendrons  in  the  peripheral  nerves  and  the  spinal  cord  undergo  sec- 
ondary atrophy.  The  disease  in  many  respects  is  the  sensory  analogue 
of  acute  poliomyelitis.  The  facial  herpes  of  pneumonia  and  other  infec- 
tions is  an  analogous  condition  (involvement  of  the  Gasserian  ganglion). 

Symptoms. — ^The  onset  may  be  abrupt,  with  fever,  malaise,  gastro- 
intestinal disturbances,  perhaps  enlargement  of  the  lymph  nodes,  etc. 
Usually  on  the  third  or  fourth  day,  and  often  preceded  by  pain  and  ten- 
derness of  the  skin,  an  herpetic  (or  vesicular)  eruption  breaks  out.  This 
is  most  common  on  the  trunk  (intercostal  nerves)  and  is  usually  unilateral ; 
it  is  confined  to  the  area  of  distribution  of  one  or  more  posterior  spinal 
roots  (segmental  distribution),  and  it  is  especially  characterized  by  a 
patchy  distribution  of  the  vesicles  corresponding  to  the  posterior,  lateral, 
and  anterior  division  or  distribution  of  the  nerves.  At  the  end  of  a  week 
or  ten  days  the  vesicles  usually  dry  up.  Small  depressed  scars  com- 
monly persist;  sometimes  also  a  postherpetic  pain  and  various  sensory 
disturbances,  and  occasionally  a  most  intractable  neuralgia.  Transient 
motor  paralysis  may  be  observed,  especially  of  the  muscles  of  the  facial 
nerve  innervation  in  trigeminal  or  occipito-cervical  nerve  herpes  (com- 
pression of  the  facial  nerve  by  a  swollen  geniculate  ganglion,  Ramsey 
Hunt). 


814  DISEASES  OF  THE  NERVES 

Treatment. — The  early  pain  may  be  relieved  by  coal-tar  derivatives, 
salicyl  preparation,  or  opium.  Zinc  stearate  or  similar  dusting  powder, 
or  a  mild  antiseptic  ointment  may  be  applied  locally.  Intractable  neu- 
ralgia, if  not  otherwise  relieved,  may  necessitate  division  of  the  posterior 
spinal  roots  involved  or  removal  or  isolation  of  the  homologous  cranial 
nerve  ganglion. 

NEUROMAS. 

Neuromas  may  be  true  or  false.  The  true  neuroma  is  a  tumor  made  up 
of  nerve  fibers,  and  sometimes  also  of  ganglion  cells ;  it  is  a  rare  growth. 
The  false  neuromas  are  of  divers  sorts:  (1)  Various  forms  of  fibromas, 
myxomas,  or  sarcomas  that  may  develop  from  the  connective  tissues  of 
the  nerves,  and  usually  give  rise  to  fusiform  swellings.  (2)  The  so-called 
amputation  neuromas — painful,  bulbous  enlargements  of  the  ends  of 
divided  nerves.  They  are  common  in  stumps  after  amputations,  and 
consist  of  a  mass  of  axons  growing  peripherally — supposedly  with  a  view 
to  reach  their  normal  endings.  (3)  Plexiform  neuromas — a  condition, 
often  hereditary '  and  congenital,  consisting  of  multiple  fibrous  tissue 
growths  that  may  involve  almost  if  not  quite  all  the  nerves  of  the  body. 
More  than  a  thousand  of  these  tumors  have  been  found  in  a  single  case. 
(4)  Generalized  neurofibromatosis  (yon  Recklinghausen's  disease),  a  con- 
dition consisting  of:  tumors  along  the  nerves  akin  to  those  of  the  plexi- 
form neuroma;  various  motor  and  sensory  phenomena  depending  upon 
the  situation  of  these  growths;  distorted  mentality,  consisting  especially  of 
general  failure  of  intellectuality  and  disorders  of  speech;  soft,  sessile,  or 
pedunculated  growths  of  the  skin  (neurofibromatosis  of  the  skin;  mol- 
luscum  fibrosum;  so-called  elephantiasis  neuromatosa,  when  of  great 
size);  and  areas  of  brownish  pigmentation  of  the  skin.  (5)  Tubercula 
dolorosa,  small,  painful,  multiple  neuromas  involving  the  cutaneous  ter- 
minations of  the  sensory  nerves,  and  found  especially  in  the  breast,  on 
the  face,  or  about  the  joints.  (6)  Dejerine's  interstitial  hypertrophic 
progressive  neuritis  of  childhood  (thickening  of  the  nerves,  with  general 
muscular  atrophy  and  the  symptoms  of  tabes  dorsalis;  page  856). 


DISEASES  OF  THE  CRANIAL  NERVES. 

I.  Olfactory  Nerve. — ^The  olfactory  nerve  may  become  diseased  in 
the  terminal  cells,  in  the  olfactory  mucous  membrane,  in  the  cells  in  the 
olfactory  bulb,  in  the  olfactory  tracts,  or  in  the  cortical  cells  in  the  unci- 
nate convolution.  The  disorders  consist  of :  (1)  Anosmia  or  hypoosmia 
(loss  of  the  sense  of  smell),  which  may  occur  in  chronic  nasal  catarrh, 
disease  of  the  bulb  or  tracts  (injuries,  meningitis,  etc.),  central  disturb- 
ance, or  hysteria  (usually  unilateral);  (2)  hyperosmia,  which  is  com- 
monly observed  in  hysterical  and  neurasthenic  women;  and  (3)  par- 
osmia—perversion  or  hallucinations  of  smell — which  may  occur  after 


DISEASES  OF  THE  CRANIAL  NERVES  815 

injuries,  in  tumors  of  the  uncinate  convolution,  in  the  insane,  and  may 
constitute  the  aura  of  epilepsy. 

II.  Optic  Nerve. — Functional  Disorders. — Functional  disorders  of  the 
retina  are  sometimes  observed,  such  as  hyperesthesia,  which  is  occa- 
sionally seen  in  hysterical  women  and  in  the  early  stages  of  meningitis 
(photophobia);  night  blindness — nyctalopia,  good  vision  in  a  strong  light 
and  poor  vision  in  twilight;  and  hemeralopia,  good  vision  in  twilight 
and  poor  or  painful  vision  in  a  bright  light;  hysterical  amblyopia  or 
amaurosis,  which  is  encountered  in  hysterical  subjects;  and  toxic 
amblyopia  or  amaurosis,  which  may  be  due  to  tobacco,  lead,  quinine,  etc. 
In  the  toxic,  especially  tobacco,  cases  there  is  gradual  bilateral  impair- 
ment of  sight,  especially  centrally  and  for  colors  (central  scotoma  for  red 
and  green).  In  advanced  cases  a  retrobulbar  neuritis  may  ensue,  with 
atrophy  of  the  macular  bundle  and  of  the  disk. 

Neuroretinitis. — Neuroretinitis  is  common  in  chronic  nephritis,  severe 
anemic  conditions,  and  leukemia,  and  it  may  be  observed  also  in 
syphilis,  malaria,  diabetes,  lead  poisoning,  etc.  The  chief  lesions  consist 
of  hemorrhages  and  opacities  of  the  retina.  The  disorder  may  be  well 
advanced  before  there  is  any  notable  impairment  of  vision. 

Optic  Neuritis;  Papillitis;  Papillcedema ;  Choked  Disk. — Papilloedema  is 
sometimes  seen  in  chronic  nephritis,  severe  anemic  states,  etc.,  in  which 
it  is  usually  associated  with  neuroretinitis;  but  it  is  especially  significant 
of  increased  intracranial  pressure,  and  is  therefore  most  common  in 
brain  tumors  (at  least  90  per  cent,  of  the  cases),  brain  abscess,  and  men- 
ingitis (in  which  it  may  be  due  to  extension  of  the  inflammation).  The 
lesions  are  usually  bilateral,  and  consist  of  congestion  and  swelling  of  the 
disk,  blurring  of  its  edges,  and  filling  of  the  physiological  cup.  Often 
there  is  an  associated  neuroretinitis.  The  process  may  subside,  but  optic 
atrophy  is  the  common  sequel.  The  early  stages  of  the  disorder  are  to 
be  recognized  only  by  ophthalmoscopic  examination,  since  considerable 
progress  may  be  made  before  there  is  notable  impairment  of  vision. 

Optic  Atrophy. — Optic  atrophy  may  occur  secondarily  to  the  causes 
that  set  up  papillitis.  Primarily  it  occurs  as  (1)  a  congenital,  family 
disease  (Leber's  disease),  most  common  in  adolescent  males,  but  usually 
transmitted  by  the  females;  and  (2)  in  tabes  dorsalis,  paretic  dementia, 
and  sometimes  in  other  nervous  disorders.  The  lesions  consist  of 
gradually  increasing  pallor  of  the  disk,  with  a  well-defined  edge,  which 
in  the  secondary  form  may  be  irregular  in  outline;  the  artery  may  ap- 
pear normal  or  become  small.     The  symptom  is  gradual  failure  of  vision. 

The  Optic  Chiasm. — ^The  chiasm  is  most  frequently  disordered  by 
tumors  of  the  brain,  especially  of  the  pituitary  body  (akromegaly).  The 
fibers  that  supply  the  inner  half  of  each  retina  (temporal  field  of  vision) 
are  commonly  first  involved,  so  that  the  symptom  is  double  temporal 
hemianopia.  Eventually,  with  progress  of  the  disease,  total  blindness 
may  ensue.  Rarely  two  symmetrically  situated  tumors  may  implicate 
the  fibers  proceeding  to  the  outer  half  of  each  retina  (nasal  field  of 
vision)  and  bilateral  nasal  hemianopia  may  ensue. 


816  DISEASES  OF  THE  NERVES 

The  Optic  Tract  and  Centre. — Disease  of  the  optic  tract  between  the 
chiasm  and  the  cortex  (cuneate  portion  of  the  occipital  lobe)  results  in 
failure  of  vision  of  the  temporal  half  of  the  retina  of  the  corresponding 
side  and  of  the  nasal  half  of  the  retina  of  the  other  side  (partial  or  com- 
plete homonymous  hemianopia).  The  lesion  may  be  in  the  fore  part  of 
the  optic  tract,  in  or  about  the  thalamus,  the  lateral  geniculate  body,  the 
corpora  quadrigemina,  the  posterior  part  of  the  internal  capsule,  the  optic 
radiation,  or  the  cuneus.  Disease  of  the  supramarginal  and  angular 
gyrus  may  result  in  crossed  amblyopia  (concentric  diminution  of  both 
fields  of  vision,  usually  more  marked  on  the  side  opposite  the  lesion)  and 
visual  aphasia  (word  blindness,  mind  blindness).  Resort  to  Wer- 
nicke's hemiopic  pupillary  reaction  may  enable  one  to  determine  whether 
the  lesion  is  in  advance  of  or  posterior  to  the  corpora  quadrigemina:  if 
throwing  a  bright  light  into  the  blind  half  of  the  retina  results  in  con- 
traction of  the  pupil,  it  shows  integrity  of  the  reflex  arc  (the  optic  nerve 
fibers,  the  centre  for  the  pupil,  and  the  third  nerve),  and  the  lesion  is  there- 
fore in  the  optic  radiation  or  the  visual  centre  in  the  cuneus.  Hemi- 
anopia usually  means  an  organic  lesion;  rarely  it  may  be  found  in 
hysterical  disorders.     Various  sorts  of  aphasia  may  be  associated  with  it. 

III.  Oculomotor  Nerve;  IV.  Trochlear  Nerve;  VI.  Abducens 
Nerve. — ^The  third  nerve  supplies  the  superior,  internal  and  inferior 
recti,  and  the  inferior  oblique  muscles  of  the  eyeball,  as  well  as  the  levator 
palpebree  superioris,  the  ciliary  muscle,  and  the  constrictor  of  the  iris. 
The  fourth  nerve  supplies  the  superior  oblique,  and  the  sixth  nerve  the 
external  rectus  muscles.  The  dilator  of  the  iris  is  innervated  by  the 
sympathetic.  Paralysis  of  the  third  nerve  results  in  ptosis,  wrinkling  of 
the  forehead  (to  compensate  for  the  lost  power  of  the  levator  palpebrse), 
divergent  strabismus,  diplopia,  and  a  fixed  and  dilated  pupil  (cycloplegia) 
inactive  to  light  and  accommodation  (iridoplegia).  The  eyeball  is 
pulled  outward  by  the  active  external  rectus,  and  may  be  moved  slightly 
downward  and  inward  by  the  active  superior  oblique.  Paralysis  of  the 
fourth  nerve  results  in  diplopia,  especially  when  the  patient  looks  down- 
ward, and  perhaps  deficient  downward  and  inward  movement  of  the 
eyeball  (usually  slight  and  unnoticed).  Paralysis  of  the  sixth  nerve 
results  in  deficient  movement  of  the  eyeball  outward  or  internal  stra- 
bismus, and  diplopia  when  the  patient  looks  outward  toward  the  aftected 
side. 

The  diplopia  that  results  from  paralysis  of  the  ocular  muscles 
may  be  homonymous  (simple)  when  the  false  image  (that  seen  by  the 
affected  eye)  is  on  the  same  side  as  the  paralyzed  eye  (usual  in  convergent 
strabismus) ;  or  the  diplopia  may  be  crossed,  when  the  false  image  is  seen 
on  the  other  side  of  the  true  image  (usual  in  divergent  strabismus).  In 
addition  to  restriction  of  movements  of  the  eyeball,  strabismus,  and 
diplopia,  paralysis  of  the  ocular  muscles  usually  leads  to  (a)  secondary 
deviation  of  the  sound  eye,  which  may  be  demonstrated  by  covering  the 
sound  eye  and  directing  the  patient  to  fix  on  an  object  with  the  paralyzed 
eye  toward  the  direction  of  paralysis;  upon  uncovering  the  sound  eye, 


DISEASES  OF  THE  CRANIAL  NERVES  817 

it  will  be  seen  to  have  been  moved  farther  in  the  direction  of  fixation  than 
the  paralyzed  eye,  on  account  of  the  greater  response  to  an  equal  inner- 
vation on  the  part  of  the  normal  muscles  of  the  non-paralyzed  eye;  and 
(6)  erroneous  projection  of  the  field  of  vision. 

Occasionally,  from  overstimulation  in  hysterical  states,  in  meningitis, 
etc.,  spasm  of  the  ocular  muscles  may  be  observed.  Nystagmus,  a  clonic, 
usually  bilateral  spasm  of  the  ocular  muscles,  causing  involuntary, 
rhythmic,  oscillatory  movements  of  the  eyeballs,  occurs  in  Friedreich's 
ataxia,  multiple  sclerosis,  and  other  diseases  of  the  nervous  system,  in 
nodding  spasms  of  children,  in  miners,  etc. 

Ophthalmoplegia. — Disease  of  the  nuclei  of  the  ocular  nerves  results  in 
the  condition  called  ophthalmoplegia  (nuclear  ocular  palsy),  which  is 
discussed  on  page  851. 

V.  Trigeminal  Nerve.— The  fifth  nerve  is  made  up  of  motor  fibers 
which  supply  the  muscles  of  mastication,  and  sensory  fibers  which, 
through  the  medium  of  its  three  great  branches  (ophthalmic,  superior  and 
inferior  maxillary),  supply  half  of  the  face  and  the  anterior  portion  of  the 
head,  the  conjunctiva,  orbit,  eyeball,  nose,  nasal  cavity,  lips,  teeth, 
mouth,  hard  and  soft  palate,  and  anterior  two-thirds  of  the  tongue.  Some 
observers  also  believe  that  the  nerve  conveys  special  taste  fibers  to  the 
anterior  two-thirds  of  the  tongue.  Paralysis  of  the  motor  portion  of  the 
nerve  gives  rise  to  loss  of  power  of  mastication  on  the  affected  side,  in- 
ability to  move  the  jaw  toward  the  sound  side  (pterygoid  muscle),  and 
deviation  of  the  jaw,  when  depressed,  toward  the  paralyzed  side.  Irri- 
tation of  this  motor  portion  gives  rise  to  spasm  of  the  muscles  of  masti- 
cation (trismus),  w^hich  may  be  tonic  (as  in  tetanus,  tetany,  hysteria, 
reflex  local  irritation)  or  clonic  (as  in  "chattering  teeth,"  chorea,  etc.). 
Disease  of  the  sensory  portion  of  the  nerve  (including  the  Gasserian 
ganglion)  may  give  rise  to :  (1)  Neuralgia,  which  usually  involves  one  of 
the  three  great  divisions,  sometimes  all  three,  and  is  often  intractable 
(tic  douloureux);  (2)  neuritis  and  herpes  zoster;  (3)  anesthesia  of  part 
or  all  the  area  of  distribution;  and  (4)  nutritional  or  trophic  disorders, 
such  as  lessening  of  the  lacrymal  secretions  (to  which  conjunctivitis  and 
ulceration  of  the  cornea  may  be  due)  ai;id  of  the  salivary  and  buccal 
secretions,  facial  hemiatrophy,  etc.  Some  observers  believe  that  loss  of 
the  sense  of  taste  over  the  anterior  two-thirds  of  the  tongue  follows  disease 
of  the  fifth  nerve,  but  the  available  evidence  is  not  conclusive. 

VII.  Facial  Nerve. — ^The  facial  nerve  innervates  the  muscles  of  the 
face;  perhaps  it  contains  also  some  sensory  fibers  (geniculate  ganglion 
and  nerve  of  Wrisberg — Hunt).  Paralysis  of  the  nerve  may  be  central 
or  peripheral. 

Central  Facial  Paralysis. — The  central  case  may  be  due  to  disease  of  (1) 
the  nuclei  in  the  pons ;  this  occurs  in  tumors,  hemorrhage,  and  softening, 
and  is  usually  associated  with  disease  of  adjacent  nuclei;  or  (2)  the 
fibers  above  the  nuclei  in  the  pons,  the  peduncle,  the  corona  radiata, 
the  internal  capsule,  or  the  cortex.  This  is  usually  a  part  of  licnii])legia, 
and  is  due  to  like  cause — hemorrhage,  softening,  tumors,  abscess,  etc.; 
52 


818  DISEASES  OF  THE  NERVES 

rarely  the  facial  nerve  may  be  involved  alone  (internal  capsule  or  cor- 
tical disease).  This  central  paralysis  differs  from  the  peripheral  type 
in  the  common  freedom  of  the  upper  branches  of  the  nerve  (so  that  the 
patient  can  wrinkle  the  forehead  and  elevate  the  eyebrow) ;  in  the  preser- 
vation of  the  normal  electrical  reactions  of  the  nerve  and  muscles;  and 
in  the  much  less  impairment  of  the  emotional  movements  (laughing, 
crying)  as  contrasted  with  the  voluntary  movements  of  the  facial 
muscles. 

Peripheral  Facial  Paralysis  (Bell's  Palsy). — Peripheral  facial  paralysis 
may  result  from  (1)  disease  of  the  pons,  usually  tumors,  softening,  or 
inflammatory  processes;  or  the  paralysis  may  be  part  of  a  hemiplegia,  in 
which  event  it  comprises  a  so-called  crossed  paralysis — involvement  of 
the  face  on  the  side  of  the  lesion  (the  facial  fibers  have  already  decus- 
sated) and  involvement  of  the  arm  and  leg  on  the  opposite  side;  (2) 
disease  at  the  cerebellopontine  angle,  at  the  base  of  the  brain  where 
the  nerve  emerges  from  the  pons — usually  tumors,  gummas,  tubercles, 
meningitis,  traumas;  (3)  disease  in  the  Fallopian  canal — caries  and 
inflammation,  especially  the  results  of  middle-ear  suppuration;  (4)  dis- 
ease outside  the  st34omastoid  foramen — traumas,  tumors  of  the  parotid 
region,  the  influence  of  cold.  The  cases  to  which  the  term  Bell's  palsy 
is  restricted  are  commonly  attributed  to  cold  and  exposure  (doubtless 
some  infection).  The  lesions  are  inflammatory  in  nature  and  are  usually 
most  marked  within  the  Fallopian  canal,  the  unyielding  wall  of  which 
leads  to  compression  and  atrophy  of  the  nerve  fibers.  The  symptoms 
(since  the  disease  is  a  disorder  of  the  lower  motor  neuron)  consist  of 
paralysis  of  muscles  innervated  by  the  nerve,  together  with  wasting  and 
fibrillary  twitchings  of  the  muscles  and  the  electrical  reactions  of  degen- 
eration. The  face  becomes  flattened,  the  nasal  fold  obliterated,  the  angle 
of  the  mouth  drooped  (that  of  the  other  side  looks  and  may  become 
retracted),  and  there  is  inab flity  to  wrinkle  the  forehead,  to  frown,  to  close 
the  eyelids,  to  show  the  teetli,  etc.  There  may  also  be  impairment  of 
hearing  (branch  nerve  to  the  stapedius),  and  of  taste  over  the  anterior 
two- thirds  of  the  tongue  (chorda  tympani).  The  cutaneous  sensibility 
is  preserved.  Complete  recovery  is  unusual ;  secondary  contractures  are 
common.  The  treatment  comprises  the  use  of  hot  applications,  counter- 
irritation,  massage,  faradization,  the  iodides,  etc. ;  the  treatment  proper 
to  any  local  disorder  that  may  be  present;  and  in  cases  not  soon 
improved  (three  to  four  months)  anastomosis  of  the  spinal  accessory 
or  the  hypoglossal  with  the  facial  nerve. 

Facial  Spasm. — Facial  spasm  may  be  an  organic  disorder  or  it  may 
arise  reflexly  from  irritation  due  to  carious  teeth,  for  instance.  The 
spasm  may  involve  some  or  all  the  muscles  supplied  by  the  facial  nerve, 
and  may  be  unilateral  or  bilateral.  Usually  the  muscles  about  the  eye, 
or  these  and  those  of  the  side  of  the  face,  reveal  rapidly  recurring  twitch- 
ings. The  disorder  is  painless,  although  the  nerve  may  have  various 
tender  spots.  Occasionally,  as  after  paralysis,  tonic  spasms  of  the  facial 
muscles  may  ensue.     Most  of  the  cases  of  facial  spasm  last  many  years, 


DISEASES  OF  THE  CRANIAL  NERVES  819 

and  are  scarcely  curable,  although  benefit  may  follow  removal  of  sources 
of  irritation,  counterirritation,  surgical  intervention,  etc. 

VIII.— Auditory  Nerve.— The  eighth  nerve  consists  of  two  parts,  the 
cochlear  nerve,  which  connects  the  organ  of  Corti  in  the  cochlea  with  the 
temporosphenoidal  lobe  and  is  the  nerve  of  hearing;  and  the  vestibular 
nerve,  which  connects  the  vestibule  and  the  semicircular  canals  with 
cerebellar  and  other  centres  and  serves  to  maintain  equilibrium. 

Cochlear  Nerve. — Disorder  of  the  cochlear  nerve  gives  rise  to  tinnitus 
aurium;  sometimes  to  hyperacute  or  painful  hearing  (hyperacusis) ; 
most  often  to  nervous  deafness.  If  a  tuning-fork  is  not  well  heard  when 
held  near  the  auditory  meatus,  but  is  well  heard  when  placed  on  the 
temporal  bone  (the  vibrations  being  transmitted  through  the  bone  to  the 
cochlea  and  vestibule),  the  deafness  is  probably  not  nervous  (not  due  to 
disorder  of  the  nerve). 

Vestibular  Nerve;  Meniere's  Disease. — Disorder  of  the  vestibular  nerve 
is  the  cause  of  so-called  auditory  vertigo,  or  Meniere's  disease,  a  symptom 
complex,  consisting  of  tinnitus  aurium,  vertigo,  nausea,  and  vomiting, 
developing  suddenly  and  sometimes  attended  by  nervous  deafness.  The 
paroxysms  occur  irregularly — at  long  or  short  intervals.  In  addition, 
there  may  be  nystagmus,  diplopia,  ataxia,  etc.  Rarely  the  disease  is 
of  the  apoplectiform  type,  due  to  hemorrhage  in  the  labyrinth;  usually 
it  occurs  in  those  the  subjects  of  acute  or  chronic  ear  disease — of  the 
Eustachian  tube,  the  middle  ear,  or  the  internal  ear;  it  may  be  due  to 
angioneurotic  disturbances  in  the  labyrinth ;  or  attacks  may  be  provoked 
by  cerumen  in  the  auditory  canal,  syringing  the  ear,  etc.  The  prog- 
nosis in  Meniere's  disease  is  not  good.  Relief  may  be  afforded  by 
treating  any  local  source  of  irritation,  correcting  refractive  errors,  the  use 
of  bromides,  nitroglycerin  in  the  event  of  arteriosclerosis  and  high  blood 
pressure,  etc. 

IX. — Glossopharyngeal  Nerve. — ^The  ninth  nerve  supplies  motor 
fibers  to  the  stylopharyngeus  muscle  and  perhaps  the  palate,  sensory  fibers 
to  the  upper  part  of  the  pharynx,  tonsil,  soft  palate,  etc.,  and  taste 
fibers  to  the  posterior  third  of  the  tongue.  The  nerve  scarcely,  if  ever,  is 
diseased  alone,  being  intimately  related  to  the  vagus.  However,  im- 
pairment of  the  sense  of  taste  on  the  posterior  third  of  the  tongue  and 
difficulty  in  swallowing  may  be  attributed  to  it. 

X.  Pneumogastric  or  Vagus  Nerve. — The  tenth  nerve  supplies  the 
pharynx,  larynx,  lungs,  heart,  oesophagus,  and  stomach,  and  is  intimately 
associated  with  the  glossopharyngeal,  spinal  accessory,  hypoglossal,  and 
sympathetic  nerves.  Disease  of  the  nuclei  of  these  nerves  constitutes 
bulbar  paralysis.  In  paralysis  of  the  pharyngeal  branches  of  the  vagus 
(together  with  the  glossopharyngeal)  there  is  difficulty  in  swallowing, 
food  is  not  passed  on  to  the  oesophagus,  and  may  regurgitate  through  the 
nostrils.  Spasm  of  the  pharyngeal  muscles  may  be  seen  in  hysterical 
subjects,  and  is  the  obtrusive  feature  of  hydrophobia.  Paralyses  of  the 
laryngeal  branches  of  the  vagus  causes  bilateral  paralysis  (nuclear  dis- 
ease) or  unilateral  paralysis  (usually  nerve  disease)  of  the  hiryngcal 


820  DISEASES  OF  THE  NERVES 

muscles.  Bilateral  paralysis  of  the  abductors  (posterior  crico-arytenoids) 
occurs  in  central  disease  (tabes,  bulbar  paralysis),  pressure  on  the  nerves, 
hysteria,  etc.,  and  is  characterized  by  inspiratory  stridor,  more  or  less 
disordered  phonation,  and  the  cadaveric  position  of  one  or  both  vocal 
cords.  Unilateral  abductor  paralysis  follows  involvement  of  one  recur- 
rent laryngeal  nerve — usually  pressure  due  to  an  aneurysm  of  the  aorta, 
and  is  characterized  by  hoarseness  of  the  voice  and  a  brassy  cough.  Ad- 
ductor paralysis  is  occasionally  seen  in  hysteria;  the  vocal  cords  are  not 
approximated  during  attempts  at  phonation,  and  the  voice  is  lost.  Spasm 
of  the  adductor  muscles  may  occur  in  the  event  of  central  or  peripheral 
irritation,  and  is  a  marked  feature  of  laryngismus  stridulus  in  rickety 
children.  The  cardiac  branches  of  the  vagus  regulate  and  inhibit  the 
action  of  the  heart;  irritation  results  in  slowing  of  the  heart  beat,  and 
paresis  or  paralysis  (removal  of  inhibiting  influence)  results  in  accelera- 
tion of  the  beat.  The  subjective  sensations  of  the  heart  beat  are  con- 
veyed to  the  brain  by  the  vagus.  Little  is  known  regarding  disorder  of 
the  pulmonary  branches  of  the  vagus,  although  these  are  said  to  influence 
the  bronchial  musculature  and  are  perhaps  in  some  way  concerned  in  the 
paroxysms  of  bronchial  asthma.  Spasm  of  the  oesophagus,  of  the  cardia, 
and  of  the  pylorus,  vomiting,  the  gastric  crises  in  tabes,  and  other  gastro- 
intestinal disturbances  are  also  related  to  disorder  of  the  vagus. 

XL  Spinal  Accessory  Nerve. — The  eleventh  nerve,  in  part,  joins 
the  vagus  nerve  and  is  distributed  with  it;  other  fibers  innervate  the 
sternomastoid  and  the  trapezius  muscles.  Paralysis  of  this  part  of  the 
nerve  results  in  paralysis  of  the  sternomastoid  muscle  and  inability  to 
rotate  the  head  to  the  opposite  side,  and  of  the  trapezius  muscle  and 
lessened  ability  to  elevate  the  shoulder,  and  the  arm  above  the  horizontal 
position.  Complete  paralysis  of  the  trapezius  does  not  ensue,  since  it  is 
innervated  in  part  by  the  cervical  nerves.  Spasm  of  the  accessory  nerve 
results  in  wryneck  (torticollis).  This  may  be  a  congenital  (permanent) 
affection,  due  to  shortening  of  the  sternomastoid  muscle  (usually  the 
right),  and  is  often  associated  with  facial  asymmetry.  An  acquired, 
spasmodic  wryneck  is  common  in  women,  especially  hysterical  subjects; 
it  has  been  attributed  to  cold.  The  spasms  may  be  tonic  or  clonic. 
When  the  sternomastoid  is  affected  alone,  the  head  is  rotated  to  the  oppo- 
site side,  the  chin  somewhat  tilted  upward,  and  the  occiput  somewhat 
depressed;  when  the  trapezius  is  also  involved,  the  head  is  still  further 
depressed  toward  the  shoulder,  and  not  so  far  rotated.  The  contracted 
muscles  stand  out  as  prominent  tense  cords.  There  is  usually  com- 
plaint of  pain  and  stiffness  of  the  neck.  The  cases  that  develop  sud- 
denly after  a  cold  usually  recover  promptly  under  the  influence  of  hot 
applications,  massage,  and  the  salicylates  internally.  In  the  other  cases 
the  outlook  is  not  so  good  and  relapses  are  common.  Relief  may  attend 
the  use  of  the  bromides,  galvanism,  mechanical  fixation  of  the  head, 
section  of  the  contracted  muscles,  division  of  the  accessory  nerve,  etc. 

XIL  Hypoglossal  Nerve. — The  twelfth   is   the  motor  nerve  of  the 
tongue.     The  tongue  is  usually  involved  in  hemiplegia  (cortical  or  supra- 


DISEASES  OF  THE  SPINAL  NERVES  821 

nuclear  lesion).  Nuclear  lesions  occiu-  in  bulbar  paralysis,  tabes  dorsalis, 
syringomyelia,  tumors,  etc.,  and  unilateral  disorder  may  follow  tumors, 
meningitis,  etc.  The  chief  symptoms  are  unilateral  or  bilateral  paralysis, 
atrophy,  and  fibrillary  twitchings  of  the  tongue;  the  mucous  membrane 
of  the  tongue  becomes  wrinkled;  and  difficulty  is  usually  experienced  in 
pronouncing  certain  words.  Spasm  of  the  tongue  is  unusual,  but  may 
be  encountered  in  hysteria,  epilepsy,  chorea,  stuttering,  etc. 


DISEASES  OF  THE  SPINAL  NERVES. 

The  Cervical  Plexus. — Cervicooccipital  neuralgia,  involving  the 
area  of  distribution  of  the  first  four  cervical  nerves  (the  occipitoparietal 
region),  may  be  due  to  the  causes  of  neuralgia  mentioned  elsewhere 
(page  808),  or  to  local  disease  of  the  bone,  the  pressure  of  tumors,  etc. 
The  phrenic  nerve,  derived  from  the  third,  fourth,  and  fifth  cervical 
roots  (Fig.  16),  may  be  paralyzed,  in  consequence  of  disease  of  the 
spinal  cord  (anterior  horns),  meninges,  or  vertebrae;  of  compression, 
as  by  a  tumor;  or  of  neuritis,  etc.  The  symptoms  consist  of  paralysis 
(immobility)  of  the  diaphragm  (unilateial  or  bilateral,  as  the  case  may 
be);  immobility  or  retraction  of  the  upper  abdomen  during  inspiration, 
and,  perhaps,  bulging  during  expiration;  and  dyspnoea  upon  exertion. 
The  inactivity  of  the  diaphragm  may  be  readily  recognized  by  radio- 
graphic examination.  The  inaction  due  to  inflammatory  conditions, 
and  the  depression  due  to  pleural  effusion,  emphysema,  etc.,  must  be 
excluded.  Spasm  of  the  diaphragm  may  be  due  to  inflammatory  or 
other  irritative  (sometimes  so-called  neurotic)  conditions  of  the  dia- 
phragm or  phrenic  nerve;  and  when  intermittent,  is  shown  by  hiccough. 

The  Brachial  Plexus. — The  brachial  plexus  is  made  up  of  the 
fifth,  sixth,  seventh,  and  eighth  cervical  and  the  first  thoracic  roots. 
Paralysis  may  be  due  to  disease  of  the  spinal  meninges  or  the  vertebrae; 
tumors  and  other  compressing  disorders  of  the  neck;  traumatism,  such 
as  fracture  or  dislocation  of  the  vertebrae;  stretching  and  laceration  of 
the  nerves;  or  neuritis.  Since  the  root  fibers  combine  variously  to  form 
the  peripheral  nerves,  the  clinical  manifestations  of  a  root  lesion  differ 
from  those  of  a  peripheral  nerve  lesion.  The  important  clinical  condi- 
tions comprise:  (1)  Obstetrical  ur  birth  paralysis  {iippcr  arm  type  of  Erb), 
which  results  from  laceration  usually  of  the  fifth  and  sixth,  sometimes  of 
all  the  roots,  due  to  forcible  stretching  apart  of  the  head  and  shoulder 
during  birth.  Usually  the  deltoid,  biceps,  supraspinatus,  infraspinatus, 
brachialis  anticus,  and  supinator  longus  are  paralyzed  and  atrophied, 
l)ut  in  some  cases  comj^lete  motoi-  and  sensory  ])aralysis  of  the  arm  may 
occur  (laceration  of  the  entire  plexus).  (2)  Lower  arm  type,  due  to 
involvement  of  the  seventh  and  eighth  cervical  and  the  first  thoracic  roots. 
This  is  followed  by  paralysis  of  the  triceps,  pronators  and  flexors  of  the 
wrist,  the  flexors  and  extensors  of  I  he  fingers,  ;ind  the  small  nniseles  of 
the  hand.     Paralysis  of  the  small  muscles  of  the  hand,  anesthesia  in 


822 


DISEASES  OF  THE  NERVES 


the  ulnar  distribution,  and  ocular  symptoms,  due  to  disorder  of   the 
cervical  sympathetic,  together  comprise  Klumpke's  paralysis.     (3)  Cer- 


FiG.  16 


7\'.  to  recUis  lateralis 

to  rectus  antic,  minor 
Anastomosis  tvith  hyjioglossal 

AnastoTnosia  wiihpneumogastric 
N.  to  rectus  antic.  Ttiajor, 
N.  to  mastoid  region,  , 

_  Qreat  auricular  n. 
-Transverse  ceTviealn . 
-J    iS*.  to  Trapezius,  Ang.  Scaj)-  and  Bhomhoid. 

Supra  clavicular  n, 
Supra-acromial  n. 
Phrcnin  n, 

K.  to  levator  ang.  8cap. 

A',  to  rhomboid 

Subscapular  n.       , 

Subclavicular  n. 


21.  to  peetoralis  major. 


Circumjienc  n, 

Musculo-eiitcmeous  n. 
Median  n., 
.Radial  n.,^ 

Vlnafn, 

Jl IntcT^al  cutaneous  n, 

.Smalliniemal  cutaneous  i 


_^  Ilio'hypogastric  7. 
_ _Ilio-ingadnul  n . 

External 

-—  Oenito-crural 


Anterior  crural  i 

Ohturatorn. 
LS 

Superior  gluteal  n^ 

.N.to  pyri/ormis 
iV.  to  gemellus  8V2Jer. 

.N,  to  gemellus  infer. 
.N,  to  guadratus 
,Small  sciatic  n . 
.Sciatic  n . 


The  relations  of  the  segments  of  the  spinal  cord  and  their  nerve  roots  to  the  bodies  and 
spines  of  the  vertebrte.      (Starr.) 


vical  rib.     An  accessory  cervical  rib,  usually  compressing  the  seventh 
or  eighth  cervical  roots  or  the  subclavian  artery,  is  a  not  uncommon 


DISEASES  OF  THE  SPINAL  NERVES  823 

cause  of  pain  and  paresthesia  of  the  arm  and  hand,  spasm  and  atrophy 
of  the  small  muscles  of  the  hand,  local  asphyxia,  and  even  gangrene  of 
the  fingers.  The  condition  may  be  familial,  and  may  not  become 
apparent  until  adult  life.  It  is  readily  recognized  upon  radiographic 
examination,  and  is  curable  upon  removing  the  accessory  rib. 

Lesions  of  the  individual  nerves  of  the  brachial  plexus  give  rise  to 
the  following  phenomena:  (1)  The  circumflex  nerve  is  often  injured  in 
dislocation  of  the  shoulder  and  other  injuries,  etc.,  and  leading  to  par- 
alysis and  atrophy  of  the  deltoid  prevents  raising  the  arm  to  the  hori- 
zontal position.  (2)  The  long  or  posterior  thoracic  nerve,  which  fixes 
and  (with  the  trapezius)  rotates  the  scapula,  when  paralyzed  gives  rise 
to  a  "winged"  scapula,  or  prominence  of  the  vertebral  border  (serratus 
paralysis),  and  imperfect  elevation  of  the  arm  above  the  shoulder  (less- 
ened rotation  of  the  scapula).  (3)  The  musculospiral  nerve  is  often 
disordered — in  consequence  of  cold,  injuries,  fracture  of  the  humerus, 
etc.;  of  pressure,  as  by  falling  asleep  with  the  arm  on  the  back  of 
a  chair,  counter,  or  bar  (bartender's  paralysis);  or  as  may  occur  in 
so-called  "bridal"  paralysis  and  other  paralyses  resulting  from  a 
weight;  and  of  lead  poisoning  and  other  forms  of  intoxication.  Usu- 
ally the  lesion  is  just  above  the  elbow,  and  results  in  paralysis  of  the 
extensor  muscles  of  the  WTist  and  the  fingers  (except  the  supinator 
longus),  and  the  characteristic  wrist-drop.  In  lesions  higher  up,  the 
triceps,  the  brachialis  anticus,  and  the  supinator  longus  are  also  involved. 
(4)  The  ulnar  nerve,  when  paralyzed,  results  in  atrophy  and  loss  of 
power  of  the  interossei,  all  the  muscles  of  the  little  finger,  the  ulnar  half 
of  the  deep  flexors  of  the  fingers,  the  adductor  and  the  inner  head  of  the 
short  flexor  of  the  thumb,  and  the  ulnar  flexor  of  the  wrist.  The  con- 
spicuous symptoms  consist  of  impaired  flexion  of  the  hand,  loss  of  power 
of  abducting  and  adducting  the  fingers,  and  of  flexing  and  extending 
the  second  and  third  phalanges.  There  is  also  anesthesia  of  both  sur- 
faces of  the  fourth  and  of  the  ulnar  half  of  the  third  fingers.  In  long- 
standing cases  the  claw-like  hand  (main-en-grift'e)  develops,  being  due 
to  the  activity  of  the  non-opposed  antagonistic  muscles  supplied  by  the 
median  nerve.  (5)  The  median  nerve  is  rarely  involved  alone,  but  if 
so,  it  may  lead  to  paralysis  of  the  muscles  arising  from  the  inner  condyle 
of  the  hmnerus  (except  the  flexor  carpi  ulnaris)  and  the  deep  muscles 
of  the  forearm;  in  consequence,  the  arm  cannot  be  pronated  beyond  the 
mid-position,  the  wrist  cannot  be  flexed  toward  the  radial  side,  the 
second  phalanges  cannot  be  flexed,  and  the  tiiunib  cannot  be  opposed 
to  the  finger  tips.  There  is  also  anesthesia  of  both  surfaces  of  the 
thumb,  and  the  first,  second,  and  the  radial  half  of  the  third  finger. 
(6)  Volhnaniis  confracture  is  a  form  of  paralysis  of  the  hand  and  fore- 
arm that  usually  follows  fractures  about  the  elbow  or  of  the  forearm 
and  undue  pressure  caused  by  splints  and  tight  bandaging.  The  nature 
of  the  disease  is  not  definitely  known;  it  lias  been  attributed  to  defective 
blood  supply  (whence  ischemic  paralysis),  to  j)riniary  disorder  of  the 
muscles,  (myositis  and  fibroid  changes),  to  neuritis,  and   to  changes 


824  DISEASES  OF  THE  NERVES 

following  sloughing  of  the  tissues  of  the  forearm  (which  is  sometimes 
observed).  The  symptoms  consist  of  atrophy  of  the  muscles  of  the 
forearm  and  hand,  with  contraction  of  the  flexors,  and  the  ultimate 
development  of  the  claw-like  hand.  Usually  there  are  no  noteworthy 
sensory  changes.  The  condition  may  be  relieved  by  passive  movements, 
massage,  electricity,  or  operative  measures. 

The  Lumbar  Plexus. — The  lumbar  plexus  is  made  up  of  the  first 
three  lumbar  roots  and  a  branch  from  the  fourth.  The  chief  causes  of 
disorder  of  the  plexus  are  regional  tumors,  disease  of  the  vertebrae,  psoas 
abscess,  and  neuritis;  and  the  obturator  nerve  may  also  be  injured 
during  parturition  or  by  other  trauma.  The  main  symptoms  consist 
of  deficient  adduction  and  rotation  of  the  thigh  (inability  to  cross  the 
leg  over  the  other).  Paralysis  of  the  anterior  crural  nerve  results  in 
paralysis  and  atrophy  of  the  extensors  of  the  knee,  loss  of  the  knee-jerk, 
and  anesthesia  of  the  anterolateral  aspect  of  the  thigh  and  of  the  inner 
aspect  of  the  leg.  Disease  of  the  external  cutaneous  nerve  may  result 
in  meralgia  parcesihetica,  a  paresthesia  of  the  outer  aspect  of  the  thigh. 

The  Sacral  Plexus. — The  sacral  plexus  is  made  up  of  a  branch 
from  the  fourth  lumbar,  the  fifth  lumbar,  the  first,  second,  and  third 
sacral,  and  a  branch  from  the  fourth  sacral  roots.  The  chief  causes  of 
disorder  of  the  plexus  are  pelvic  growths  and  inflammations,  disease  of 
the  vertebrae  and  the  spinal  meninges,  parturition,  and  neuritis.  In- 
volvement of  the  sciatic  nerve  causes  sciatica  (page  809).  Paralysis  of  the 
nerve  results  in  inability  to  flex  the  leg  upon  the  thigh  and  loss  of  power 
of  all  the  muscles  below  the  knee;  anesthesia  of  the  outer  aspect  of  the 
leg  and  of  the  sole  and  most  of  the  dorsum  of  the  foot;  and  ultimate 
wasting  of  the  muscles.  Paralysis  of  the  external  popliteal  (or  peroneal) 
nerve  results  in  loss  of  power  of  the  peroneal  muscles,  the  extensors  of 
the  toes,  and  the  tibialis  anticus,  with  ensuing  "foot-drop"  and  a  char- 
acteristic, so-called,  steppage  gait.  Paralysis  of  the  internal  popliteal 
nerve  results  in  loss  of  plantar  flexion  of  the  foot  and  of  the  power  to 
flex  the  toes,  and  anesthesia  of  the  outer  and  posterior  aspect  of  the 
lower  leg  and  sole  of  the  foot. 


DISEASES  OF  THE  CERVICAL  SYMPATHETIC  NERVES. 

The  cervical  sympathetic  system  supplies  vasomotor,  secretory,  and 
motor-nerve  fibers  to  the  head  and  neck  and  part  of  the  arm  and 
chest :  vasomotor  fibers  to  the  bloodvessels,  secretory  fibers  to  the  sweat 
glands  and  the  submaxillary  salivary  glands,  and  motor  fibers  to  the 
dilator  muscle  of  the  iris,  the  involuntary  muscle  fibers  of  the  upper  eye- 
lids, and  the  orbital  muscle  of  Mtiller.  The  sympathetic  nerves  may  be 
paralyzed  or  irritated,  paralysis  being  much  the  more  common.  The 
symptoms  of  paralysis  consist  of  unilateral  ptosis,  or  narrowing  of  the 
palpebral  fissure  (paralysis  of  the  unstriped  muscle  of  the  upper  eyelid); 
enophthalmos  or  retraction  of  the  eyeball  (paralysis  of  Miiller's  muscle) ; 


MENINGEAL  HEMORRHAGE  825 

contraction  of  the  pupil  and  no  dilatation  when  it  is  shaded  (unopposed 
action  of  the  sphincter  muscle  of  the  iris  supplied  by  the  intact  third 
cranial  nerve,  which  is  also  responsible  for  preservation  of  contraction  of 
the  pupil  to  light  and  in  accommodation);  unilateral  pallor  and  lessened 
secretion  of  sweat  (anidrosis);  and  perhaps  dryness  of  one  nostril  and 
one-half  of  the  mouth.  Irritation  of  the  sympathetic  nerves  causes 
contrary  symptoms:  widening  of  the  palpebral  fissure,  protrusion  of  the 
eyeball  (exophthalmos),  dilatation  of  the  pupil,  flushing  of  the  skin,  and 
increased  sweating  (hyperidrosis). 


DISEASES  OF  THE  CEREBEOSPINAL  MENINGES. 

MENINGEAL  HEMORRHAGE. 

Etiology.— Meningeal  hemorrhage  may  be  extradural  or  intradura 
(subdural).  Extradural  cerebral  hemorrhage  is  almost  always  trau- 
matic, though  it  may  result  from  erosion  of  a  vessel  by  caries  of  the  bone. 
The  middle  meningeal  artery  is  usually,  but  not  always,  the  source  of 
the  hemorrhage.  Intradural  cerebral  hemorrhage  (hemorrhage  from 
the  vessels  of  the  pia-arachnoid)  may  be  due  to  traumatism  (rather 
unusual),  internal  hemorrhagic  pachymeningitis  and  associated  disorders 
of  mentality,  rupture  of  an  aneurysmal  dilatation  of  a  vessel,  the  hemor- 
rhagic diathesis,  severe  anemic  states,  paroxysms  of  whooping  cough, 
the  chronic  congestion  of  cardiac,  pulmonary,  and  advanced  renal  dis- 
eases; and  it  may  occur  from  compression  of  the  skull  at  birth.  Spinal 
meningeal  hemorrhage  may  or  may  not  be  associated  with  cerebral  hemor- 
rhage; when  it  occurs  it  may  be  due  to  like  causes;  or  it  may  result 
from  local  traumatism,  and  is  then  usually  extradural. 

Symptoms. — The  symptoms  vary,  depending  upon  the  situation  of 
the  hemorrhage,  upon  whether  it  is  small  or  excessive,  and  whether  it 
occurs  slowly  or  rapidly.  In  sudden,  large,  cerebral  meningeal  hemor- 
rhage the  symptoms  are  much  like  those  of  intracerebral  apoplexy,  with 
the  added  evidences  of  cortical  irritation  or  paralysis.  In  other  cases 
the  manifestations  of  the  injury  itself  sometimes  overshadow  those  of 
the  hemorrhage,  especially  if  the  hemorrhage  occurs  slowly  and  is  not 
directly  over  the  motor  area.  In  this  event  the  patient  may  even  con- 
tinue at  his  occupation  for  several  hours,  perhaps  complaining  only  of 
headache;  in  other  cases,  there  may  be  also  some  mental  confusion, 
vertigo,  and  vomiting,  and  the  patient  gradually  loses  consciousness. 
Sometimes  convulsions,  which  may  be  severe,  occur;  they  may  be  uni- 
lateral and  succeeded  by  })aresis  or  paralysis  (monoplegia  or  lu-nn'plegia). 
In  other  cases,  depending  upon  the  seat  of  the  hemorrliage,  other  symp- 
toms develop,  such  as  aphasia,  sensory  disturbances,  oculomotor  palsy 
(occipital  region),  etc.  In  favorable  cases  the  coma  lessens  and  partial 
recovery  of  the  Jjalsy  supervenes. 


826  DISEASES  OF  THE  CEREBROSPINAL  MENINGES 

The  symptoms  of  spinal  meningeal  heTnorrhage  consist  of  pain  and 
distress  in  the  back,  which  are  usually  of  sudden  onset  (in  traumatic  cases 
especially);  radiation  of  the  pain  along  the  nerve  roots  and  peripheral 
nerves,  especially  into  the  legs;  and  some  muscular  spasm.  The  deep 
reflexes  may  be  temporarily  lessened;  usually  they  become  exaggerated. 
In  the  event  of  compression  of  the  cord,  more  or  less  paralysis  super- 
venes and  control  of  the  vesical  and  rectal  sphincters  may  be  lost. 

Treatment. — The  treatment  of  cerebral  meningeal  hemorrhage  is  simi- 
lar to  that  of  intracerebral  hemorrhage;  but  in  every  case  the  head 
should  be  shaved  and  searched  for  subcutaneous  hemorrhage  or  frac- 
ture, and  the  question  of  operative  removal  of  the  clot  must  be  consid- 
ered. When  in  doubt,  it  is  probably  wise  to  operate,  since  a  large 
hemorrhage  may  result  in  death  from  compression,  and  a  small  hemor- 
rhage, if  recovered  from,  may  determine  traumatic  epilepsy  or  insanity 
in  later  life.  In  spinal  meningeal  hemorrhage  resort  should  be  had  to 
lumbar  puncture,  with  a  view  to  relieve  pressure;  but  if  symptoms  of 
compression  of  the  cord  ensue,  laminectomy  should  be  performed  and 
the  fluid  and  clotted  blood  removed;  otherwise,  the  treatment  consists 
of  rest  and  quiet, 

EXTERNAL  PACHYMENINGITIS. 

Etiology. — Inflammation  of  the  outer  surface  of  the  dura  mater  is 
practically  always  a  secondary  affection,  and  is  usually  acute,  although 
it  may  be  chronic.  It  results  from  trauma  (injuries  to  the  skull  or  ver- 
tebrae) or  bacterial  infection — most  commonly  in  consequence  of  necrosis 
of  the  petrous  portion  of  the  temporal  bone  in  middle-ear  disease,  or  of 
streptococcic  or  staphylococcic,  less  commonly  of  tuberculous  or  syph- 
ilitic, disease  of  the  bones  or  adjacent  tissues.  The  chronic  cases  are 
virtually  always  due  to  syphilis  or  tuberculosis. 

Pathology. — In  acute  cases  the  dura  is  swollen,  softened,  hemor- 
rhagic, and  frequently  suppurative.  The  pus  collects  between  the 
membranes  and  the  skull  or  vertebrse,  and  may  extend  into  and  between 
the  two  layers  of  the  membrane  (causing  thrombosis  of  the  sinuses),  and 
involving  the  pia-arachnoid.  In  syphilitic  and  tuberculous  cases  the 
dura  may  be  greatly  thickened  and  considerable  pus  may  be  present, 
although  the  inner  surface  may  be  quite  smooth.  In  chronic  pachy- 
meningitis the  lesions  consist  of  the  formation  of  the  new  fibrous  tissue. 

Symptoms. — The  symptoms  in  mild  cases  are  indefinite;  in  the  cerebral 
cases  there  may  be  only  headache.  In  severe  cases  the  symptoms  of 
the  primary  disturbance  often  mask  the  pachymeningitis.  Symptoms, 
when  present,  consist  of  headache,  malaise,  and  perhaps  convulsions, 
followed  by  drowsiness  and  stupor,  and  in  case  of  suppuration,  by 
chills  and  fever,  and  often  sweats  and  leukocytosis.  Sometimes  the 
symptoms  are  only  those  of  pressure,  which  may  be  sufficient  to  cause 
paralysis  of  the  opposite  side  of  the  body.  Choked  disk  has  also  been 
noted.      Sinuses    communicating    with    the    exterior    usually    suggest 


INTERNAL  PACHYMENINGITIS  827 

syphilis.  The  symptoms  in  the  spinal  cases  are  those  of  compression  of 
the  spinal  cord,  which  are  usually  clue,  in  part,  also  to  associated  lesions. 
Treatment. — The  treatment  varies  with  the  cause.  In  the  lighter 
grades  of  the  disease,  antiphlogistic  measures  and  counterirritants  are 
indicated;  in  the  severer  grades,  operative  interference;  and  in  syph- 
ilitic cases,  mercury  and  potassium  iodide. 

INTERNAL  PACHYMENINGITIS. 

Three  forms  of  internal  pachymeningitis  are  usually  described:  The 
hemorrhagic,  the  purulent,  and  the  pseudomembranous.  The  purulent 
and  the  pseudomembranous  forms  are  uncommon  and  rarely  recognized 
before  death.  The  purulent  form  is  usually  secondary  to  inflammation  of 
the  pia-arachnoid,  but  it  may  follow  softening  of  a  sinus  thrombus  or 
result  from  traumatism.  The  pseudomembranous  form  is  of  obscure 
etiology,  though  it  may  result  from  trauma,  or  syphilis,  or  follow  hemor- 
rhagic or  suppurative  pachymeningitis.  The  lesions  may  be  purely 
fibrous  or  partly  osseous. 

Internal  hemorrhagic  pachymeningitis  may  involve  the  cerebral 
or  the  spinal  meninges.  The  lesions  are  most  common  in  the  brain 
(hematoma  of  the  dura  mater),  and  occur  chiefly  in  males  over  fifty 
years  of  age,  though  they  are  by  no  means  rare  in  children.  The  most 
frequent  causes  are:  (1)  Chronic  alcoholism;  (2)  different  nervous  dis- 
turbances, such  as  paretic  dementia,  chronic  hereditary  chorea,  senile 
dementia,  etc. — whence  it  is  frequently  seen  in  insane  asylums  and 
almshouses;  (3)  cranial  injuries;  (4)  different  infectious  diseases;  (5) 
diseases  of  respiration,  of  circulation,  and  of  nutrition. 

Pathology. — The  lesions  are  usually  confined  to  the  area  of  distribu- 
tion of  the  middle  meningeal  artery  and  are  often  bilateral;  they  consist 
of  the  development  of  a  very  delicate  vascular  membrane  (the  result  of 
the  organization  of  an  inflammatory  exudate),  the  bloodvessels  of. which 
commonly  rupture  and  give  rise  to  the  extravasation  of  a  greater  or  less 
amount  of  blood  (hematoma).  Through  the  successive  formation  of 
such  vascular  membrane  and  the  occurrence  of  hemorrhage,  lamelhv 
of  membrane  and  hemorrhage  are  formed,  which  may  be  3  to  5  mm. 
thick.  The  lamellated  structure  is  well  shown  on  section,  and  frequently 
the  successive  layers  may  be  stripped  oif.  The  brain  is  correspond- 
ingly compressed.  Occasionally,  in  consequence  of  the  imperfect  organ- 
ization of  the  blood  clot,  a  collection  of  serous  fluid  or  a  cyst  results 
(hygroma  dura  matris).  Involving  the  spinal  meninges,  the  lesions  are 
most  common  in  the  cervical  region — hypertr()j)hic  cervical  pachy- 
meningitis. A  new  formation,  analogous  to  that  in  the  brain,  develops 
between  the  dura  and  the  spinal  cord,  compressing  the  cord  and  the 
nerve  roots,  and  often  leading  to  secondary  degenerations. 

Symptoms. — In  many  cases  of  the  cerebral  disorder  symptoms  are 
wanting,  especially  when  the  hemorrhage  is  small  and  has  occurred 
slowly;  and  in  the  insane,  in  whom  the  insanity  often  masks  the  symp- 


828  DISEASES  OF  THE  CEREBROSPINAL  MENINGES 

toms  of  the  pachymeningitis.  Characteristic  symptoms,  however,  consist 
of  recurring  apoplectiform  attacks  (referable  to  repeated  hemorrhages), 
evidences  of  increasing  intracranial  pressure,  and  paresis  or  paralysis  of 
cortical  origin.  Headache  is  common.  The  symptoms  of  increasing 
intracranial  pressure  consist  of  increasing  headache,  somnolence,  pro- 
gressing in  some  cases  to  coma,  nausea,  vomiting,  slowing  and  irregu- 
larity of  the  pulse,  and  contracted  pupils  (with  marked  or  complete  loss 
of  reaction  to  light).  Paralysis  of  one  limb,  or  of  a  single  cranial  nerve 
(such  as  the  facial  or  hypoglossal),  and  circumscribed  or  unilateral 
convulsions,  suggest  the  cortical  seat  of  the  disorder.  The  patient  often 
recovers  from  minor  attacks,  the  manifestations  of  the  apoplectiform 
insult  gradually  (within  several  weeks)  subsiding,  though  paresis  or 
paralysis,  headache,  intellectual  disturbances,  muscular  weakness  and 
awkwardness,  etc.,  often  persist.  In  severe  cases  the  manifestations  are 
often  bilateral,  and  the  patient  may  die  in  coma — an  event  that  happens 
sooner  or  later  in  all  cases,  whether  the  lesions  are  unilateral  or  bilateral. 

The  symptoms  of  the  spinal  disorder  consist  of  severe  neuralgic  pains 
in  the  neck  and  arms  (corresponding  to  the  cervical  roots  involved),  with 
associated  hyperesthesia,  paresthesia,  and  perhaps  anesthesia.  In  the 
course  of  time  muscular  weakness  and  atrophy  supervene;  these  depend 
upon  the  situation  and  extent  of  the  nerve-root  involvement,  but  are 
usually  most  marked  in  the  small  muscles  and  the  flexors  of  the  hands. 
The  extensors  often  remaining  intact,  gradually  lead  to  the  development 
of  the  claw-like  hand.  In  some  cases  the  hands,  forearms,  upper  arms, 
and  shoulders  may  be  markedly  involved  (cervical  paraplegia).  Ulti- 
mately spastic  paraplegia  may  develop  in  the  legs  from  secondary 
degeneration  in  the  cord. 

Diagnosis. — The  diagnosis  of  the  cerebral  disorder  is  always  difficult; 
it  is  suggested  by  the  etiological  factors  and  recurring  apoplectiform 
attacks,  with  evidences  of  cortical  irritation.  The  spinal  disorder  must 
be  differentiated  from  tumors  and  other  forms  of  compression,  amyo- 
trophic lateral  sclerosis  (absence  of  severe  initial  pains  and  sensory 
changes),  and  syringomyelia  (characteristic  sensory  changes). 

Prognosis. — The  outlook  in  both  types  of  the  disorder  is  bad. 

Treatment. — The  causal  condition  demands  first  attention,  and  the 
symptoms  should  be  treated  as  they  arise:  during  the  stage  of  hemor- 
rhage— rest  in  bed,  elevation  of  the  head,  an  ice-cap  or  leeches  to  the 
base  of  the  head  or  behind  the  ears,  hot  foot  baths,  venesection,  free 
purgation,  etc. ;  and  during  the  subsequent  stages — merciu'ials,  potassium 
iodide,  and  antispasmodics.  Should  the  diagnosis  of  a  focus  of  cortical 
irritation  be  possible,  especially  with  evidences  of  increasing  intracranial 
pressure,  an  operation  for  the  removal  of  the  clot  may  be  undertaken. 

LEPTOMENINGITIS. 

Etiology. — Inflammation  of  the  pia-arachnoid  (leptomeningitis,  pia- 
arachnitis)  may  be  primary  or  secondary,  and  acute  or  chronic.     The 


LEPTOMENINGITIS  829 

priiiiarv  acute  form,  even  the  sporadic  cases,  is  commonly  the  cerebrospinal 
fever  (meningococcic  infection)  already  discussed  (page  86),  although 
tuberculous  and  pneumococcic  infections  also  may  occasion  lesions  onlv, 
or  most  marked,  in  the  meninges.  Secondary  leptomeningitis  may  be 
due  to:  (1)  Bacterial  infection,  and  is  seen  most  commonly,  as  a  com- 
plication or  sequel,  in  the  acute  infectious  diseases,  especially  in  pneu- 
monia, septicemia,  erysipelas,  acute  infective  endocarditis,  typhoid 
fever,  smallpox,  measles,  scarlet  fever,  gonorrhoea,  influenza,  acute 
rheumatic  fever,  lung  abscess,  empyema,  etc.  It  results  also  from 
extension  of  infection  from  caries  of  adjacent  bones,  from  purulent  otitis 
media,  disease  of  the  frontal  sinuses,  nasal  cavities,  or  pharynx,  brain 
abscess,  etc.  (2)  Trauma  of  the  bones  of  the  skull,  affecting  the  men- 
inges directly;  but  in  most  of  these  cases,  trauma  and  infection  are 
associated.  (3)  As  a  terminal  infection  in  many  chronic  diseases,  such 
as  nephritis,  diabetes,  arteriosclerosis,  etc.  The  exciting  causes  may  be 
the  microorganisms  provocative  of  the  primary  infection,  but  often  they 
are  the  common  pyogenic  bacteria,  the  infection  of  the  meninges  being 
hemogenic,  lymphogenic,  or  occurring  by  contiguity  of  tissue. 

Pathology. — The  lesions  vary  much  in  different  cases.  Basal  menin- 
gitis, convexity  meningitis,  and  ventricular  meningitis  are  terms  used 
to  denote  the  seat  of  the  marked  lesions;  but  in  many  cases  the  lesions 
are  more  or  less  widespread.  In  the  meningitis  following  pneumonia 
and  sepsis  the  convexity  on  both  sides  is  usually  involved;  in  that 
occurring  in  children  the  posterior  basic  region  is  especially  involved 
(posterior  basic  meningitis),  and  this  is  also  true  of  that  occurring  in 
Bright's  disease,  diabetes,  and  other  cachectic  conditions.  Anatomic- 
ally, three  varieties  may  be  distinguished  —  the  serous  meningitis  of 
Quincke,  tuberculous  meningitis  (page  122),  and  puz"ulent  meningitis. 

The  serous  meningitis  of  Quincke  is  a  rare  condition,  in  which  the  pia- 
arachnoid  is  the  seat  of  serous  inflammation,  especially  marked  on  the 
convexity,  and  in  which,  by  lumbar  puncture,  the  cerebrospinal  fluid  is 
found  under  greater  pressure  than  the  normal  40  to  60  mm.  of  water, 
and  it  contains  at  least  twice  as  much  as  the  normal  (0.5  per  cent.)  of 
albumin. 

Generally,  however,  the  lesions  are  purulent  and  confined  to,  or  at 
least  most  marked  on,  the  convexity  of  the  brain  (convexity  meningitis). 
In  some  cases,  especially  in  infants  or  children,  they  are  more  marked  at 
the  base  (posterior  basic  meningitis).  In  other  cases  the  lesions  are 
widespread,  and  consist  of  swelling,  congestion,  and  suppuration  of  the 
pia-arachnoid,  sometimes  its  more  superficial  layers,  especially  marked 
along  the  course  of  the  vessels,  and  sometimes  so  marked  as  completely  to 
obscure  the  convolutions.  They  are  usually  bilateral,  although  they  may 
be  unilateral,  especially  in  cases  due  to  extension  from  midtlle  ear  disease, 
etc.,  when  they  may  be  accompanied  by  sinus  thrombosis.  The  ventricles 
may  contain,  and  are  sometimes  distended  with,  serous  or  seropurulent 
fluid;  the  lesions  may  extend  to,  or  simultaneously  involve,  the  s])inal 
meninges  (cerebrospinal  meningitis);  and  in  some  cases  small  foci  of 


830  DISEASES  OF   THE  CEREBROSPINAL  MENINGES 

hemorrhage  may  be  detected  in  the  superficial  layers  of  the  brain 
(meningo-encephalitis) . 

Chronic  leptomeningitis  is  quite  uncommon;  it  may  be  due  to  syphilis 
or  tuberculosis;  rarely  the  meningococcic  (epidemic  or  sporadic)  cases, 
posterior  basic  meningitis,  and  the  serous  meningitis  of  Quincke  may 
run  a  chronic  course. 

Symptoms. — The  symptoms  are  sometimes  divided  into  the  pro- 
dromal, the  irritative,  and  the  paralytic.  Prodromal  symptoms  are 
frequently  absent,  but  sometimes  for  a  day  or  two  there  may  be  general 
malaise,  irritability,  headache,  and  perhaps  vomiting;  but  these  are 
often  overshadowed  or  masked  by  the  evidences  of  the  primary  disorder. 
The  disease  is  often  ushered  in  with  high  fever,  perhaps  a  chill  or  chilli- 
ness, and  headache  which  is  extreme,  persistent,  sometimes  more  marked 
in  the  frontal  region,  but  usually  widespread — constituting  a  most  char- 
acteristic symptom  of  the  disease.  With  the  progress  of  the  inflamma- 
tion, the  headache  increases  in  severity,  and  is  often  subject  to  exacer- 
bations of  great  severity  (occasioning  the  so-called  "hydrocephalic 
cry"),  and  disorders  of  consciousness — delirium,  stupor,  coma — super- 
vene. Furthermore,  manifestations  of  cerebral  irritation  develop,  and 
vary  somewhat  with  the  seat  of  the  most  marked  lesions;  they  com- 
prise vomiting  (often  frequent  and  persistent,  especially  in  basilar  menin- 
gitis); slowing  and  irregularity  of  the  pulse;  retraction  of  the  head  and 
rigidity  of  the  neck  muscles  (opisthotonos),  especially  when  the  lesions 
are  posterior,  and  basal,  and  cervical;  crunching  of  the  teeth;  pupillary 
miosis;  strabismus;  nystagmus;  photophobia;  undue  sensitiveness  of  the 
auditory  apparatus;  ptosis;  muscular  irritability  and  twitchings;  con- 
vulsive seizures  in  the  facial  muscles  (trismus)  and  in  the  extremities; 
increase  of  the  reflexes;  Kernig's  sign  (inability  to  extend  the  leg  when 
the  thigh  is  flexed  on  the  abdomen);  general  cutaneous  and  muscular 
hyperesthesia;  etc.  These  are  soon  followed  by  evidences  of  paresis 
or  paralysis  (paralytic  stage):  coma  instead  of  the  previous  delirium 
and  stupor;  increased  frequency  of  the  pulse  (not  constant);  pupillary 
differences  or  mydriasis;  sometimes  optic  neuritis  (basilar  meningitis); 
paralysis  of  certain  cranial  nerves  (especially  the  facial)  or  paresis  of  the 
extremities  of  cortical  nature;  loss  of  reflexes;  retraction  of  the  abdomen; 
loss  of  control  over  the  sphincters;  etc.  Fever  is  present  throughout  the 
course  of  the  disease;  it  is  usually  irregular,  varying  up  to  102°  or  103°  F., 
but  occasionally  hyperpyrexia  is  observed,  and  sometimes  but  little  fever 
(in  terminal  infections).  Repeated  chills  are  not  uncommon.  Herpes 
labialis  is  quite  common,  but  especially  in  the  meningococcic  infections. 
The  urine  is  diminished  and  often  contains  albumin  and  casts;  the 
bowels  are  constipated,  until  the  final  stage,  when  incontinence  often 
supervenes.     Leukocytosis  is  usually  present. 

Diagnosis. — The  diagnosis  is  usually  comparatively  easy,  but  in  doubt- 
ful cases  the  antecedent  history,  disordered  cerebration,  high  fever,  slow 
pulse,  and  the  other  symptoms  narrated,  together  with  the  data  men- 
tioned on  page  89,  should  clear  up  the  diagnostic  uncertainty. 


CEREBROSPINAL  LOCALIZATION  831 

Prognosis. — The  outlook  depends  upon  the  nature  of  the  infection, 
the  severity  of  the  lesions,  and  the  associated  conditions.  Quincke's 
serous  meningitis  may  eventuate  in  recovery;  the  purulent  cases  are 
almost  always  fatal;  and  the  non-fatal  cases  may  be  followed  by  divers 
sequels  (page  89). 

Treatment. — The  treatment  is  that  mentioned  on  page  89.  Perhaps 
in  the  future  we  may  secure  a  serum  or  bacterin  for  each  specific  type  of 
meningitis. 


DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD. 

CEREBROSPINAL  LOCALIZATION. 

Diseases  of  the  brain  and  the  spinal  cord  may  be  somewhat  arbitrarily 
divided  into  two  classes:  (1)  The  so-called  system  diseases — those  in 
which  the  lesions  are  more  or  less  strictly  limited  to  certain  tracts  or 
collections  of  neurons  functionally  homologous;  if  only  one  tract  is 
involved,  the  disorder  is  spoken  of  as  a  single  system  disease;  if  more 
than  one,  as  a  combined  system  disease.  (2)  The  non-system  (focal  or 
diffuse)  diseases — those  in  which  the  lesions  are  not  limited  to  a  system 
or  systems  of  neurons.  The  system  diseases  involve  variously  the  dif- 
ferent motor  and  sensory  neurons,  of  which  mention  is  made  on  page 
802  and  thereafter,  and  which  are  shown  in  their  course  in  the  spinal 
cord  on  Plate  II.  (page  805). 

The  accurate  localization  of  irritative  or  destructive,  system  or  non- 
system,  disorders  of  the  brain  and  spinal  cord  depends  upon  a  knowl- 
edge of  the  functional  activity  and  the  mutual  relations  of  the  different 
parts  of  the  brain  and  the  cord.  The  characteristic  features  of  disease 
of  the  upper  and  the  lower  motor  neuron  and  of  the  sensory  neuron 
are  mentioned  on  pages  802,  803,  and  804.  When  diseased  focally, 
that  is,  when  the  seat  of  non-system  diseases,  most  parts  of  the  brain 
and  cord  exhibit  sensible  evidence  of  the  local  lesions  that  permit  of 
definite  localization;  but  there  are  certain  so-called  silent  areas  in  the 
brain,  the  functions  of  which  are  unknown,  and  disease  (especially 
tumors)  of  which,  although  causing  general  manifestations,  provoke 
no  localizing  symptoms.  In  the  diagnosis  of  local  lesions,  especially 
timiors  of  the  brain,  one  must  remember:  (1)  That  focal  signs  are 
of  the  greater  value  the  nearer  to  the  general  symptoms  in  point  of 
time  they  develop;  (2)  that  some  of  the  signs  are  often  due  to  irritation 
or  paralysis  of  adjacent  areas  of  the  brain  or  of  tracts  that  may  pass 
through  or  near  the  seat  of  disease,  and  that  this  is  more  likely  to  be 
the  case  the  longer  after  the  onset  of  the  general  symptoms  these  local- 
izing signs  develop;  and  (3)  that  in  advanced  cases  many  of  the  signs  are 
often  due,  not  so  much  to  the  primary  lesion  (tumor,  abscess,  etc.)  as  to 
secondary  conditions,  such  as  meningitis,  hydroceplialus,  secondary 
tumors  or  abscesses,  hemorrhage  into  tumors,  and  so  forth. 


832 


DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 


The    Brain. — Frontal   Lobes;  Prefrontal   Region. — The   frontal 
lobes  anterior  to  and  above  the  ascending  and  the  third  frontal  convo- 


FiG.  17 


CONCRLTE  CONCEPT 


The  lateral  surface  of  the  human  brain,  showing  the  localization  of  the  different  functions.    (Mills.) 

Fig.  18 


The  mesial  surface  of  the  human  brain,  showing  the  localization  of  the  different  functions.    (Mills). 

lutions  are  believed  to  subserve  the  higher  mental  and  psychic  func- 
tions, such  as  general  intelligence,  memory,  reasoning  powers,  judgment, 


CEREBROSPINAL  LOCALIZATION 


833 


attention,  Abolition,  and  abstract  concepts  (Figs.  17  and  18).  Mills  and 
other  observers  assign  these  functions  especially  to  the  left  side  in  right- 
handed  persons,  and  to  the  right  side  in  left-handed  persons.  Tumors 
and  other  destructive  lesions  of  the  prefrontal  region  are  said  by  Mills  to 
be  always  associated  with  disorder  of  these  higher  mental  functions. 

Motor  Cortex;  Ascending  Frontal  Convolutions. — The  cor- 
tical centres  for  voluntary  muscular  movements  are  situated  in  the 
ascending  frontal,  second  frontal,  and  paracentral  lobules,  the  different 
centres  being  as  represented  in  Fig.  19.  A  tumor  or  other  lesion  of  the 
motor  cortex,  or  immediately  subjacent  thereto  (subcortical),  may  pro- 
duce, first,  irritation  of  the  area  involved  and  spasm  or  convulsions  of  the 
muscles  of  the  opposite  side  of  the  body  therein  represented  (focal  or 
Jacksonian  epilepsy).     Soon  localized  paresis  or  paralysis  supervenes, 


Fig.  19 


The  functional  areas  of   the  cerebral  cortex  of  the  left  hemisphere,  to  show  especially  the  cortical 
centres  for  voluntary  muscular  movements.      (Starr.) 


and  if  at  first  limited  to  certain  groups  of  muscles,  may,  as  the  tumor 
grows,  become  monoplegic  or  hemiplegic;  it  usually  becomes  spastic 
in  type  (degeneration  of  the  upper  motor  neuron).  In  addition,  there 
is  likely  to  be  disorder  of  epicritic  sensibility,  especially  lessening  of 
tactile  sensibility  and  of  the  power  of  cutaneous  localization.  This  is 
usually  due  to  pressure  or  secondary  involvement  of  the  ascending 
parietal  convolution  where  sensibility  has  its  cortical  representation. 
Homologous  muscles  that  act  together  are  not  likely  to  show  marked 
or  permanent  disability  from  unilateral  cortical  or  subcortical  lesions, 
since  the  muscles  of  both  sides  may  be  iimervated  from  the  one  cerebral 
hemisphere. 

Sensory  Cortex;   Parietal  IvObe. — The  cortical  centres  for  sen- 
sation are  situated  in  the  parietal  lobe,  especially  in  the  ascending 
53 


834  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

parietal  convolution  and  the  gyrus  fornicatus.  According  to  Mills, 
these  centres  correspond  with,  and  are  about  on  a  level  with,  the  related 
motor  centres  in  the  neighboring  frontal  convolutions.  Tumors  and 
other  destructive  lesions  of  the  parietal  lobe  causes  disturbances  of 
epicritic,  protopathic,  and  deep  (or  muscular)  sensibility — that  is,  dis- 
order of  the  sensations  of  touch,  pain,  temperature,  and  stereognosis. 
Usually  also  there  are  motor  disturbances  from  compression  by  or  exten- 
sion of  the  tumor  to  the  frontal  convolutions,  or  subcortical  implication 
of  the  motor  fibers  in  the  corona  radiata. 

Occipital  Lobe. — Irritative  lesions  of  the  occipital  lobe  may  cause 
convulsions  with  visual  warnings.  Destructive  lesions  involving  the 
cuneate  lobule  cause  simple  or  homonymous  hemianopsia;  those  involving 
the  angular  gyrus  cause  bilateral  contraction  of  the  field  of  vision, 
greater  on  the  side  opposite  the  tumor,  and  visual  aphasia  (word-blind- 
ness), especially  if  situated  on  the  left  side. 

Temporosphenoidal  Lobe. — Irritative  lesions  of  the  temporosphe- 
noidal  lobe  may  cause  convulsions  with  auditory  warnings  or  auditory 
hallucinations.  Destructive  lesions  cause  deafness  on  the  opposite  side, 
and  sensory  aphasia  (word-deafness),  especially  if  situated  on  the  left 
side.  Lesions  of  the  uncinate  gyrus  may  cause  olfactory  and  gustatory 
•hallucinations. 

Centrum  Ovale. — Lesions  of  the  centrum  ovale  may  involve  the 
motor,  sensory,  or  association  fibers  that  pass  through  it.  Subcortical 
lesions  cause  motor  or  sensory  disturbances  similar  to  those  mentioned 
in  connection  with  the  motor  and  the  sensory  cortex,  but  varying  with 
the  situation  of  the  lesion  (the  fibers  implicated).  Convulsions  do  not 
occur  unless  the  motor  cortex  is  involved;  if  they  do  supervene,  it  is 
not  until  the  paralysis  has  been  present  for  some  time  (the  reverse  of 
cortical  lesions).  Lesions  of  the  centrum  ovale  lower  down  resemble 
those  of  the  internal  capsule. 

Internal  Capsule. — In  the  comparatively  constricted  region  of  the 
internal  capsule  practically  all  of  the  motor  and  sensory  projection 
fibers  of  the  cerebral  cortex  are  closely  packed  together.  The  internal 
capsule  is  made  up  of  a  so-called  knee;  an  anterior,  lenticulo-caudate 
(lenticulo-striate)  limb;  and  a  posterior  limb,  of  which  the  anterior 
two-thirds  is  called  the  lenticulo-optic  (lenticulo-thalamic)  segment,  and 
the  posterior  one-third  the  retrolenticular  segment.  The  different  sets 
of  neurons  passing  through  the  internal  capsule  are  shown  in  Fig.  20.  A 
lesion  of  the  anterior  segment,  if  not  large,  may  cause  only  disorders  of 
the  higher  mental  and  psychic  faculties.  A  lesion  of  the  knee  gives  rise 
to  disturbances  of  the  motor  nerves  of  the  eye,  the  motor  part  of  the 
trigeminus,  the  facial,  and  the  hypoglossal;  in  consequence,  in  addition 
to  the  obvious  paralyses,  disorders  of  articulation  ensue,  and  if  the  lesion 
be  on  the  left  side,  aphasia.  A  lesion  just  posterior  to  the  knee  (the 
pyramidal  tract),  implicating  in  order  the  neurons  for  the  face,  arm,  and 
leg,  causes  usually  hemiplegia  of  the  opposite  half  of  the  body;  mono- 
plegia is  very  rare,  the  lesion  scarcely  ever  being  small  enough  to  involve 


CEREBROSPINAL  LOCALIZATION 

Fig.  20 


835 


Sypcylossm. 


rlic. 

•Aifdit'ory 
'  tract 


A  horizontal  section  through  the  right  hemisphere  to  show  especially  the  internal  capsule,  the 
situation  of  common  lesions  therein,  and  their  consequences:  B.  Kn.,  knee  of  the  corpus  callosuni; 
F/...  anterior  horn  of  the  lateral  ventricle;  F„  inferior  part  of  the  third  frontal  convolution; 
.  8<r»c.,  lenticulo-striate  di^dsion  of  the  internal  capsule;  Knic.ic,  knee  of  the  internal  capsule- 
I.  oplic,  lenticulo-optic  division  of  the  internal  capsule;  Th.,  optic  thalamus;  J  ,  island  of  Reil- 
cl  claustrum;  Operc,  operculum;  T„  first  temporal  co.ivolution;  r.  lie,  retrolenticular  region  of 
the  internal  capsule;  C.  A.,  ammon's  horn;  calc,  calcarine  fissure;  Hh.,  posterior  horn  of  the 
lateral  ventricle;  SS  optic  radiation  of  Gratiolet;  T„  second  temporal  convolution;  Facialis, 
position  in  the  capsule  of  the  motor  tract  to  the  face;  Hypofjlossus,  position  of  tlie  tract  to  the 
tongue;  Arm,  position  of  the  tract  to  the  arm;  Bein,  position  of  the  tract  to  the  leg-  S  B 
sensory  fibers;  ,S..  visual  tract;   Auditory  trad,  auditory  tract.      (After  von  Monakow  )  '      '      " 


836  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

only  the  neurons  innervating  one  limb.  A  lesion  of  the  posterior  third 
(the  retrolenticular  segment)  of  the  posterior  limb  of  the  internal  capsule 
(which  transmits  sensory  fibers  for  the  entire  body,  as  well  as  the  optic 
and  auditory  neurons)  gives  rise  to  hemianesthesia  (and  related  sensory 
changes)  of  the  opposite  half  of  the  body,  homonymous  hemianopsia, 
and  deafness  on  the  opposite  side.  In  most  cases,  however,  notably  in 
cerebral  hemorrhage  (of  which  the  internal  capsule  is  the  common  seat), 
the  results  are  usually  varying  combinations  of  those  mentioned. 

Thalamus. — Lesions  of  the  thalamus  usually  implicate  also  the  internal 
capsule,  so  that  the  symptoms  are  likely  to  be  chiefly  those  just  mentioned. 
In  addition,  there  may  be  also  loss  of  control  of  the  facial  expression 
and  of  emotional  movements,  and  perhaps  also  imperfect  control  of  the 
posture  of  the  body,  athetoid  movements  of  the  extremities,  etc. 

Corpora  Quadrigemina. — Lesions  (usually  a  tumor)  of  the  anterior 
bodies  of  the  corpora  quadrigemina  cause  oculomotor  paralysis  (pressure 
on  the  nuclei  or  subcortical  interruption  of  impulses),  dilated  pupils 
inactive  to  light  and  accommodation,  and,  perhaps,  nystagmus.  Lesions 
of  the  posterior  bodies  give  rise  to  auditory  disturbances,  deafness, 
difficulty  in  maintaining  equilibrium,  and  a  tendency  to  fall,  usually  to 
the  opposite  side. 

Crus;  Cerebral  Peduncle. — A  lesion  of  one  peduncle,  as  of  the 
internal  capsule,  causes  hemiplegia  (face,  arm,  and  leg)  and  hemianes- 
thesia on  the  opposite  side  of  the  body;  paralysis  of  the  ocular  motor 
nerve  of  the  same  side  (involvement  of  the  nucleus  or  fibers);  perhaps, 
also,  if  the  lesion  (tumor)  is  large,  paralysis  of  the  fourth,  fifth,  and  sixth 
nerves. 

Pons. — ^A  lesion  in  the  pons  causes  contralateral  hemiplegia  and 
hemianesthesia,  and  usually  paralysis  of  the  face  (facial  nuclei)  of  the 
same  side  (crossed  paralysis).  In  some  cases  there  is  also  homolateral 
paralysis  of  the  third,  the  fourth,  the  motor  division  of  the  fifth,  and  the 
sixth  nerves;  contralateral  hemianesthesia  (arm  and  leg)  and  homo- 
lateral anesthesia  in  the  area  of  distribution  of  the  sensory  division  of  the 
fifth  nerve  (crossed  hemianesthesia);  or  homolateral  deafness  (involve- 
ment of  the  eighth  nerve).  The  lesion  (tumor)  if  situated  and  growing 
near  the  median  line  of  the  pons,  may  cause  motor  paralysis  (sometimes 
sensory  paralysis)  of  one  side;  and  paralysis  of  both  facial  (rarely  other 
cranial)  nerves. 

Medulla. — ^A  lesion  in  the  medulla  may  involve  one  or  both  pyram- 
idal tracts  (which  here  are  close  together),  and  cause,  therefore,  unilateral 
or  bilateral  paralysis  (usually  more  marked  on  one  side  than  the  other); 
and  also  paralysis  of  any  or  all  of  the  cranial  nerves  from  the  eighth  to 
the  twelfth  (bulbar  paralysis,  page  850).  There  may  be  also  disturb- 
ances of  respiration,  disorders  of  the  rate  and  rhythm  of  the  heart, 
and  glycosuria  or  polyuria. 

Pituitary  Body. — Tumors  of  the  pituitary  body  (akromegaly,  page 
356)  usually  compress  the  optic  chiasm  and  cause  at  first  double  temporal 
hemianopsia  (involvement  of  the  fibers  that  supply  the  inner  half  of  each 


CEREBROSPINAL  LOCALIZATION  837 

retina,  the  temporal  field  of  vision).  Eventually,  with  growth  of  the 
tumor  and  involvement  of  the  temporal  portions  of  the  optic  chiasm 
and  nerves  (nasal  field  of  vision),  more  or  less  complete  blindness 
ensues. 

Cerebellopontine  Angle. — Tumors  of  the  cerebellopontine  angle 
cause  homolateral  disturbances  of  hearing  and  of  equilibration  from 
involvement  of  the  auditory  nerve,  which  with  the  tumor  seems  usually  to 
be  intimately  related;  homolateral  paresis  or  paralysis  of  the  fifth,  sixth, 
and  seventh  cranial  nerves  (from  compression) ;  controlateral  hemiplegia 
and  hemianesthesia  from  compression  of  the  motor  and  sensory  tracts 
in  the  pons;  and  evidences  of  disturbance  of  the  cerebellum  of  the  same 
side. 

Cerebellum. — Lesions  (tumors)  of  the  cerebellum  give  rise  to  homo- 
lateral motor  weakness  and  hypotonia  of  the  arm,  leg,  neck,  and  trunk; 
sometimes  contralateral  hemiplegia  (from  pressure  on  the  pons  and 
medulla);  incoordination,  usually  more  marked  on  the  side  of  the  lesion; 
inability  to  maintain  equilibrium,  an  unsteady  gait,  and  a  tendency  to 
turn  and  fall,  usually  toward  the  side  of  the  tumor;  and  nystagmus.  Any 
of  the  regional  cranial  nerves  may  be  affected  by  compression.  Vertigo 
is  often  very  marked,  and  suggests  Meniere's  disease.  Muscular 
rigidity,  especially  of  the  muscles  of  the  neck,  back,  and  trunk  (opisthot- 
onos) may  occur,  and  may  be  associated  with  muscular  twitchings  or 
tonic  spasms,  especially  in  disease  of  the  middle  lobe;  in  this  event,  the 
tendency  may  be  to  fall  backward. 

Spinal  Cord. — The  localization  of  focal  lesions  of  the  spinal  cord  pre- 
supposes a  knowledge  of  the  functions  of  the  segments  of  the  cord,  of 
the  segmental  muscular  and  sensory  innervations,  and  of  the  reflex 
arcs  represented  in  each  segment.  These  are  shown  in  Plate  I,  page 
803,  and  in  the  accompanying  tables,  I,  II,  and  III,  arranged  by  M.  A. 
Starr  (pages  838  and  839). 

Total  Transverse  Lesions.^A  total  transverse  lesion,  one  in 
which  that  part  of  the  cord  below  the  segmental  level  of  the  lesion  is 
entirely  removed  from  all  influences  emanating  from  above,  gives  rise 
to:  (1)  Complete  flaccid  paralysis  of  all  the  muscles  innervated  by  the 
cord  below  the  segmental  level  of  the  lesion  (this  is  in  contrast  to  sub- 
total transverse  lesions  in  which  spastic  paralysis  occurs);  (2)  complete 
anesthesia  below  the  segmental  level  of  the  lesion;  (3)  absent  knee- 
jerks,  and  other  deep  reflexes  below  the  segmental  level  of  the  lesion  (occa- 
sionally certain  of  the  cutaneous  reflexes,  such  as  the  plantar  reflex — dorsal 
flexion  of  the  toe,  the  Babinski  sign — may  be  preserved) ;  (4)  atrophy  of 
the  paralyzed  muscles;  (5)  partial  or  complete  reactions  of  degeneration; 
and  (6)  loss  of  control  over  the  vesical  and  rectal  sphincters. 

Subtotal  Transverse  Lesions. — Subtotal  transverse  lesions  give 
rise  to  motor  paralyses  varying  with  the  segmental  level  (Table  I,  page 
838),  segmental  sensory  changes  shown  in  Plate  I,  page  803,  and 
disturbances  of  reflexes  shown  in  Table  II,  page  839.  In  general,  the 
important  symptoms  are  those  of  myelitis  (page  880). 


838 


DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 


Unilateral  Lesions  (Brown-Sequard  Paralysis). — Lesions  lim- 
ited to  one  lateral  half  of  the  spinal  cord  are  occasionally  seen  in  stab 
wounds,  bullet  wounds,  syphilis,  and  tumors,  and  are  rarely  observed 
also  in  syringomyelia  and  spinal  hemorrhage.  They  give  rise  to 
the   following   characteristic   symptom-complex,   named   after   Brown- 


Table  I, — Showing  the  Muscles  Represented  in  Groups  of  Cells  in  the  Various 
Segments  of  the  Spinal  Cord. 


II.,  ni. 

IV. 

V, 

VI. 

VII. 

vin. 

L 

Cervical. 

Cervical. 

Cervical. 

Cervical. 

Cervical. 

Cervical. 

Dorsal. 

Diaphragm. 

Diaphragm. 

Stern  0- 

Lev.ang.scap. 

mastoid. 

Rhomboid. 

Rhomboid. 

Trapezius. 

Supra-  and 

Supra-  and 

Scalenus. 

infraspin. 
Deltoid. 
Supin.  long. 
Biceps. 

infraspin. 
Deltoid. 
Supin.  long. 
Biceps. 
Supin.  brev. 
Serratus  mag. 
Pect.  (clav. ). 
Teres  minor. 

Biceps. 

Serratus  mag. 
Pect.  (clav.). 
Pronators. 
Triceps. 
Brach.  ant. 
Long  exten- 
sors of  wrist. 

Pronators. 

Triceps. 
Brach.  ant. 

Long  exten- 
sors of  wrist 
and  fingers. 

Pect.  (costal). 

Latis.  dorsi. 

Teres  major. 

Long  flexors 
of  wrist  and 
fingers. 

Long  flexors 

of  wrist  and 

fingers. 
Extensor  of 

thumb. 
Intrinsic 

muscles  of 

hands. 

Extensor  of 

thumb. 
Intrinsic 

muscles  of 

hands. 

I,    Lumbar. 

II,    Lumbar, 

III.    Lumbar. 

IV.    Lumbar. 

V.    Lumbar. 

Quadr,  lumb. 

Obliqui. 

Transversalis. 

Psoas. 

Psoas. 

Hiacus. 

Iliacus. 
Sartorius. 
Quad.  ext.  cruris. 

Quad.  ext.  cruris. 

Obturator. 

Adductores. 

Obturator. 

Adductores. 

Glutei. 

Glutei, 

Biceps  femoris. 

Semi-tend. 

Popliteus. 

I.    Sacral. 

n.    Sacral. 

III.     Sacral. 

IV.  and  V.  Sacral. 

Biceps  femor. 
Semi-memb. 
Ext.  long.  dig. 
Gastroc. 
Tibialis  post. 

Gastroc. 

Tibialis  post. 

Tibialis  auticus. 

Peronel. 

Intrinsic  muscles  of  foot. 

Peronei. 

Intrinsic  muscles  of  foot. 

Sphincter  ani  et  vesicse. 
Perineal  muscles. 

CEREBROSPINAL  LOCALIZATION  839 

Sequard:  (1)  On  the  side  of  the  lesion:  (a)  motor  paralysis  on  a  level 
with  and  below  the  lesion — flaccid  paralysis  and  atrophy,  with  the  re- 
actions of  degeneration,  of  the  muscles  innervated  by  the  segment  of 
cord  destroyed,  and  spastic  paralysis  of  the  muscles  innervated  by  lower 
motor  neurons  below  the  destroyed  segment  of  the  cord  (due  to  degen- 
eration of  the  pyramidal  tract — upper  motor  neuron);  (b)  a  segmental 
zone  of  complete  anesthesia  (protopathic,  epicritic,  and  deep  sensi- 
bility) corresponding  to  the  spinal-cord  segment  destroyed;  and  (c)  below 


Table  II. — Localization  of  Muscular  Meflex  Acts  in  the  Spinal  Cord. 

Reflex  acts.  Localization  in  segment. 

Pupillary  reflex  through  the  sjTnpathetic  :  Dil-     Fourth  cervical  to  first  dorsal. 

atation  of  the  pupil  produced  by  irritation  of 

the  neck. 
Scapular  reflex  :  Irritation  of  the  skin  over  the     Fifth  cervical  to  first  dorsal. 

scapula  produces  contraction  of  the  scapular 

muscles. 
Biceps  and   supinator  longus  :    Tapping  their     Fifth  and  sixth  cervical. 

tendons  produces  flexion  of  the  forearm. 
Triceps  reflex  :   Tapping  tendon  produces  ex-     Sixth  cervical. 

tension  of  forearm. 
Scapulohumeral  reflex  :  Tapping  the  inner  lower    Seventh  cervical. 

edge  of  the  scapula  causes  adduction  of  the 

arm. 
Tapping  extensor  tendons  at  the  wrist  causes  ex-     Sixth  to  eighth  cervical. 

tension  of  the  hand. 
Tapping  flexor  tendons  at  the  wrist  causes  flexion    Seventh  to  eighth  cervical. 

of  the  hand. 
Palmar  reflex  :  Stroking  palm  causes  closure  of    Eighth  cervical  to  first  dorsal. 

fingers  ;  finger  clonus. 
Abdominal  reflex  :   Stroking  side  of  abdomen     Ninth  to  twelfth  dorsal. 

causes  retraction. 
Genital  reflex  :   Squeezing  the   testicle  causes     First  to  third  lumbar. 

contraction  of  the  abdominal  muscles. 
Patella  tendon  :  Striking  tendon  at  knee  causes    Second  and  third  lumbar. 

extension  of  the  leg  ;  "knee-jerk." 
Achilles  tendon  reflex  :   Tapping  the  Achilles     First  to  third  sacral. 

tendon  causes  flexion  of  ankle. 
Foot   clonus  :    Extension    of    Achilles   tendon     First  to  third  sacral. 

causes  flexion  of  the  ankle. 
Plantar   reflex  :   Tickling  sole  of  foot  causes    First  to  third  sacral. 

flexion  of  the  toes. 
Babinski's  reflex  :  Scratching  sole  of  foot  causes 

extension   of  great   toe  and   flexion   of  the 

others. 
^Mendel's  reflex :  Tapping  the  tendons  of  the 

toes  causes  flexion  or  extension  of  the  toes. 


Table  III.  — Localization  of  Shin  Reflexes  in  the  Spinal  Cord. 

Eeflex  acts.  Localization  in  segment. 

Epigastric  reflex  :  Stroking  breast  causes  dim-     Seventh  to  ninth  dorsal. 

1)1  ing  of  tlie  epigastrium. 
Cremasteric  reflex  :  Strolcing  inner  side  of  thigh     First  and  second  lumbar. 

causes  retraction  of  scrotum. 
Gluteal  i-eflex  :   Stroking  buttock  causes  dim-     Fourth  to  fifth  lumbar. 

pling  in  the  fold. 


840 


DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 


the  level  of  the  lesion — normal  or  increased  protopathic  and  epicritic 
sensibility,  but  usually  lessening  of  the  deep  sensibility  (muscle  sense). 
(2)  On  the  side  opposite  the  lesion:  (a)  lessened  protopathic  (pain) 
and  epicritic  (tactile  and  temperature)  sensibility;  and  (b)  normal  deep 
sensibility,  muscular  power,  and  reflexes. 


APHASIA. 


The  following  statements  are  largely  adapted  from  Starr's  discussion 
of  aphasia : 

The  basis  of  language  is  a  series  of  memory  pictures  of:  (1)  The  sound 
of  a  word;  (2)  the  effort  necessary  to  enunciate  it;  (3)  the  appearance 
that  its  printed  or  written  symbols  present;  and  (4)  the  effort  needed  to 


Fig.  21 
Hand  rj.^^-^ 


Voice 


Hearing 


Diagram  to  illustrate  aphasia.  The  cortical,  sensory,  and  motor  centres  are  indicated  by  the 
arrows.  The  secondary  cortical  centres  of  memories  are  indicated  by  circles.  /,  visual,  of  objects; 
//,  visual,  of  words;  ///,  tactile;  IV,  auditory;  V,  speech;  VI,  writing.  These  are  joined  to  one 
another  by  association  fibers  which  transmit  impulses  in  both  directions.  Subcortical  lesions  in 
these  fibers  as  well  as  lesions  in  the  cortex,  cause  aphasia.     (Starr.) 


produce  these  symbols  in  writing.  These  memory  pictures  are  inti- 
mately connected  with  one  another  by  means  of  association  fibers 
which  pass  in  all  directions  between  the  areas  in  which  they  are  located, 
and  they  are  also  joined  to  the  memory  pictures  which  make  up  the  con- 
cept (Fig.  21).     They  are  so  intimately  joined  that  if  one  is  lost  all  the 


APHASIA  841 

otheis  feel  the  effect,  and  a  break  in  the  mechanism  leads  to  a  defect 
in  the  act  of  speech.  The  loss  of  speech  or  of  the  power  of  compre- 
hending the  spoken  or  written  language  is  termed  aphasia;  the  loss  of 
concepts  (inability  to  understand  the  uses  of  familiar  objects)  is  termed 
apraxia. 

Etiology. — ^Aphasia  is  occasionally  said  to  be  functional  in  nature, 
being  due  to  a  temporary  disturbance  of  the  speech  centres,  such  as  may 
occur  in  epilepsy,  hysteria,  intoxications  like  alcoholism,  uremia,  etc., 
and  angiospasm  of  the  cerebral  bloodvessels  (in  which  condition  there 
is  usually  also  some  anatomical  disorder  of  the  vessels).  In  the  great 
majority  of  cases,  however,  aphasia  is  due  to  a  destructive  anatomical 
lesion,  such  as  cerebral  hemorrhage,  softening  (embolism  or  throm- 
bosis,) abscess,  or  tumor;  and  the  lesion  may  involve  the  centres  (cortical 
aphasia)  or  the  tracts  (subcortical  aphasia). 

Types  of  Aphasia. — Aphasia  is  broadly  divided  into  sensory  and  motor. 
Sensory  aphasia  consists  in  a  lack  of  power  to  recognize  or  to  recall  the 
sound  or  appearance  of  words.  If  the  sound  alone  is  lost,  the  condition 
is  termed  word-deafness;  if  the  appearance  is  lost,  the  condition  is 
termed  word-blindness.  Motor  aphasia  consists  in  a  lack  of  power  to 
initiate  the  effort  and  set  in  action  the  motor  mechanism  needed  to  pro- 
nounce or  to  write  a  word.  The  former  is  termed  motor  or  ataxic 
aphasia,  the  latter  motor  agraphia;  they  are  usually  combined. 

Word-deafness. — If  the  memory  of  the  sound  of  a  word  is  lost, 
the  word  cannot  be  called  to  mind  and  cannot  be  recognized  when 
heard.  If,  having  been  shown  a  watch  or  other  familiar  object,  the 
patient  is  unable  to  name  it,  and  does  not  recognize  the  correct  name 
when  stated,  he  is  totally  word-deaf,  unable  to  understand  what  is 
said  to  him.  The  lesion  is  in  the  middle  part  of  the  cortex  of  the 
first  and  second  temporal  convolutions  in  the  left  hemisphere  in  right- 
handed,  and  in  the  right  hemisphere  in  left-handed  persons.  Since  the 
patient  is  unable  to  call  to  mind  the  sound  of  a  word,  he  is  unable  to  say 
it;  but  the  motor  act  of  pronunciation  may  be  initiated  if  the  impulse 
can  be  sent  to  its  centre  without  passing  through  the  auditory  centre. 
This  is  the  case  in  exclamations,  when  one  does  not  choose  his  words; 
many  patients  can  swear,  although  they  cannot  talk.  If  the  patient 
exhibits  recognition  of  the  name  of  a  familiar  object  when  it  has  been 
stated,  he  has  only  partial  word-deafness,  or  auditory  amnesia.  He 
retains  the  sound-memory  picture  (in  the  cortex),  and  it  can  be  aroused 
by  hearing  it  (transmission  by  the  auditory  tract  to  the  cortex);  but  he 
cannot  make  the  connection  between  the  sight  of  the  object  and  tlie 
sound-memory  picture.     The  lesion,  therefore,  is  subcortical. 

Word-blindness  (Alexia,  Visual  Aphasia). — If  the  memory  of  the 
appearance  of  a  word  is  lost,  the  usual  image  of  it  cannot  be  called  to 
mind  or  recognized;  the  patient  is  therefore  unable  to  read,  because  the 
shapes  of  the  letters  and  words  seen  arouse  no  recollection,  and  he  is 
unable  to  write  spontaneously,  because  he  cannot  remember  how  the 
letter  looks  that  he  wishes  to  write.     Persons  who  are  word-blind  can 


842  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

sometimes  ^Tite  at  dictation  or  copy,  and  yet  show  no  evidence  of  under- 
standing what  has  been  written;  the  ^^T-iting  centre  has  been  called  into 
activity  through  some  association  tract  without  the  intervention  of  the 
word-memory  picture.  A  distinction  must  be  made  between  those  who 
have  lost  the  memory  picture  (cortical  word-blindness)  and  those  in 
whom  it  cannot  be  recalled  by  ordinary  means  (subcortical  word- 
blindness).  Visual  amnesia  with  word-blindness  is  due  to  a  lesion 
involving  the  inferior  parietal  convolutions  and  angular  gyrus  in  the  left 
hemisphere  in  right-handed  persons,  and  vice  versa.  It  may  be  associ- 
ated with  psychical  blindness.  Word-deafness  and  word-blindness  fre- 
quently occur  together;  the  lesion  involves  the  temporal  convolutions 
and  the  angular  gyrus. 

Optical  Aphasia,  Transcortical  Aphasia,  or  Intercortical  Sen- 
sory Aphasia. — ^AMien  the  association  fibers  between  the  memories  of 
sight  and  the  memories  of  sound  are  severed,  a  condition  of  aphasia  re- 
sults, which  is  characterized  by  an  inability  to  recall  the  name  of  a  thing 
seen  and  to  picture  to  the  mind  the  appearance  of  a  thing  named;  yet 
the  name  is  recognized  when  heard,  and  the  object  is  recognized  when 
seen.  The  lesion  lies  in  the  long  association  tract  within  the  temporal 
and  occipital  lobes. 

Motor  Aphasia  (Aphemia). — If  the  memory  of  the  effort  needed  to 
pronounce  a  word  is  lost,  a  true  paralysis  of  active  speech  occurs, 
although  the  muscles  may  not  be  weakened.  The  loss  of  speech  in- 
volves a  loss  of  the  power  of  repeating  words  after  one  another,  as  well 
as  of  voluntary  speech,  and  is  not  accompanied  by  any  inability  to 
understand  spoken  or  "vsTitten  language.  This  is  the  ordinary  form  of 
motor  aphasia  and  is  due  to  a  lesion  of  Broca's  centre  in  the  posterior  part 
of  the  left  third  frontal  convolution  in  right-handed  persons. 

Agraphia. — Loss  of  the  effort  memories  necessary  for  T\Titing  is 
known  as  agraphia:  the  pen  cannot  be  used;  copying,  wTiting  at  dic- 
tation, and  voluntary  writing,  are  all  lost.  The  condition  is  usually  asso- 
ciated with  motor  aphasia.  ^Mien  a  word  cannot  be  recalled  to  mind, 
or  read,  or  mentally  enunciated,  in  the  majority  of  persons  it  cannot  be 
written;  but  words  then  can  often  be  VvTitten  at  dictation,  if  the  person 
is  one  who  has  WTitten  much.  Hence,  sensory  agraphia  and  motor 
agraphia  must  be  distinguished,  the  former  being  a  part  of  word- 
blindness,  the  latter  not  at  all  associated  with  inability  to  read.  The 
lesion  in  motor  agraphia  is  not  certainly  known,  though  a  few  facts 
point  to  the  posterior  part  of  the  second  frontal  convolution  as  the  prob- 
able seat  of  this  function. 

Paraphasia,  or  Intercortical  Motor  Aphasia;  Aphasia  of  Con- 
duction.— ^The  several  memory  pictures  which  are  united  in  the  word- 
image  may  reasonably  be  regarded  as  separate  from  one  another  in  their 
location  in  the  brain.  But  since  they  are  joined  together  to  form  the 
word-image,  it  follows  that  the  association  fibers  joining  the  various 
areas  are  as  necessary  to  the  use  of  even  a  single  word  as  the  various 
areas  with  their  memories;  it  is  really  by  association  only  that  an  object 


APHASIA 


843 


or  a  word  becomes  a  subject  of  thought  or  use.  If  these  associations  are 
broken,  the  result  is  a  defect  of  language,  characterized  by  the  misplace- 
ment of  words,  and  the  patient  talks  a  jargon.  There  are  as  many 
phases  of  this  so-called  paraphasia,  or  intercortical  aphasia,  as  there  are 
association  tracts.  In  intercortical  motor  aphasia  the  patient  can  under- 
stand what  is  heard  or  seen,  and  can  enunciate  words  clearly,  but  is 
unable  to  repeat  after  another  person  a  word  heard;  he  talks  rapidly 
and  constantly,  trying  hard  to  convey  his  ideas,  but  he  cannot  be  under- 
stood on  account  of  the  mingling  of  nonsense  words  or  of  syllables  with 
words  (jargon). 

Some  lesion  of  these  association  fibers  is  found  at  the  necropsy  in 
almost  all  cases  of  aphasia,  so  that  aphasia  of  purely  cortical  origin  is 
rare.  The  lesion  of  these  fibers  necessarily  causes  great  confusion  in  the 
mental  processes  of  association,  so  that  defects  of  intelligence  are  very 
striking  in  all  cases  of  aphasia.  Marie  states  that  in  almost  all  cases  a 
lesion  can  be  shown  in  the  lenticular  zone  lying  at  the  bottom  of  the 
Sylvian  fissure  and  outside  of  the  lenticular  nucleus — the  zone  through 
which  the  majority  of  these  association  fibers  pass.  This  he  terms  the 
"intellectual  centre  of  language."  He  regards  the  motor  centre  in 
Broca's  convolution  as  wholly  subsidiary,  and  he  considers  that  its 
lesion  causes  anarthria  (difficulty  in  the  proper  muscular  act  of  speaking 
without  disturbance  of  intelligence)  rather  than  aphasia.  Marie's  opin- 
ions have  not  yet  been  accepted. 

The  accompanying  table  (Starr's)  shows  the  chief  defects  in  each 
variety  of  aphasia: 


Table  IV. —  The  Symptoms  in  Diffeeent  Forms  op  Aphasia. 


Variety. 

Understand- 
ing of 
language. 

Power  to  re- 
peat words. 

Power  to  talk. 

Power  to  read. 

Power  to  write. 

1.   Word-deafness. 

(a)  cortical, 

Lost. 

Lost. 

Retained 

(not  to  answer). 

Retained 
(not  aloud). 

Retained. 

(b)  subcortical. 

Lost. 

Lost. 

Imperfect 
(not  to  answer). 

Retained 
(not  aloud). 

Retained. 

2.    Word-blindness. 

(a)  cortical, 

Retained. 

Retained. 

Retained. 

Lost. 

Lost. 

(6)  subcortical. 

Retained. 

Retained. 

Retained. 

Lost. 

Imperfect. 

3.  Intercortical, 

between  T.  and  0. 

Imperfect. 

Retained. 

Retained. 

Imperfect 
(without  com- 

Retained 
(not  at  dicta- 

4. Molor  aphasia. 

prehension). 

tion). 

(a)  cortical. 

Retained. 

Lost. 

Lost. 

Retained 
(not  aloud). 

Lost. 

(6)  subcortical. 

Retained. 

Lost. 

Lost. 

Imperfect 
(not  aloud). 

Lost. 

5.  Agraphia. 

la)  cortical, 

Retained. 

Retained. 

Retained. 

Retained. 

Lost. 

{b)  subcortical. 

Retained. 

Retained. 

Retained. 

Retained. 

Imperfect. 

C.  Intercortical, 

between  T.  and  F. 

Imperfect. 

Lost. 

Jargon. 

Imperfect. 

Lost    or    im- 
perfect. 

Apraxia,  the  loss  of  concepts,  includes  psychical  blindness,  psychical 
deafness,  amnesia,  and  astereognosis. 


844  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

Psychical  blindness  is  a  condition  in  which  there  is  a  loss  of  visual 
memories,  so  that  the  recognition  of  objects  seen  is  imperfect  and  the 
mind  cannot  recall  the  appearance  of  things  formerly  familiar;  the 
members  of  the  patient's  family,  for  instance,  may  not  be  recognized  by 
sight  (optic  asymbolia),  although  they  may  be  identified  by  the  sound  of 
their  voices;  objects  once  familiar  cannot  be  named  (anomia).  The  lesion 
in  these  cases  is  in  the  cortex  of  the  occipital  lobe,  in  the  convexity  (wide 
area  of  the  location  of  visual  memory  pictures),  as  well  as  in  the  cuneus; 
commonly  in  the  left  hemisphere  in  right-handed  subjects,  and  vice 
versa.  Hemianopsia  is  usually  also  present,  always  when  the  cuneus  is 
destroyed;  and  word-blindness  (really  a  part  of  psychical  blindness) 
may  also  be  associated,  although  it  may  occur  without  psychical  blind- 
ness. 

Psychical  deafness  (mind  deafness)  is  a  condition  in  which  the 
patient  loses  the  auditory  memory  of  sounds,  of  musical  melodies  and 
harmonies  (amusia),  and  of  words  (word-deafness),  although  he  may  retain 
the  power  of  hearing;  he  no  longer  recognizes  sounds  or  noises,  or 
musical  melodies  or  harmonies  once  familiar,  or  words  once  well  known. 
The  lesion  is  in  the  left  temporal  cortex  in  right-handed  persons,  and 
vice  versa. 

Amnesia  comprises  a  destruction  of  the  power  of  memory — an  inability 
to  recall  a  whole  or  a  part  of  past  experiences.  In  some  cases  the  power 
to  recall  these  experiences  is  only  partially  lost,  lessened,  or  impeded 
(delayed),  a  condition  spoken  of  as  hypomnesia;  or  the  condition  may 
be  one  of  perversion  of  memory  (paramnesia). 

AsTEREOGNOSis  is  a  condition  in  which  the  patient  is  unable  to 
recognize  objects  by  the  sense  of  touch  (without  the  aid  of  sight). 
The  stereognostic  sense  is  a  complex  made  up  of  tactile,  temperature, 
pressure  (weight),  and  other  memories;  it  is  represented  in  the  sensory 
area  of  the  parietal  cortex,  especially  in  the  middle  third  of  the  posterior 
central  convolution  and  the  adjacent  part  of  the  inferior  parietal  lobule, 
since  stereognostic  impressions  are  in  greatest  number  received  by  the 
hands.  Astereognosis,  therefore,  occurs  as  a  symptom  of  disease  of  the 
sensory,  cortical,  or  subcortical  area. 

Diagnosis. — Starr  states  that  to  examine  an  aphasic  subject  thor- 
oughly it  is  necessary  to  test:  (1)  The  power  to  recognize  objects  seen, 
heard,  felt,  tasted,  or  smelled,  and  their  use.  This  will  determine 
whether  the  condition  of  apraxia,  or  disturbance  in  the  power  of  recalling 
any  part  of  a  concept,  is  present.  (2)  The  power  to  recall  the  spoken 
name  of  objects  seen,  heard,  handled,  tasted,  or  smelled.  (3)  The 
power  to  understand  speech  and  musical  tunes.  (4)  The  power  to 
recall  to  mind  objects  named.  This  will  test  the  integrity  of  the  audi- 
tory speech  area  and  of  the  association  tracts  between  other  sensory 
areas  and  the  temporal  convolutions.  (5)  The  power  to  understand 
printed  or  written  words.  (6)  The  power  to  read  aloud  and  to  under- 
stand what  is  read.  (7)  The  power  to  recall  objects  the  names  of 
which  are  seen.      (8)  The  power  to  write  spontaneously  and  to  WTite 


LATERAL  SCLEROSIS  845 

the  names  of  objects  seen,  heard,  etc.  (9)  The  power  to  copy  and  to 
write  at  dictation.  (10)  The  power  to  read  understandingly  what  has 
been  written.  These  tests  will  determine  the  condition  of  the  usual 
word  memories  in  the  angular  gyrus  and  of  the  connections  between 
this  area  and  surrounding  sensory  and  motor  areas.  (11)  The  power  to 
speak  voluntarily,  and,  if  it  is  lost,  the  character  of  the  defects.  (12) 
The  power  of  repeating  words  after  another.  This  will  test  the  integrity 
of  Broca's  centre  and  its  association  tracts. 


SYSTEM  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD. 

Diseases  of  the  Upper  (Central)  Motor  Neuron. 

LATERAL  SCLEROSIS. 

(Spastic  Sjniial  Paralysis,  or  Para/plegia,  of  Adults;  Spastic  Tabes.) 

Lateral  sclerosis,  or  spastic  spinal  paralysis  (Erb),  is  a  primary  de- 
generation of  the  upper  motor  neuron — that  is,  of  the  pyramidal  tracts. 

Etiology. — The  disease  is  most  common  in  early  adult  life — after  the 
twentieth  year — although  an  analogous  condition  may  develop  in  chil- 
dren; and  the  disorder  may  be  familial.  The  cause  of  the  disease  is  not 
known;  it  has  been  attributed  to  infections,  especially  syphilis.  Doubt- 
less there  is  a  congenital  weakness  (abiotrophy)  of  the  upper  motor 
neuron,  or  some  primary  nutritional  change  in  the  motor  cells  of  the 
cerebral  cortex,  although  some  observers  doubt  whether  this  ever  occurs. 

Pathology. — The  lesions  consist  of  degeneration  of  the  upper  motor 
neuron,  that  is,  of  the  pyramidal  tracts;  this  may  be  confined  to  the 
cord  or  may  extend  to  the  cerebral  cortex.  Following  the  nerve-fiber 
degeneration  there  is  a  secondary  overgrowth  of  neuroglia. 

Symptoms. — The  symptoms,  which  usually  develop  in,  and  may  be 
for  a  very  long  time,  if  not  entirely,  confined  to,  the  legs,  consist  of  a 
sense  of  fatigue  upon  slight  exertion,  progressive  muscular  weakness 
and  spasticity,  and  exaggerated  reflexes — knee-jerks,  ankle  clonus,  and 
the  Babinski  sign.  The  rigidity  of  the  muscles  occasions  a  spastic 
gait,  adduction  of  the  thighs  (scissors  gait),  a  tendency  to  stub  the  toe, 
etc.  There  is  no  muscular  atrophy,  no  sensory  disturbance,  no  ataxia, 
and  no  disorder  of  the  sphincters. 

Diagnosis. — The  diagnosis  must  be  made  with  circumspection,  bearing 
in  mind  that  primary  lateral  sclerosis  is  very  rare.  Progressive  mus- 
cular weakness  and  spasticity,  increased  reflexes,  and  the  Babinski  sign 
indicate  disorder  of  the  lateral  columns,  but  this  may  be  due  to  dis- 
seminated or  multiple  sclerosis,  chronic  myelitis,  vertebral  caries,  or 
spinal  tumor  and  compression,  etc.;  it  may  be  part  of  a  combined  system 
disease;  it  may  be  secondary  to  a  cerebral  lesion,  such  as  apoplexy, 
softening,  or  tumor;  or  it  may  be  hysterical.  The  concomitant  symp- 
toms will  aid  in  the  diagnosis. 


846     SYSTEM  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

Prognosis. — The  disease  is  slowly  progressive^  and  may  continue  more 
than  twenty  years  (Erb). 

Treatment. — ^In  the  primary  cases  little  benefit  can  be  hoped  for, 
although  massage  and  passive  movements  may  promote  the  comfort  of 
the  patient.  Spiller  has  suggested  surgical  division  of  some  of  the  pos- 
terior lumbar  roots,  with  a  view  to  lessen  the  spasticity,  and  has  had  the 
operation  done  with  benefit. 


SPASTIC  PARALYSIS  OF  INFANTS. 

(Cerebral  Palsies  of  Children;  Birth  Palsies;  Spastic  Diplegia,   or  Paraplegia,   or 
Hemiplegia  of  Infants;  Spastic  Cerebral  Paraplegia;  Little's  Disease.) 

The  spastic  paralyses  of  infants  and  children  comprise  several  groups 
of  cases:  (1)  In  most  cases  the  disorder  dates  from  birth;  the  labor,  as 
a  rule,  was  difficult,  and  forceps  perhaps  were  used.  The  primary 
lesion  consists  of  a  more  or  less  extensive  meningeal  hemorrhage  (usually 
venous),  which  may  be  limited  to  the  motor  area,  but  may  also  extend 
to  the  frontal  lobes  (when  the  intelligence  is  likely  to  suffer).  Secondary 
sclerosis  and  non-development  of  the  brain  ensue.  (2)  In  another  series 
of  cases  there  is  more  or  less  extensive  agenesis  of  the  brain — convolu- 
tions, a  lobe,  or  a  hemisphere — due  to  imperfect  blood  supply  (hemor- 
rhage, thrombosis,  or  embolism).  There  may  be  associated  porencephalus. 
(3)  In  some  cases  there  is  a  foetal  meningo-encephalitis,  which  may  be 
s}'philitic.  (4)  Other  infants  are  born  prematurely,  before  the  p}Tamidal 
tracts  have  properly  developed,  and  an  arrested  development  is  believed 
to  be  the  cause  of  the  disease  (Little's  disease).  In  the  different  types  of 
cases,  syphilis,  alcoholism,  and  neuropathies  in  the  parents  are  looked 
upon  as  etiological  factors.  Some  cases  follow  postnatal  traumatism  to 
the  child's  head,  the  infectious  diseases,  etc. 

Symptoms. — The  symptoms  vary  somewhat  with  the  type  of  the  dis- 
order. In  the  cases  due  to  injury  during  birth,  paralysis  may  be  notice- 
able during  the  early  days  of  life,  and  is  likely  to  be  paraplegic  (two 
extremities)  or  diplegic  (four  extremities).  In  other  cases  the  child  per- 
haps may  have  had  conM_ilsions  during  early  life,  but  noteworthy  symp- 
toms are  not  manifest  until  the  child  should  begin  to  walk,  when  stiffness 
and  inability  to  use  the  muscles,  especially  of  the  legs,  become  apparent. 
In  still  other  cases  there  may  be  a  sudden  onset,  attended  by  uncon- 
sciousness and  convulsions,  and  followed  by  paralysis — ^which  is  likely 
to  be  hemiplegic,  sparing  the  face.  AMien  fully  developed  there  is 
paralysis — diplegic  or  paraplegic;  the  legs  are  most  commonly  involved, 
but  the  arms  also  may  be  affected,  and  the  child  may  not  be  able  to 
sit  up  or  support  its  head  (involvement  of  the  neck  muscles).  The 
involved  muscles  are  stiff  and  rigid;  the  adductor  spasm  of  the  thigh 
muscles  causes  approximation  of  the  knees  or  crossing  of  the  legs,  and 
impedes  or  prevents  walking.  The  reflexes  are  exaggerated;  irregular, 
spasmodic  movements  of  the  muscles  are  common,  especially  on  volun- 


AMAUROTIC  FAMILY  IDIOCY  847 

tary  movement  (spastic  chorea  or  athetosis,  usually  bilateral);  epilepsy 
is  a  frequent  sequel;  the  mentality  is  usually  imperfectly  developed,  and 
imbecility  or  idiocy  may  ensue. 

Diagnosis. — The  diagnosis  is  usually  apparent  from  the  history  of  the 
development  of  the  disease  and  the  mentioned  symptoms. 

Prognosis. — -The  outlook  is  bad,  although  some  improvement  in  the 
physical  and  mental  condition  may  be  effected  by  carefully  supervised 
physical  and  educational  measures. 

Treatment.^The  treatment  of  the  developed  disorder  comprises  general 
hygienic  measures,  massage,  electricity,  and  orthopedic  appliances,  but 
they  usually  avail  very  little.  More  attention  should  be  paid  to  mental 
training,  which  often  results  in  notable  improvement  in  the  mentality  of 
the  children.  Since  most  of  the  cases  result  from  meningeal  hemorrhage 
during  birth.  Gushing  has  advised  and  practised  with  good  result, 
opening  the  skull  and  removing  the  blood  clot  soon  after  birth. 


HEREDITARY  SPASTIC  SPINAL  PARALYSIS. 

(Hereditary  Spastic  Paraplegia.) 

Hereditary  spastic  spinal  paralysis  is  a  rare  disorder,  occurring  in 
several  members  of  the  same  family — in  one  or  more  generations.  The 
conspicuous  lesions  consist  of  degeneration  of  the  pyramidal  tracts 
throughout  the  cord,  although  often  most  marked  in  the  lower  thoracic 
and  the  lumbar  regions.  The  nature  of  the  disorder  is  not  known;  it 
is-  assumed  to  be  an  abiotrophy — imperfect  development  and  deficient 
potentiality  of  the  upper  motor  neuron,  in  consequence  of  which  it  suc- 
cumbs in  early  life.  The  symptoms  consist  of  the  development  during 
infancy,  childhood,  or  adolescence  of  muscular  rigidity  and  paralysis, 
involving  especially  the  legs;  and  increased  reflexes,  including  the 
Babinski  sign.  There  are  no  sensory  disturbances  and  no  disorders 
of  mentality.  The  disorder  is  usually  slowly  progressive,  and  is  not 
amenable  to  any  treatment. 


AMAUROTIC  FAMILY  IDIOCY. 

(Hereditary  Spastic  Paraplegia — Cerebral  Type;  Tay-Sachs'  Disease.) 

Amaurotic  family  idiocy  is  described  by  Sachs  as  a  family  disease  of 
infancy  of  unknown  etiology,  and  of  which  the  basis  is  "a  nervous  system 
so  inadequate  to  the  demands  imposed  upon  it  that  its  cells,  after  having 
performed  their  function  for  a  few  weeks  or  months  undergo  complete 
disintegration."  The  condition,  therefore,  is  also  an  abiotrophy,  and  is 
akin  to  hereditary  spastic  spinal  paralysis;  both  disorders  are  often 
described  as,  respectively,  the  spinal  and  the  cerebral  type  of  hereditary 
spastic  paraplegia.  The  chief  symptoms  of  the  cerebral  type,  or  amau- 
rotic family  idiocy,  are  thus  summarized  by  Sachs:  Mental  impairment 


848     SYSTEM  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

during  the  first  months  of  life,  leading  to  absolute  idiocy;  paresis,  or 
paralysis  of  the  greater  part  of  the  body,  which  may  be  flaccid  or  spastic; 
normal,  deficient,  or  increased  reflexes;  diminution  of  vision,  terminating 
in  absolute  blindness  (the  cherry-red  spot  in  the  region  of  the  macula 
lutea,  and  later  a  simple  optic  atrophy);  marasmus,  and  a  fatal  termi- 
nation, as  a  rule,  before  the  age  of  two  years;  the  occurrence  of  the 
affection  in  several  members  of  the  same  family;  and  in  some,  but  not 
all,  cases,  nystagmus,  strabismus,  hyperacusis,  and  convulsions.  Since 
the  disease  has  been  frequently  observed  in  the  children  of  blood  rela- 
tions, Sachs  advises  discouraging  consanguineous  marriages,  with  a  view 
to  prevent  the  birth  of  such  amaurotic  children. 


UNILATERAL  ASCENDING  AND  UNILATERAL  DESCENDING 

PARALYSIS. 

Unilateral  ascending  and  unilateral  descending  paralyses  comprise 
symptom-complexes,  first  described  by  Mills,  in  which  unilateral  primary 
degeneration  of  the  pyramidal  tract  (upper  motor  neuron)  occurs,  and 
of  which  the  clinical  expression  is  unilateral  spastic  paralysis,  beginning 
as  a  rule,  in  the  lower  extremity  and  ascending.  Mills  states  that  the 
disorder  may  be  a  primary  degeneration  of  the  pyramidal  tracts,  or 
may  occur  in  focal  disease  (tumor  or  softening)  of  the  brain  or  cord,  in 
multiple  sclerosis,  in  cerebrospinal  syphilis,  in  hysteria,  and  as  unilatera 
amyotrophic  lateral  sclerosis  or  paralysis  agitans. 


Diseases  of  the  Lower  (Peripheral)  Motor  Neuron. 

CHRONIC  ANTERIOR  POLIOMYELITIS. 

(Progressive  Spinal  Muscular  Atrophy;  Progressive  Muscular  Atrophy  of  the 
Duchenne-Aran  and  the  Vulpian  Type.) 

Etiology. — Chronic  anterior  poliomyelitis,  or  progressive  spinal  mus- 
cular atrophy,  is  most  common  in  middle  life  (excluding  the  infantile 
cases).  It  may  develop  upon  an  obsolete  acute  poliomyelitis  (page  270), 
or  may  be  due  to  syphilis,  lead  poisoning,  etc. 

Pathology.^ — The  lesions  consist  of  degeneration  and  atrophy  of  the 
motor  nuclei  in  the  anterior  cornua  of  the  spinal  cord,  and  corresponding- 
atrophy  of  the  motor  roots.  In  some  cases  there  are  associated  degen- 
erative changes  in  the  pyramidal  tracts  (amyotrophic  lateral  sclerosis). 

Symptoms. — The  chief  symptoms  consist  of  muscular  atrophy  and 
proportionate  weakness  and  flaccidity  (flaccid  paralysis),  which  are 
usually  first  manifest  in  the  small  muscles  of  one  or  both  hands  (Du- 
chenne-Aran type),  less  commonly  in  the  muscles  of  the  shoulder  girdle 
(Vulpian  type),  and  rarely  in  the  muscles  of  the  feet  or  the  trunk  There 
are  also  diminished  or  lost  reflexes,  fibrillary  twitchings  of  the  affected 


PROGRESSIVE  NEURAL  MUSCULAR  ATROPHY  849 

muscles,  and  the  reactions  of  degeneration  (partial  or  complete).  The 
atrophy  is  progressive,  and  ultimately  leads  to  the  development  of  the 
claw-like  hand  (main-en-griff e) ;  beginning  in  the  hands,  it  may  later 
implicate  the  muscles  of  the  forearm,  arm,  shoulder,  and  trunk.  There 
are  no  sensory  changes  nor  involvement  of  the  sphincters.  Occasionally 
exacerbations  of  the  process  are  observed  (subacute  poliomyelitis). 

Werding  and  Hoffman  have  described  a  similar  disorder,  beginning  in 
infancy  or  childhood,  often  hereditary,  and  affecting  several  members 
of  the  same  family. 

Diagnosis. — The  disease  should  be  distinguished  from  multiple  neu- 
ritis (pain  and  tenderness  of  the  nerve  trunks  and  sensory  changes), 
amyotiophic  lateral  sclerosis  (exaggerated  tendon  reflexes),  progressive 
neural  muscular  atrophy,  the  muscular  dystrophies,  syringomyelia,  etc. 
Some  neurologists  distinguish  between  chronic  anterior  poliomyelitis  and 
progressive  spinal  muscular  atrophy,  the  chief  distinction  being  the  absence 
of  periods  of  exacerbation  in  progressive  spinal  muscular  atrophy. 

Prognosis. — The  disorder  is  usually  progressive,  but  arrest  sometimes 
occurs. 

Treatment. — Massage,  electricity,  passive  movements,  tonics,  etc.,  are 
sometimes  useful,  but  commonly  avail  little. 


PROGRESSIVE  NEURAL  MUSCULAR  ATROPHY. 

(Progressive  Muscular  Atrophy  of  the  Charcot-Marie-Tooth  Type;  Peroneal  Type  of 
Progressive  Muscular  Atrophy.) 

Etiology. — Progressive  neural  muscular  atrophy  is  more  common  in 
males  than  females;  it  is  often  an  hereditary  or  family  disease,  and 
commonly  develops  before  the  twentieth  year.     No  cause  is  known. 

Pathology. — The  lesions  consist  of  degeneration  of  the  axons  and  con- 
nective-tissue overgrowth  of  the  peripheral  nerves,  atrophy  of  the  cells 
of  the  anterior  cornua  of  the  spinal  cord,  degeneration  of  the  posterior 
roots  and  columns,  slight  degeneration  of  the  pyramidal  tracts,  and 
atrophy  of  the  muscle  fibers,  with  connective-tissue  overgrowth. 

Symptoms. — The  chief  symptoms  consist  of  progressive  muscular 
atrophy,  weakness,  and  flaccidity  (flaccid  paralysis),  beginning  in  the 
small  muscles  of  the  feet,  and  later  involving  the  peroneal  muscles,  so 
that  foot-drop  ensues.  In  the  course  of  time  the  muscles  of  the  thigh  may 
become  involved,  as  well  as  the  small  muscles  of  the  hands,  and  perhaps 
the  forearm.  The  muscles  of  the  upper  arm,  neck,  trunk,  and  face  are 
rarely  implicated.  Associated  with  the  paralyses  there  are  fibrillary 
twitchings  of  the  affected  muscles,  diminished  or  lost  reflexes,  reactions 
of  degeneration  (partial  or  complete),  and  often  paresthesia,  lessened 
sensibility,  and  slight  pain  in  the  affected  peripheral  regions. 

Diagnosis. — The  hereditary  or  family  occurrence  of  the  disease,  its 
development  in  early  life,  the  almost  if  not  quite  complete  limitation 
of  the  atrophic  and  other  changes  to  the  periphery,  and  the  prominence 
54 


850     SYSTEM  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

of  the  motor  as  contrasted  with  the  sensory  phenomena,  are  character- 
istic of  the  disease  and  distinguish  it  from  progressive  spinal  muscular 
atrophy  (chronic  anterior  poliomyelitis),  multiple  neuritis,  and  the  mus- 
cular dystrophies. 

Prognosis. — The  disease  is  slowly  progressive,  but,  having  reached  its 
height,  it  may  remain  stationary  for  years. 

Treatment. —  No  known  treatment  is  of  any  noteworthy  avail,  but 
massage,  electricity,  passive  movements,  and  orthopedic  appliances  may 
afford  symptomatic  relief. 


BULBAR  PARALYSIS. 

(Inferior  Polioencephalitis.) 

Bulbar  palsy  is  a  paralysis  of  the  motor  nuclei  of  the  bulb  (pons  and 
medulla) — that  is,  the  motor  trigeminal,  the  facial,  the  glossopharyngeal, 
the  vagus,  the  spinal  accessory,  and  the  hypoglossal  nuclei. 

Acute  bulbar  palsy  (inferior  polioencephalitis)  may  be  due  to 
acute  inflammation  (akin  to  acute  anterior  poliomyelitis),  or  to  embo- 
lism, thrombosis,  or  hemorrhage  of  the  vessels  supplying  the  bulbar 
nuclei.  The  lesions  are  analogous  to  those  of  acute  poliomyelitis  (page 
270),  or  to  those  of  embolism,  thrombosis,  or  hemorrhage  occurring  else- 
where in  the  brain.  The  onset  is  usually  sudden,  and  may  be  attended 
by  headache,  vertigo,  and  vomiting.  If  death  does  not  soon  ensue 
(which  is  common,  on  account  of  respiratory  and  cardiac  failure)  the 
muscles  of  the  lower  part  of  the  face,  the  lips,  the  tongue,  the  palate,  and 
the  pharynx  are  found  to  be  paralyzed.  Death  may  eventually  ensue. 
In  some  cases  there  is  associated  ophthalmoplegia  (superior  polio- 
encephalitis) or  acute  poliomyelitis.  The  cases  due  to  hemorrhage  or 
softening  (embolism  or  thrombosis)  may  sometimes  be  distinguished 
from  those  due  to  infection  or  toxemia  (inflammation)  by  their  being  more 
sudden  in  onset,  and  usually  attended  by  motor  (paralytic)  and  sensory 
phenomena  due  to  implication  of  the  related  tracts  passing  through  the 
pons  and  medulla;  and  sometimes  by  the  absence  of  fever  and  other  signs 
of  infection. 

Chronic  bulbar  palsy  (glosso-labio-laryngeal  and  pharyngeal 
paralysis)  occurs  especially  after  the  fortieth  year,  and  is  of  unknown 
etiology;  it  is  probably  an  abiotrophy.  The  lesions  consist  of  bilateral 
degeneration  of  the  motor  nuclei  of  the  bulb,  especially  the  vagus,  spinal 
accessory,  and  hypoglossal. 

Symptoms. — The  symptoms  consist  of  the  gradual  onset  and  pro- 
gression of  difficulty  in  articulating  (hypoglossal  involvement),  which 
is  especially  marked  in  connection  with  labials,  such  as  b,  p,  and  v, 
and  linguals,  such  as  1,  m,  r,  and  t.  Soon  there  is  difficulty  in  swal- 
lowing (vagus  and  spinal  accessory  involvement),  and  fluids  regurgitate 
through  the  nose  (paralysis  of  the  palatal  and  pharyngeal  muscles); 
food  may  pass  into  the  larynx  (loss  of  the  pharyngeal  reflex),  and  the 


OPHTHALMOPLEGIA  851 

voice  takes  on  a  nasal  quality  and  becomes  weak.  In  the  course  of  time 
the  muscles  of  the  lips  (orbicularis  oris,  supplied  by  the  hypoglossal), 
lower  part  of  the  face  (facial  nerve),  and  tongue  become  paralyzed  and 
atrophied,  and  exhibit  fibrillary  twitchings  and  the  reactions  of  degener- 
ation; the  tongue  cannot  be  protruded;  the  lips  cannot  be  puckered  (as 
in  whistling);  the  saliva  drools  from  the  mouth;  the  palatal,  pharyngeal, 
and  laryngeal  reflexes  lessen  and  finally  disappear;  and  in  the  course  of 
several  years  the  patient  dies  from  respiratory  or  cardiac  failure,  if  he 
has  not  earlier  succumbed  to  an  intercurrent  infection.  Intelligence  is 
preserved  throughout  the  course  of  the  disease  and  there  are  no  sensory 
changes.     In  some  cases  there  is  an  associated  ophthalmoplegia. 

Diagnosis. — The  diagnosis  is  rarely  diflScult.  Some  confusion  may  occur 
with  pseudobulbar  palsy,  a  disorder  caused  by  supranuclear  (cerebral) 
lesions;  but  in  this  there  is  usually  a  history  of  apoplectiform  attacks,  the 
lesions  are  unilateral  or  asymmetrical  in  distribution  and  non-progressive 
(in  the  absence  of  succeeding  apoplectiform  attacks),  and  muscular 
atrophy,  fibrillary  twitchings,  and  the  reactions  of  degeneration  do  not 
occur.  So-called  asthenic  bulbar  paralysis,  or  myasthenia  gravis  (a  dis- 
order of  unknown  nature,  although  probably  toxic,  and  muscular  rather 
than  nervous  in  origin),  may  be  distinguished  by  the  rapid  exhaustion 
of  the  muscles  upon  slight  exertion,  and  their  recovery  upon  resting;  by 
involvement  of  muscles  other  than  those  innervated  by  the  bulb  (such  as 
the  limbs  and  the  ocular  muscles),  and  the  absence  of  atrophy  and  fibrillary 
twitchings  of  the  affected  muscles;  and  by  the  presence  of  the  myasthenic 
reaction  (early  exhaustion  of  the  muscle,  especially  when  stimulated  by 
the  faradic  current,  and  recovery  after  resting).  Postdiphtheritic  and 
other  forms  of  multiple  neuritis  and  the  cases  due  to  tumor,  meningitis, 
etc.,  should  be  readily  distinguished. 

Prognosis, — The  disease,  as  a  rule,  is  steadily  progressive. 

Treatment, — There  is  no  satisfactory  treatment.  Benefit  often  attends 
general  hygienic  measures,  electricity,  and  strychnine.  Special  care 
must  be  taken  in  feeding  the  patient  to  prevent  aspiration  of  food  and 
consecutive  bronchopneumonia. 


OPHTHALMOPLEGIA. 

(Superior  Polioencephalitis.) 

Ophthalmoplegia,  or  paralysis  of  the  motor  nuclei  of  the  eyeball,  is  a 
disorder  in  every  way  allied  to  bulbar  palsy,  with  which  it  is  often  asso- 
ciated; like  it,  it  may  be  acute  or  chronic,  and  the  etiological  factors  are 
analogous.  The  acute  cases  may  be  sudden  in  onset,  attended  by  head- 
ache, vertigo,  and  vomiting,  and  are  characterized  by  rapidly  developing 
paralysis  of  the  ocular  muscles — except,  in  some  cases,  the  elevator  of 
the  upper  lid  and  the  sphincter  of  the  iris.  In  some  cases  death  ensues 
in  stupor  or  coma;  in  other  cases  the  patient  may  recover  (usually  neu- 
ritic  cases),  or  chronic  ophthalmoplegia  may  ensue.     This  may  also  be 


852     SYSTEM  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

a  chronic  process  from  the  beginning,  and  is  characterized  by  gradually 
progressing  paralysis  of  the  ocular  muscles,  commonly  bilateral.  The 
paralysis  may  be  partial  or  complete  and  may  involve  one  or  ail  the 
muscles.  Diplopia  is  the  chief  complaint,  but  it  may  disappear  in 
advanced  cases.  Ptosis  may  or  may  not  be  present.  In  some  cases 
only  the  extraocular  muscles  are  involved  (external  ophthalmoplegia); 
in  some  cases  only  the  internal  muscles  (internal  ophthalmoplegia);  in 
other  cases,  both.  The  disorder  is  usually  found  in  association  with 
syphilis,  tabes  dorsalis,  paretic  dementia,  and  progressive  muscular 
atrophy.  The  treatment  is  unsatisfactory,  but  the  salicylates  seem  to 
be  of  value  in  some  acute  cases,  and  the  iodides  in  some  of  the  chronic 
cases,  even  in  the  absence  of  a  history  of  syphilis;  in  the  event  of  syph- 
ilis the  iodides  should  be  combined  with  mercury.  The  chronic  cases 
are  occasionally  benefited  by  electricity  and  strychnine;  and  the  diplopia 
may  be  corrected  by  glasses. 


Disease  of  the  Upper  (Central)  and  the  Lower  (Peripheral) 

Motor  Neurons. 

AMYOTROPHIC  LATERAL  SCLEROSIS. 

(Progressive  Muscular  Atrophy;  Charcot's  Disease.) 

Etiology. — Amyotrophic  lateral  sclerosis  is  a  disease  of  adult  life  and 
is  somewhat  more  common  in  men  than  in  women.  It  is  doubtless  an 
abiotrophy,  but  has  been  attributed  to  intoxications  like  lead  poisoning, 
and  to  infections,  such  as  syphilis,  etc.;  but  a  definite  causal  relationship 
has  not  been  shown. 

Pathology. — The  lesions  consist  of  degeneration  and  atrophy  of  the 
upper  and  the  lower  motor  neurons — that  is,  of  the  pyramidal  tracts, 
the  nerve  cells  of  the  anterior  cornua  of  the  spinal  cord,  the  anterior  nerve 
roots,  the  peripheral  nerves,  and  the  muscles.  The  degeneration  of  the 
pyramidal  tracts  sometimes  extends  to  the  cerebral  cortex,  involving 
both  the  axons  and  the  nerve  cells. 

Symptoms. — The  symptoms  consist  of  a  combination  of  those  of 
lateral  sclerosis  (weakness  and  spasticity  of  the  muscles  of  the  legs,  with 
increased  knee-jerks,  ankle  clonus,  and  the  Babinski  sign),  and  of 
progressive  muscular  atrophy,  beginning  in  the  small  muscles  of  the 
hands,  and  associated  with  fibrillary  twitching  and  partial  or  complete 
reactions  of  degeneration.  In  the  beginning  the  symptoms  in  the  legs 
or  in  the  arms  may  be  in  the  ascendancy,  but  the  atrophy  in  the  course 
of  time  extends  to  the  forearm  and  the  upper  arm  and  may  involve  the 
muscles  of  the  trunk  (with  ensuing  kyphosis  or  lordosis)  and  the  thigh; 
those  of  the  lower  leg  are  usually  relatively  uninvolved.  Sensory  phe- 
nomena are  in  abeyance,  although  there  may  be  slight  pain.  Rarely  the 
atrophic  and  other  changes  begin  in  the  muscles  of  the  shoulder  girdle, 


TABES  DORSALIS  853 

or  in  those  supplied  by  the  motor  nuclei  of  the  bulb  (a  type  of  glosso- 
labio-laryngeal  and  pharyngeal  paralysis). 

Diagnosis. — ^The  diagnosis  is  to  be  based  upon  the  co-existence  of  the 
signs  of  lateral  sclerosis  and  of  progressive  muscular  atrophy  (involve- 
ment of  the  cells  of  the  anterior  cornua  of  the  spinal  cord). 

Prognosis. — The  disease  is  slow^ly  progressive  and  commonly  termi- 
nates fatally  within  one  to  three  or  four  years. 

Treatment. — Treatment  is  not  of  much  avail.  Symptomatic  relief  may 
follow  the  use  of  electricity,  massage,  passive  movements,  strychnine,  etc. 


Diseases  of  the  Sensory  Neuron. 

TABES  DORSALIS. 

{Locomotor  Ataxia;  Posterior  Sclerosis.) 

Etiology. — Tabes  dorsalis  is  almost  ten  times  as  common  in  men  as  in 
women;  it  develops  usually  during  the  fourth  decade  of  life,  but  cases 
are  occasionally  encountered  in  very  young  subjects  (second  decade — 
juvenile  cases  due  to  hereditary  syphilis),  and  even  about  or  after  the 
sixtieth  year.  In  about  95  per  cent,  of  the  cases  (Erb)  tabes  dorsalis 
follows  syphilitic  infection,  developing,  as  a  rule,  in  from  five  to  twenty 
years  after  the  initial  lesion;  rarely,  it  ensues  within  a  year  or  two. 
Trauma,  exposure  to  wet  and  cold,  infections  other  than  syphilis,  ex- 
treme bodily  and  mental  exertion,  sexual  excesses,  etc.,  are  sometimes 
said  to  be  of  etiological  significance. 

Pathology. — Tabes  dorsalis  is  a  disease  of  the  sensory  neuron:  of  the 
dorsal-root  fibers  (exogenous  fibers),  and  not  of  the  fibers  that  run  from 
one  part  of  the  cord  to  another  (endogenous  fibers);  following  primary 
degeneration,  secondary  sclerosis  occurs.  The  situation  of  the  primary 
lesion  has  not  been  positively  determined.  Obersteiner  and  Redlich 
have  accentuated  the  importance  of  inflammation  of  the  dorsal  pia- 
arachnoid  with  involvement  of  the  root  fibers,  which,  as  they  pierce  the 
pia-arachnoid,  are  poor  in  myelin  and  have  no  neurilemma;  Nageotte 
believes  the  process  to  originate  in  a  meningoneuritis  of  the  dorsal  roots 
centrally  to  the  dorsal  ganglia,  w^here  they  are  still  covered  by  tlie  dura 
mater;  Starr  states  that  the  primary  lesion  is  in  the  posterior  spinal 
ganglia  and  the  ganglia  of  the  cranial  nerves.  In  the  spinal  cord  the 
degenerative  and  sclerotic  lesions  are  found  in  the  pathway  of  the  dorsal- 
root  or  exogenous  fibers.  Most  of  these  enter  directly  into  the  postero- 
external column  (Burdach);  some  pass  into  the  gray  matter;  others 
later  run  in  the  postero-internal  column  (Goll),  on  account  of  the 
superior  fibers  crowding  toward  the  median  line  those  fibres  that  have 
entered  lower  down;  and  they  end  in  the  nuclei  in  the  dorsal  columns 
of  the  medulla.  Other  of  these  root  fibers  enter  directly  into  a 
small  bundle  of  fibers  (Lissauer's  tract)  at  the  apex  of  the  posterior 
cornua  and  ascending  or  descending  a  short  distance,  enter  the  cornua, 


854     SYSTEM  DISEASES  OF  THEf  BRAIN  AND  SPINAL  CORD 

where  some  of  them  end;  others  pass  forward  to  the  cells  of  the  ante- 
rior cornua  or  cross  over  to  the  opposite  side  and  enter  the  antero- 
lateral column.  Involving  these  pathways,  the  sclerosis  usually  begins, 
or  is  most  marked,  in  the  lumbar  region  and  commonly  decreases  from 
below  upward;  rarely  it  may  begin  in  the  sacral,  thoracic,  cervical,  or 
bulbar  regions.  Changes  are  often  found  in  the  cranial  nerves  and 
nuclei,  especially  the  optic  and  ocular  nerves,  the  pneumogastric,  etc.; 
in  the  motor  tracts  and  anterior  horns  of  the  spinal  cord  (this  accounting 
for  the  muscular  atrophy  of  some  cases);  and  in  the  cerebral  cortex 
(tabo-paralysis;  paretic  dementia). 

The  lesions  are  commonly  described  as  parasyphilitic  rather  than 
truly  syphilitic,  but  the  radicular  meningitis  often  found  and  the  ready 
demonstration  of  the  Wassermann  reaction  indicate  the  essentially 
syphilitic  nature  of  the  process. 

Symptoms. — The  symptoms  are  quite  variable  in  their  mode  of  devel- 
opment and  in  their  mutual  association.  They  can  perhaps  be  best 
comprehended  by  bearing  in  mind:  (1)  That  they  result  from  dorsal -root 
lesions,  and  that  a  dorsal  root  conveys  fibers  for  epicritic,  protopathic, 
and  deep  sensibility  (page  803),  as  well  as  fibers  composing  part  of  a 
reflex  arc;  (2)  that  the  disease  may  begin  at  varying  levels  of  the  cord; 
and  (3)  that  not  all  the  fibers  in  a  dorsal  root  are  diseased  at  once  or  to 
the  same  extent.  The  disease  is  sometimes  divided  clinically  into  the 
first,  incipient,  painful,  or  pre-ataxic  stage,  the  second  or  ataxic  stage, 
and  the  third  or  paralytic  stage.  In  practice  these  are  not  always 
separable  the  one  from  the  other. 

The  chief  symptoms  of  the  early  stage  of  the  disease  consist  of:  Sharp 
shooting,  fulgurant,  or  lancinating  pains,  usually  in  the  legs,  rarely  in 
the  arms  (cervical  tabes);  loss  of  the  deep  reflexes,  especially  the  laiee- 
jerk  (Westphal's  sign),  and  of  the  Achilles  teijdon  reflex;  inequality  of 
the  pupils  and  the  Argyll  Robertson  pupil  (immobility  to  light,  but 
contraction  during  convergence  and  accommodation);  and  swaying  of 
the  body,  perhaps  progressing  to  falling  when  the  eyes  are  closed  (Rom- 
berg's sign).  In  some  cases  complaint  is  of  dull  aching,  rather  than  of 
sharp  pains,  and  these  being  interpreted  as  "rheumatic,"  the  disease  is 
for  a  long  time  overlooked.  Other  patients  complain  early  of  various 
paresthetic  phenomena — such  as  numbness  or  tingling  of  the  feet,  a 
sensation  as  if  walking  on  cotton  or  eggs,  etc.;  or  of  delay  or  difficulty 
in  emptying  the  bladder;  or  of  loss  of  sexual  power  and  desire;  or  of 
transient  or  permanent  diplopia  (involvement  of  the  cranial  nerves) ;  or 
of  gradually  increasing  dimness  of  vision  (primary  optic  atrophy);  or 
of  so-called  visceral  crises,  such  as  gastric  crises  (severe  epigastric  pains 
and  vomiting),  laryngeal  crises  (dyspnoea  and  stridor),  renal  crises  (simu- 
lating renal  colic),  rectal  crises,  etc.  These  symptoms,  if  they  do  not 
occur  early,  are  likely  to  come  on  later,  and  in  varying  combinations. 
Sensory  disturbances,  as  a  rule,  are  readily  found  early  if  searched  for, 
and  commonly  consist  of  segmental  hyperthesia  or  anesthesia,  often  about 
the  chest  or  abdomen  or  in  the  legs  and  soles  of  the  feet. 


TABES  DORSALIS  855 

In  the  course  of  time  ataxia  supervenes :  the  patient  at  first  experiences 
difficulty  in  walking  in  the  dark;  the  Romberg  sign  will  be  found  upon 
examination,  but  soon  the  characteristic  ataxic  gait  supervenes — the  foot 
being  considerably  elevated,  thrown  out  with  an  ill-controlled  jerk  and 
brought  down  with  a  thud,  and  an  effort  being  made  to  control  these 
movements  by  close  attention  with  the  eyes.  Ataxia  may  also  supervene 
in  the  arms.  About  this  time  hypotonia  of  the  muscles  may  be  observed, 
although  it  often  precedes  the  ataxia;  it  consists  of  abnormal  flaccidity 
of  the  muscles  (and  sometimes  also  of  the  ligaments),  so  that  passive 
movements  of  the  limbs  much  beyond  the  normal  range  are  possible, 
although  there  may  be  no  loss  of  muscular  power.  There  are  varied 
sensory  disturbances:  the  pains  and  paresthetic  phenomena  may  con- 
tinue; bands  of  segmental  hyperesthesia  or  anesthesia  are  common;  the 
transmission  of  painful  stimuli  and  the  response  thereto  are  delayed; 
and  the  deep  sensibility,  especially  the  sense  of  location,  becomes  im- 
paired. Trophic  manifestations  also  ensue,  especially  herpes  zoster,  a 
perforating  (usually  painless)  ulcer  of  the  sole  of  the  foot  near  the  meta- 
tarsophalangeal joint  of  the  great  toe,  and  Charcot's  arthropathies — 
painless  swelling  of  the  large  joints,  especially  the  knee  (due  to  increase 
of  fluid,  enlargement  and  exostosis  of  the  ends  of  the  bones,  and 
atrophy  and  absorption  of  the  bone  and  the  articulating  cartilage). 
The  bones  may  become  brittle  and  readily  fractured. 

After  some  years,  if  the  patient  does  not  sooner  die,  the  third,  or  para- 
lytic stage,  develops:  the  patient,  in  addition  to  being  ataxic,  becomes 
muscularly  weak,  unable  to  walk,  and  finally  bedridden. 

In  a  certain  proportion  of  the  cases  tabes  becomes  associated  with 
general  paralysis  of  the  insane  (general  paresis,  paralytic  dementia), 
giving  rise  to  a  condition  sometimes  spoken  of  as  tabo-paralysis.  Some 
writers  maintain  the  essential  etiological  (syphilitic)  and  pathogenetic 
identity  of  the  two  disorders,  and  believe  that  the  onie  or  the  other  may 
be  the  antecedent  or  the  secondary  disorder  in  a  given  case.  The  ma- 
jority of  cases  of  tabes  dorsalis,  nevertheless,  are  devoid  of  noteworthy 
mental  symptoms,  and  general  paretic  subjects,  as  a  rule,  are  not  tabetic. 
However,  in  some  cases  of  tabes,  after  the  lapse  of  time,  evidences  of 
cerebral  disorder  (chronic  meningo-encephalitis)  supervene:  the  subject 
becomes  irritable;  his  character  changes,  he  becomes  intemperate,  licen- 
tious, and  neglectful  of  himself,  his  family,  and  his  business;  and  his 
memory  fails.  Soon  mental  deterioration  becomes  more  marked,  the 
general  condition  being  that  of  exaltation  and  well-being  and  delusions 
of  grandeur,  or  there  may  be  alternating  periods  of  exaltation  and  of 
depression.  In  addition  there  are  disturbances  of  speech,  which  be- 
comes slowed;  there  is  special  difficulty  in  pronouncing  labials  and 
linguals;  tremors  of  the  lips,  tongue,  face,  and  hands  (especially  obvious 
in  attempting  to  write)  become  noticeable;  and  the  patient  gradually 
develops  a  general  muscular  weakness,  although  the  mental  disorder 
may  lead  him  to  deny  any  bodily  infirmity.  Transient  paralyses,  in- 
volving the  cranial  nerves,  or  hemiplegia,  attacks  of  stupor,  coma,  or 


856     SYSTEM  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

momentary  loss  of  consciousness,  convulsive  seizures,  especially  of  the 
face  or  arm,  may  supervene.  Finally  the  dementia  becomes  aggra- 
vated, the  patient  takes  permanently  to  his  bed,  and  ultimately  dies. 
The  significant  symptoms  of  tabes  are  variously  associated  with  these 
manifestations  of  the  cerebral  disorder. 

Diagnosis. — The  diagnosis  of  tabes  dorsalis  should  be  readily  made  by 
attention  to  the  aforementioned  symptoms.  Efi^orts  should  be  made 
to  recognize  the  disease  in  its  earliest  stage;  the  presence  of  any  two  of 
the  following  signs  is  of  the  greatest  diagnostic  importance:  lightning 
pains,  Argyll  Robertson  pupil,  lost  knee-jerks  and  other  deep  reflexes,  and 
Romberg's  sign;  and  any  one  of  these  in  association  with  two  of  the  other 
mentioned  symptoms  warrant  the  diagnosis.  In  doubtful  cases  a  history 
of  syphilitic  infection,  a  positive  Wassermann  reaction,  or  an  excess  of 
lymphocytes  in  the  cerebrospinal  fluid,  will  furnish  material  diagnostic 
aid.  Multiple  neuritis  should  be  readily  excluded  by  the  absence  of 
motor  paralysis,  muscular  atrophy,  tender  nerve  trunks,  etc. 

Prognosis. — The  disease  may  pursue  a  slow  or  a  comparatively  rapip 
course,  and,  having  made  more  or  less  progress,  it  may  come  to  a 
standstill.  Slow  progression  in  the  past  is  a  promise  of  slow  progress 
in  the  future.  The  existence  of  lightning  pains  for  years  prior  to  the  loss 
of  knee-jerks  augurs  slow  progression  or  standstill,  and  the  cases  with 
early  optic  atrophy  are  likely  also  to  show  delayed  onset  of  ataxia  and 
slow  progression  of  the  other  symptoms.  Degeneration  of  the  columns 
in  the  spinal  cord,  once  effected,  of  course,  cannot  be  remedied. 

Treatment. — If  the  patient  is  in  good  physical  condition  and  the  disease 
is  not  far  advanced,  a  course  of  efficient  antisyphilitic  treatment  should 
be  instituted,  especially  if  the  infection  were  poorly,  or  not  all,  treated. 
Otherwise,  attention  should  be  directed  to  improving  the  general  nutri- 
tion of  the  patient  by  good  food,  rest,  and  tonics,  such  as  iron,  quinine, 
and  strychnine,  and  hydropathic  measures,  massage  and  electricity. 
Arsenic  and  silver  nitrate  have  been  recommended.  The  lightning  pains 
may  be  benefited  by  aspirin,  acetphenetidin,  and  other  coal-tar  deriva- 
tives, aluminum  chloride,  codeine,  and  morphine  (which  are  almost 
certain  to  engender  the  habit).  The  ataxia  may  be  markedly  improved 
by  exercises — which  have  been  systematized  for  the  tabetic  subject  by 
Fraenkel. 


INTERSTITIAL  HYPERTROPHIC  PROGRESSIVE  NEURITIS  OF 

CHILDHOOD. 

Interstitial  hypertrophic  progressive  neuritis  of  childhood  is  a  heredi- 
tary or  familial  disorder,  studied  especially  by  Dejerine,  that  develops  in 
childhood  or  adolescence  from  unknown  causes,  although  it  has  been 
attributed  to  syphilis.  The  chief  lesions  consist  of  degeneration  of 
the  posterior  roots  and  columns  of  the  cord  (as  in  tabes  dorsalis)  and 
of  parenchymatous  and  interstitial  changes  in  the  peripheral  nerves, 


HEREDITARY  OR  FAMILY  CEREBELLAR  ATAXIA         857 

especially  of  the  legs.  The  symptoms  consist  of  those  of  tabes,  especially 
ataxia  of  the  arms  and  legs,  severe  pains,  sensory  disturbances  (as  in 
tabes,  with  retardation  of  the  appreciation  of  painful  stimuli),  inequality 
of  the  pupils,  Argyll  Robertson's  sign,  etc.;  general  muscular  atrophy, 
especially  marked  at  the  periphery;  and  kyphoskoliosis  (due  to  weak- 
ness of  the  trunk  muscles).  The  palpable  nerve  trunks  are  thickened 
and  indurated.     There  is  no  satisfactory  treatment. 

Combined  System  Diseases. 

HEREDITARY  OR  FAMILY  ATAXIA. 

{Friedreich' s  Ataxia.) 

Etiology. — Friedreich's  ataxia  is  a  family  disease,  that  may  or  may  not 
have  occurred  in  the  antecedents.  It  is  slightly  more  common  in  males 
than  in  females,  and  is  likely  to  develop  in  early  life — often  in  childhood, 
and  in  the  great  majority  of  cases  before  puberty.  The  cause  is  not 
known.  Alcoholism  and  syphilis  in  the  parents  seem  to  be  inoperative. 
Evidently  the  disease  is  an  abiotrophy. 

Pathology. — The  lesions  consist  of  degeneration  and  consequent  scle- 
rosis of  the  posterior,  lateral,  and  direct  cerebellar  tracts,  and  sometimes 
also  of  Gowers'  anterolateral  tracts. 

Symptoms. — The  symptoms  consist  of  the  gradual  development  during 
early  life  of  ataxia.  This  occurs  first  in  the  legs,  and  gives  rise  to  a 
swaying  or  stumbling  gait,  which  usually  becomes  aggravated  on  closing 
the  eyes  (Romberg's  sign);  developing  later  in  the  arms,  it  occasions 
irregular  choreiform  movements.  The  head  also  may  be  subject  to 
similar  movements;  and  irregular,  oscillatory  movements  may  affect  the 
body  when  it  is  erect  at  rest,  or  a  limb  when  it  is  extended  (static  ataxia). 
Nystagmus  and  a  slow  scanning  or  stumbling  speech  often  supervene. 
The  deep  reflexes  are  lost;  the  skin  reflexes  are  usually  preserved;  there 
are  no  noteworthy  sensory  changes.  In  advanced  cases,  on  account  of 
muscular  weakness  and  atrophy,  talipes  equinus,  hammer-toes,  or  spinal 
curvature  may  occur. 

Diagnosis. — The  diagnosis  should  be  quite  apparent  from  the  onset  of 
the  aforementioned  symptoms  in  early  life,  especially  if  several  members 
of  a  family  are  affected 

Prognosis. — The  disorder  is  slowly  progressive. 

Treatment. — No  satisfactory  treatment  is  known;  the  available  treat- 
ment is  purely  symptomatic. 

HEREDITARY  OR  FAMILY  CEREBELLAR  ATAXIA. 

{Marie's  Ataxia;  Hereditary  or  Family  Spastic  Paraplegia.) 

Hereditary  or  family  cerebellar  ataxia  is  a  family  disorder,  that  tends 
to  develop  after  puberty  or  in  early  adult  life  (tlie  third  decade),  and  is 
characterized  anatomically  by  gross  atrophy  of  the  cerebellum  or  by 


858     SYSTEM  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

microscopic  atrophy  of  the  cells  of  Purkinje.  Clinically,  the  disorder 
resembles  Friedreich's  ataxia  in  the  family  occurrence,  the  ataxia 
(although  the  gait  is  likely  to  be  less  awkward),  the  Romberg's  sign, 
the  choreiform  movements,  the  nystagmus,  and  the  disturbances  of  speech; 
but  it  differs  from  Friedreich's  ataxia  in  its  onset  later  in  life,  normal  or 
exaggerated  knee-jerks,  ultimate  spasticity  of  the  legs  (attributable  to 
degeneration  of  the  pyramidal  tracts),  and  the  absence  of  deformities  of 
the  feet  and  trunk. 

ATAXIC  PARAPLEGIA. 

(Posterolateral  Sclerosis.) 

Etiology. — Ataxic  paraplegia  occurs  most  commonly  in  males  in  the 
fourth  and  fifth  decades.  No  cause  can  be  assigned;  it  is  not  due  to 
syphilis;  it  has  been  attributed  to  cold  and  wet,  traumatism,  etc.;  it  is 
probably  an  abiotrophy. 

Pathology. — The  lesions  consist  of  degeneration  and  consequent 
sclerosis  of  the  posterior  and  the  lateral  columns;  that  of  the  posterior 
columns  differs  from  that  of  tabes  in  being  equally  marked  in  the  lumbar 
and  thoracic  regions  and  in  sparing  the  dorsal -root  zones;  that  of  the 
lateral  columns  is  most  marked  in  the  pyramidal  tracts,  but  may  also 
involve  the  direct  cerebellar  and  the  direct  pyramidal  tracts. 

Symptoms. — The  symptoms  consist  of  gradually  developing  weariness, 
muscular  weakness,  and  difficulty  and  unsteadiness  in  walking.  Ex- 
amination reveals  well-marked  incoordination  (as  in  tabes  dorsalis), 
which  may  extend  to  the  arms;  and  Romberg's  sign.  The  deep  reflexes 
are  exaggerated,  including  ankle  clonus  and  the  Babinski  sign.  In  the 
course  of  time  rigidity  and  spasticity  of  the  muscles  of  the  legs  ensue 
(spastic  paraplegia),  and  may  somewhat  overshadow  the  ataxic  phe- 
nomena. Sensory  and  ocular  symptoms  are  rare.  Late,  the  sphincters 
may  become  involved,  and  mental  symptoms,  suggesting  paretic  dementia, 
may  develop. 

Diagnosis. — The  disease  should  be  readily  recognized  from  the  ataxic 
gait,  the  increased  knee-jerks,  and  muscular  rigidity,  and  the  absence  of 
the  lightning  pains,  sensory  changes,  and  ocular  signs  of  tabes. 

Prognosis. — The  disease  is  slowly  progressive,  as  a  rule,  but  sometimes 
arrest  occurs. 

Treatment. — The  treatment  is  that  of  primary  lateral  sclerosis  (page 
845),  plus  Fraenkel's  method  for  the  reeducation  of  muscles,  useful  in 
tabes  dorsalis. 

TOXIC  COMBINED  SCLEROSIS. 

(Subacute  Combined  Sclerosis  of  the  Spinal  Cord,  Putnam;  Diffuse  Secondary  De- 
generation of  the  Spinal  Cord;  Anemic  Degeneration  of  the  Spinal  Cord.) 

Etiology. — The  disorder,  or  disorders,  comprised  within  the  term  toxic 
combined  sclerosis  of  the  spinal  cord  occur  secondarily  in  the  course  of 
toxic  and  anemic  conditions,  such  as  pernicious  anemia,  severe  secondary 


MULTIPLE  SCLEROSIS  859 

anemias,  cachectic  conditions  generally,  acute  and  chronic  infections, 
prolonged  suppuration,  lead  poisoning,  ergotism,  pellagra,  etc. 

Pathology. — The  lesions  consist  of  degeneration  and  sclerosis  of  the 
posterior  columns,  usually  most  marked  in  the  thoracic  and  cervical 
regions;  and  sometimes  also  of  the  crossed  pyramidal  tracts;  rarely  of 
other  tracts.     The  degeneration  is  sometimes  focal  rather  than  systemic. 

Symptoms. — The  symptoms  consist  of  early  numbness  and  tingling  of 
the  feet  and  legs  and  mild  spastic  or  ataxic  paraplegia.  Similar  phe- 
nomena may  develop  in  the  arms,  and  those  in  the  legs  become  aggra- 
vated, so  that  the  patient  then  exhibits  the  phenomena  of  well-marked 
spastic  paraplegia,  with  diminution  or  loss  of  all  forms  of  sensibility  in 
the  legs  and  perhaps  the  lower  part  of  the  trunk.  Finally,  a  stage  of 
flaccid  paralysis  may  supervene. 

Diagnosis. — The  development  of  the  mentioned  symptoms  in  the 
course  of  any  of  the  diseases  that  may  occasion  them  should  serve  for 
the  diagnosis. 

Prognosis. — The  outlook  depends  more  upon  the  primary  disorder 
than  upon  the  nervous  manifestations.  As  a  rule,  a  fatal  outcome 
supervenes  within  a  few  months. 

Treatment. — The  treatment  is  wholly  that  of  the  primary  disorder. 

NON-SYSTEM    DISEASES   OF   THE   BRAIN   AND 

SPINAL  CORD. 

MULTIPLE  SCLEROSIS. 

{Disseminated  Sclerosis;   Insular  Sclerosis.) 

Multiple  or  disseminated  sclerosis  is  a  disorder  characterized  by 
small  islets  or  foci  of  sclerotic  neuroglial  tissue  scattered  irregularly 
throughout  the  brain  and  spinal  cord. 

Etiology. — ^Multiple  sclerosis  occurs  especially  in  early  adult  life  (be- 
fore the  thirtieth  year);  it  affects  the  sexes  about  equally.  The  exciting 
cause  is  not  known.  Some  cases  are  believed  to  be  congenital — an 
abiotrophy;  others  appear  to  follow  some  of  the  infectious  diseases 
(typhoid  fever,  scarlet  fever,  smallpox,  pneumonia,  etc.),  and  still  others 
are  attributed  to  metallic  poisons  (lead,  mercury,  etc.). 

Pathology. — The  lesions  consist  of  foci  or  islets  of  sclerotic  neuroglial 
tissue  scattered  throughout  the  brain  and  spinal  cord,  and  sometimes  also 
in  the  peripheral  (especially  the  cranial)  nerves.  They  are  much  more 
common  in  the  white  than  in  the  gray  matter,  and  they  vary  in  size  from 
those  microscopic  to  those  3  to  5  mm.  or  more  in  diameter.  The  primary 
lesion  seems  to  be  a  neuroglial  proliferation  (perhaps  toxic  in  origin), 
with  consecutive  destruction  of  the  medullary  sheaths  of  the  neurons. 
The  lesions  are  not  systemic  (that  is,  not  confined  to  definite  tracts);  and 
sparing,  at  least  for  a  very  long  time,  the  axons,  they  do  not  give  rise  to 
secondary  degenerations  of  tracts  or  fibers. 

Symptoms. — The  onset  of  the  symptoms  is  insidious  and  their  progress 
slow,  and  they  vary  extraordinarily  with  the  seat  of  the  lesions.     In  the 


860     NON-SYSTEM  DISEASES  OF  THE  BRAIN  AND  SPINAL  CORD 

so-called  typical  cases  the  early  complaint  may  be  stiffness  and  weakness 
of  one  or  both  legs,  rarely  of  an  arm.  Gradually  spastic  paralysis  of 
the  legs  develops  and  is  associated  with  increased  knee-jerks,  ankle 
clonus,  and  the  Babinski  sign;  the  deep  reflexes  of  the  arm  also  are 
usually  increased,  but  the  superficial  reflexes,  especially  of  the  abdomen 
and  the  cremasteric  reflex,  may  be  abolished.  In  most  cases  there  is 
more  or  less  ataxia  and  a  staggering  gait  (involvement  of  the  posterior 
and  cerebellar  tracts).  Muscular  tremors  develop — usually  first  and 
most  markedly  in  the  arms,  but  they  may  involve  the  legs  and  the 
head.  They  are  characterized  by  being  absent  or  ceasing  during  rest,  by 
developing  upon  voluntary  motion  of  any  kind,  such  as  writing,  taking 
hold  of  an  object  (so-called  volitional  or  intention  tremor),  by  their  general 
coarseness,  and  by  increasing  in  amplitude,  jerkiness,  and  irregularity 
upon  continuation  of  the  voluntary  movement.  Nystagmus  is  common 
and  may  develop  spontaneously  or  only  upon  voluntary  movement  of 
the  eyes;  it  may  be  associated  with  weakness  of  one  or  more  ocular 
muscles  and  diplopia.  Optic  atrophy  is  often  present  and  is  rather 
commonly  confined  to  the  temporal  half  of  one  or  both  disks.  The 
pupils  usually  react  normally  to  light  and  in  accommodation.  There  is, 
in  most  cases,  more  or  less  disorder  of  speech,  which  is  commonly  slow, 
scanning,  staccato,  syllabic,  and  in  a  monotone.  Mental  impairment 
ensues  to  a  greater  or  less  degree,  and  the  patient  becomes  emotionally 
unstable,  laughing  or  crying  upon  little  or  no  provocation. 

There  are  a  number  of  other  symptoms  that  occur  variously  in  dif- 
ferent cases,  such  as  vertigo,  apoplectiform  or  epileptiform  attacks,  pares- 
thesias, patchy  anesthesias,  disorder  of  the  vesical  and  rectal  sphincters, 
etc.  The  disease  is  often  characterized  by  notable  improvement  or  dis- 
appearance of  some  of  the  obtrusive  symptoms  and  by  relapse  or  recur- 
rence. 

Diagnosis. — A  combination  of  the  symptoms  mentioned  is  quite  char- 
acteristic. In  the  early  and  ill-developed  cases  (especially  in  young 
women)  care  must  be  taken  not  to  confound  the  disease  with  hysteria; 
in  hysteria,  however,  intention  tremors,  nystagmus,  optic  atrophy,  scan- 
ning speech,  and  the  Babinski  sign  are  absent,  and  various  hysterical 
stigmas  are  likely  to  be  present.  Cerebrospinal  syphilis  may  simulate 
multiple  sclerosis,  but  it  is  likely  to  exhibit  pupillary  and  other  phe- 
nomena, and  rarely,  if  ever,  shows  intention  tremors,  nystagmus,  and 
scanning  speech.  Paralysis  agitans  also  is  characterized  by  a  tremor, 
but  this  occurs  while  the  parts  are  at  rest  and  is  fine,  nystagmus  and 
scanning  speech  are  absent,  and  the  disease  occurs  in  advanced  life. 
Friedreich's  and  cerebellar  ataxia  should  be  readily  excluded. 

Prognosis. — The  disease  is  of  slow  progress;  remissions  are  quite 
common;  standstill  may  ensue,  but  recovery  is  not  likely. 

Treatment. — The  treatment  is  symptomatic:  rest,  the  avoidance  so  far 
as  possible  of  muscular  movements  (talking,  walking,  exercise,  etc.), 
warm  baths,  massage,  electricity  (galvanism),  and  tonics,  such  as  iron, 
quinine,  arsenic,  etc. 


ANEMIA   OF  THE  BRAIN  861 

DIFFUSE  AND  FOCAL  DISEASES  OF  THE  BRAIN. 
HYPEREMIA  OF  THE  BRAIN. 

Active  hyperemia  of  the  brain  occurs  in  the  many  and  varied  condi- 
tions that  increase  the  force  and  rapidity  of  the  heart's  action,  especially 
the  acute  infectious  diseases,  alcoholism  and  other  intoxications,  pro- 
longed mental  strain,  and  emotional  disturbances;  and  it  is  a  part  of 
sunstroke,  meningitis,  and  encephalitis.  Although  in  these  circum- 
stances more  blood  passes  through  the  brain  in  a  given  time,  it  is  not 
definitely  known  that  more  than  a  normal  amount  is  present  at  any  one 
time  (on  account  of  the  relative  inexpansibility  of  the  brain  and  the 
absence  of  local  vasomotor  control);  nor  is  it  likely  that  the  condition 
of  itself  gives  rise  to  any  noteworthy  symptoms;  the  cerebral  symptoms 
that  do  occur  are  much  more  likely  due  to  the  initiating  infectious  or 
toxic  factor. 

Passive  hyperemia  of  the  brain  occurs  in  conditions  of  general  venous 
engorgement,  such  as  develop  in  failure  of  the  heart  induced  by  any 
cause  (myocardial,  endocardial,  pericardial,  or  chronic  pulmonary  dis- 
ease), and  local  conditions,  such  as  venous  or  sinus  thrombosis,  tumors 
and  abscess  of  the  brain,  and  tumors,  aneurysms,  and  other  factors 
obstructing  the  circulation  in  the  neck.  The  symptoms  consist  of  head- 
ache, with  a  feeling  of  general  tenseness  and  perhaps  pulsation,  and  of 
pressure  behind  the  eyes,  vertigo,  tinnitus  aurium,  mental  irritability 
and  incapacity,  etc.  The  diagnosis  should  always  be  made  w^ith  cir- 
cumspection, since  the  symptoms  mentioned  are  more  likely  to  be  due 
to  some  cause  (toxic?)  other  than  mere  congestion;  and,  assuredly,  in 
the  chronic  cases.  The  treatment  of  such  cases  as  may  be  recognized  con- 
sists of  attention  to  the  underlying  causative  factor;  the  use  of  general 
depletive  measures,  especially  calomel,  or  blue  mass  and  saline  cathartics, 
hot  foot  baths,  counterirritation  to  the  back  of  the  neck;  an  ice-cap  to  the 
head;  and  the  administration  of  the  bromides,  ergot,  etc. 

ANEMIA  OF  THE  BRAIN. 

Anemia  of  the  brain  may  result  from:  (1)  Acute  or  chronic,  primary 
or  secondary,  anemia.  The  symptomatology  and  treatment  are  men- 
tioned on  page  365  et  seq.  (2)  Disorder  of  the  vasomotor  influences 
acting  in  the  splanchnic  area  and  the  skin.  When,  for  instance,  the 
vasomotor  centre  becomes  inhibited,  as  may  happen  under  tlie  influ- 
ence of  emotions,  or  when  it  becomes  of  lessened  functional  activitv,  as 
may  occur  in  infectious  and  toxic  processes,  the  circulation  in  the  brain 
may  become  readily  disturbed.  In  the  first  mentioned  case  the  abdom- 
inal vessels  dilate,  and  the  general  blood  pressure  in  consequence  falling, 
the  heart  is  no  longer  able  to  maintain  an  efficient  circulation  in  the 


862  DIFFUSE  AND  FOCAL  DISEASES  OF  THE  BRAIN 

brain,  cerebral  anemia  ensues,  and  the  patient  faints;  in  the  second 
mentioned  case,  a  satisfactory  cerebral  circulation  may  be  maintained 
in  the  recumbent  posture,  but  sudden  exertion,  emotional  disturb- 
ances, or  the  assumption  of  the  sitting  or  erect  posture,  may  similarly 
induce  cerebral  anemia  and  fainting.  A  like  result  may  also  follow  the 
sudden  liberation  of  excessive  intra-abdominal  pressuie — withdrawal  of 
ascites,  removal  of  an  abdominal  tumor,  etc.  The  treatment  consists  of 
the  recumbent  posture  (to  favor  the  ready  access  of  blood  to  the  brain) 
and  the  use  of  diffusible  stimulants.  (3)  Localized  anemia  of  the  brain 
may  occur  in  arteriosclerosis  and  in  what  may  be  interpreted  as  a  condition 
of  angiospasm;  foci  of  temporary  stasis  of  the  blood  are  doubtless  often 
associated.  The  symptoms  consist  of  momentary  inability  to  perform 
special  cerebral  acts,  depending  upon  the  area  involved,  such  as  think, 
speak,  see,  move  certain  muscles,  etc.  (page  482).  These  may  or  may  not 
be  associated  with  temporary  (momentary)  loss  of  consciousness.  The 
conditions  have  been  likened  to  intermittent  claudication  (page  493). 
The  treatment  is  that  of  arteriosclerosis  (page  493). 


(EDEMA  OF  THE  BRAIN. 

(Edema  of  the  brain  may  occur:  (1)  In  conditions  associated  with 
passive  congestion;  (2)  in  chronic  nephritis,  in  which  the  oedema  may 
be  widespread  or  localized,  is  doubtless  toxic  in  nature,  and  is  answer- 
able for  some  of  the  uremic  manifestations;  (3)  in  traumatic  disorders, 
such  as  concussion  and  contusion;  (4)  about  abscesses  and  tumors; 
and  (5)  in  congenital  atrophic  disorders,  in  which  the  oedema  and  in- 
creased cerebrospinal  fluid  fills  up  potential  spaces.  The  symptoms, 
except  in  chronic  nephritis,  are  due  to  associated  conditions  rather  than 
to  the  oedema  per  se. 


CEREBRAL  HEMORRHAGE. 

(Apoplexy;  A  Stroke;  Hemiplegia.) 

Etiology. — Hemorrhage  into  the  substance  of  the  brain  is  most  com- 
mon in  male  subjects  after  the  fortieth  year.  The  etiological  factors  are 
those  of  arteriosclerosis  (page  489),  especially  syphilis,  chronic  alcoholism, 
chronic  nephritis,  excessive  muscular  work,  plumbism,  gout,  diabetes, 
etc.  The  exciting  cause  of  the  hemorrhage  is  often  some  undue  increase 
of  blood  pressure,  such  as  may  be  provoked  by  exertion  (running,  lifting 
heavy  bodies,  straining  at  stool,  etc.),  or  emotional  disturbances;  but  in 
many  cases  the  rupture  of  the  bloodvessel  occurs  during  quietude  (as 
sleep)- — in  which  event  one  may  assume  that  the  gradually  weakened 
vessel  finally  becomes  unable  to  sustain  the  ordinary  blood  pressure 
of  that  individual.  Cerebral  hemorrhage,  however,  may  occur  into 
tumors;  it  may  develop  in  conditions  of  blood  dyscrasia,  such  as  per- 


CEREBRAL  HEMORRHAGE 


863 


nicious  anemia,  leukemia,  purpura,   scurvy,   septicopyemia,  etc.;  and 
occasionally  it  is  observed  in  children. 

Pathology. — In  about  three-fourths  of  the  cases  the  hemorrhage  occurs 
from  one  of  the  several  branches  of  the  middle  cerebral  (sylvian)  artery, 
which,  penetrating  the  anterior  perforated  space,  supply  the  corpus 
striatum  and  the  internal  capsule,  especially  the  lenticulostriate  branch 
(Duret^s  artery;  Charcot's  artery  of  cerebral  hemorrhage)  and  the  len- 
ticulothalamic  branch  (Fig.  22).  In  about  one-fourth  or  more  of  the  cases 
the  hemorrhage  occurs  variously  from  any  of  the  many  branches  of  the 
cerebral  arteries,  and  into  the  brain  cortex,  the  peduncles,  the  pons,  the 
medulla,  or  the  cerebellum.  The  lesions  consist  of  the  ordinary  changes 
of  advanced  arteriosclerosis  (page  489);  small,  so-called  miliary  aneurysms 
are  common,  and  rupture  of  these  is  the  usual  cause  of  the  bleeding. 
Rarely,  as  in  toxic  states  and  the  various  blood  dyscrasies,  there  may 
be  an  undue  permeability  of  the  vessel  walls  and  an  undue  fluidity  of  the 


Fig.  22 


Mid.  C. 


Ant.  Cerebral 
Int.  Car.     jnt.  Car. 

Mid.  C. 


The  distribution  of  the  bloo^dvessels  to  the  internal  capsule:  E,  the  lenticulostriate  arteries 
(external  arteries  of  the  corpus  striatum).  /,  the  lenticulothalamic  arteries  (the  internal  arteries 
of  the  corpus  striatum).      (Buret.) 

blood.  The  hemorrhage  may  be  large  or  small ;  in  most  cases  it  is  large 
enough  to  destroy  the  outer  portion  of  the  lenticular  nucleus,  the  internal 
capsule,  and  the  thalamus;  but  it  may  extend  to  the  caudate  nucleus  and 
the  insula,  and  in  extreme  cases  it  may  involve  almost,  if  not  quite,  all 
of  the  hemisphere  and  invade  the  lateral  ventricles.  In  other  cases  the 
hemorrhage  may  be  small — pinhead  in  size,  for  instance — but  such  a 
small  hemorrhage,  if  occurring  in  the  pons  or  medulla,  may  be  attended 
by  very  serious  consequences,  even  death.  The  blood,  soon  after  being 
poured  out,  clots;  ultimately  the  clot  may  be  entirely  absorbed,  and 
represented  by  a  scar,  or  a  cyst  may  be  the  residual  manifestation. 
Secondary  degeneration  of  those  fibers  of  the  upper  motor  neuron 
deprived  of  continuity  with  their  cell  bodies  in  the  cerebral  cortex  ensues. 
Symptoms. — In  a  few  cases  symptoms  described  as  premonitory  are 
noted.  Men  of  an  apoplectic  habitus  (short,  rather  stout  body,  with  a 
short,  thick  neck,  prominent  arteries,  and  ruddy  complexion)  are  still 


864 


DIFFUSE  AND  FOCAL  DISEASES  OF  THE  BRAIN 


believed  by  some  persons  to  be  predisposed  to  cerebral  hemorrhage;  but 
the  question  is  solely  one  of  the  cerebral  arteries  and  the  mode  of  life. 
In  these,  as  well  as  other  subjects  with  sclerotic  vessels  and  high  blood 
pressure,  there  may  be  attacks  of  headache,  vertigo,  and  transitory  inca- 
pacities (mentioned  on  page  862) ;  or  slight  paresis  or  paralysis  involving 
the  cranial  nerves  (especially  ptosis,  strabismus,  or  disturbances  of 
vision),  and  due  perhaps  to  small  hemorrhages,  may  ensue;  or  actual 


Fig.  23 


Scheme  of  the  motor  tract  to  show  the  effect  of  hemorrhagic  or  softening  (thrombotic  or 
embolic)  lesions  at  different  positions:  1,  cortical  or  subcortical  lesion,  causing  monoplegia  of 
the  left  arm;  2,  capsular  lesion,  causing  left  hemiplegia;  3,  crus  lesion,  causing  left  hemiplegia 
and  right  third  nerve  palsy;  4,  pons  lesion,  causing  alternating  paralysis  of  the  right  face  and 
the  left  arm  and  leg;  S,  sylvian  fissure;  OT,  optic  thalamus;  NL,  lenticular  nucleus;  C,  crus; 
NC,  caudate  nucleus;   VII,   facial  nerve;  M,  medulla.      (Starr.) 

hemorrhages  may  be  detected  in  the  retina;  or  paresthetic  phenomena 
(numbness  and  tingling),  or  choreiform  or  other  movements  may  occur 
in  an  arm  or  a  leg. 

In  the  great  majority  of  cases,  however,  the  apoplectic  attack  comes 
on  suddenly,  without  warning,  The  patient,  in  apparently  good  health, 
while  sitting  quietly,  or  walking,  or  after  some  exertion  or  emotion,  sud- 
denly becomes  dizzy  and  falls  to  the  ground  unconscious;  he  may  vomit 
and  exhibit  some  convulsive  movements.  In  the  usual  cases,  those  due 
to  hemorrhage  from  the  lenticulostriate  artery  or  into  the  internal  capsule 
(Fig,  23),  and  in  any  event  if  the  hemorrhage  is  of  at  least  moderate  size. 


CEREBRAL  HEMORRHAGE  865 

the  patient  is  soon  found  to  have  a  livid  or  ashen-gray  countenance, 
bathed  in  sweat,  a  full,  bounding,  rather  infrequent  pulse  under  increased 
pressure,  and  a  normal  or  subnormal  temperature;  to  be  breathing 
slowly  or  stertorously,  and  "flapping"  one  cheek  (paralysis),  or  exhibiting 
the  Cheyne-Stokes  rhythm;  and  to  be  paralyzed  on  one  side  of  the  body, 
which,  however,  may  be  difficult  to  determine  on  account  of  complete 
muscular  relaxation.  In  addition,  the  head  and  the  eyes  may  be  turned 
toward  the  side  of  the  lesion  in  the  brain  (paralytic  conjugate  deviation); 
the  pupils  are  likely  to  be  unequal  or  dilated  (especially  on  the  side  of 
the  lesion),  and  to  be  inactive  to  light  if  the  patient  is  in  deep  coma; 
and  control  over  the  vesical  and  rectal  sphincters  may  be  lost.  In  some 
cases  the  paralysis  and  other  phenomena  are  noted  only  when  the  patient 
awakes  in  the  morning;  or,  not  awakening,  he  is  found  to  have  died  of 
apoplexy  during  the  night.  In  other  cases  the  onset  is  slower:  there 
may  be  at  first  only  headache  and  vertigo,  and  perhaps  vomiting,  with 
gradual  loss  of  power  in  the  arm  and  leg;  but  in  the  course  of  a  few 
hours  or  a  day  unconsciousness  supervenes  and  deepens  into  coma — 
so-called  ingravescent  apoplexy,  due  often  to  slow  leakage  of  blood 
into  the  external  capsule,  and  its  gradual  breaking  through  into  the 
internal  capsule  and  perhaps  the  lateral  ventricle. 

One  of  several  eventualities  may  ensue:  (1)  The  patient  may  die  soon, 
or  within  several  hours  of  the  onset  of  the  apoplexy.  (2)  The  coma 
may  continue,  or  it  may  lessen  somewhat  and  become  associated  with 
delirium  and  fever — 102°  to  104°  (so-called  febrile  reaction) — and  then, 
recurring,  the  patient  may  die  at  the  end  of  a  week  or  thereabouts.  In 
some  of  the  cases,  neither  improving  much  nor  retrograding,  a  sudden 
increase  of  the  symptoms  may  occur;  muscular  rigidity  and  perhaps 
convulsions  may  ensue,  and  spasmodic  conjugate  deviation  of  the  head 
and  the  eyes  away  from  the  side  of  the  lesion  may  supervene.  In  some 
of  these  cases  sudden  inundation  of  the  ventricles  is  answerable  for  the 
finally  fatal  symptoms.  (3)  With  more  or  less  return  of  consciousness, 
although  not  complete  mental  clearness,  fever  may  set  in;  trophic 
changes  may  ensue,  especially  bed  sores  and  sloughing  on  the  paralyzed 
side;  congestion  of  the  bases  of  the  lungs  (in  some  way  related  to  the 
cerebral  disorder)  may  supervene;  and  with  bronchopneumonia  or 
septicopyemia  the  patient  may  die  in  two  or  three  weeks.  (4)  The 
coma  may  gradually  subside  and  the  paralysis  become  obtrusive.  This 
is  unilateral,  and  may  involve  the  leg,  arm,  and  one-half  of  the  face  and 
tongue  (complete  hemiplegia),  or  only  one  of  these  parts  (sometimes 
called  partial  hemiplegia).  The  paralysis  at  first  is  flaccid,  and  is  asso- 
ciated with  lessened  or  absent  deep  reflexes;  soon  an  early  rigidity  may 
develop  and  be  associated  with  increased  reflexes  and  the  Babinski  sign. 
The  speech  is  indistinct;  aphasia  (page  840)  may  occur  in  left-sided 
lesions.     There  may  be  slight  or  no  sensory  phenomena. 

Hemorrhage  into  the  cms  gives  rise  to  paralysis  of  the  face,  arm,  and 
leg  of  the  side  opposite  the  lesion,  and  paralysis  of  the  oculomotor  nerve 
of  the  same  side  (syndrome  of  Weber;  crossed  or  alternate  hemiplegia). 
55 


866  DIFFUSE  AND  FOCAL  DISEASES  OF  THE  BRAIN 

There  may  also  be  contralateral  hemianesthesia  from  extension  to  the 
tegmentum. 

Hemorrhage  into  the  jions  and  medulla  is  usually  fatal  within  a  few 
hours;  but,  if  the  patient  survives,  there  is  likely  to  be  convulsions,  deep 
coma,  contracted  pupils,  and  high  fever;  and  in  many  cases  bilateral 
paralysis,  because  of  involvement  of  both  motor  tracts.  If  the  hemor- 
rhage is  small,  there  is  contralateral  hemiplegia  and  homolateral  dis- 
turbance with  the  functions  of  the  nerve  nuclei  therein  located  (crossed 
hemiplegia);  loss  of  sensation  in  the  area  of  trigeminal  distribution; 
paralysis  of  the  muscles  supplied  by  the  facial  nerve;  or  the  phenomena 
described  under  acute  bulbar  paralysis  (page  850). 

Hemorrhage  into  the  cerebellum  gives  rise  to  few  symptoms  significant 
in  themselves.  Coma,  convulsions,  and  vomiting  are  common;  par- 
alysis may  result  from  pressure  on  the  nuclei  or  tracts  in  the  medulla 
or  pons;  characteristic  symptoms,  such  as  vertigo,  staggering  gait,  and 
inability  to  maintain  muscular  balance  and  the  erect  posture,  can 
scarcely  be  ascertained.     Death  usually  ensues. 

Occasionally,  after  the  lapse  of  several  weeks  all  evidences  of  the 
apoplexy  and  paralysis  have  disappeared  and  the  patient  appears  to  be 
as  well  as  before  the  attack.  In  the  majority  of  cases,  however,  at  the 
end  of  a  month  or  six  weeks  the  patient  exhibits  the  permanent  results 
of  the  hemorrhage — the  secondary  symptoms,  or  the  chronic  stage.  As 
a  rule,  the  paralysis  is  less  than  at  first;  some  power  has  returned  in 
the  arm  and  the  leg — in  the  leg  first,  and  to  a  greater  degree;  the  par- 
alysis of  the  face  and  the  tongue  and  any  sensory  disturbances  originally 
present  may  have  wholly  disappeared.  In  the  usual  cases  (hemorrhage 
into  the  internal  capsule),  however,  more  or  less  unilateral  paralysis  of 
the  upper  motor  neuron  type  persists.  This  is  most  marked  in  the  arm 
and  the  leg;  muscles  that  act  bilaterally,  such  as  those  of  the  face 
(wrinkling  the  forehead,  frowning,  closing  the  eyes)  and  of  the  trunk 
(respiration,  etc.),  are  likely  to  show  relatively  slight  impairment  of 
function,  since  they  doubtless  may  be  innervated  by  stimuli  from  one 
side  of  the  brain;  and  movements  associated  with  emotional  disturbances 
(laughing  and  crying)  also  are  usually  well  executed,  although  the 
patient  may  not  be  able  voluntarily  to  move  the  angle  of  his  mouth.  In 
addition,  rigidity  (so-called  late  rigidity)  of  the  affected  muscles  develops 
and  usually  progresses  to  deformities  (contraction  of  the  flexors  and  adduc- 
tors overcoming  the  extensors  and  abductors);  in  walking,  the  great  toe 
is  dragged  along  the  "ground,  and  the  leg,  as  a  whole,  circumducted 
(swung  on  an  arc  of  a  circle  from  the  hip);  the  deep  reflexes  are  exag- 
gerated, and  ankle  clonus  and  the  Babinski  sign  become  apparent;  there 
is  little,  if  any,  wasting  of  the  muscles  aside  from  what  may  be  attributed 
to  disuse.  Sometimes  there  is  persisting  hemianesthesia  (involvement  of 
the  posterior  part  of  the  internal  capsule),  and  rarely  pain  (irritation  of 
the  sensory  neuron).  Athetoid  and  choreiform  movements  may  develop 
in  the  paralyzed  limbs  (posthemiplegic  chorea  and  athetosis).  In  most 
cases  there  is  at  best  slight  impairment  of  mentality;  in  many  cases 


CEREBRAL  HEMORRHAGE  867 

mental  irritability,  emotional  disturbances  on  slight  provocation,  failure 
of  memory,  etc.,  supervene,  and  dementia  may  occur. 

Diagnosis. — At  the  time  of  the  apoplectic  attack  one  must  differentiate 
it  from  coma  due  to  other  causes,  such  as:  (1)  Embolism  and  throm- 
bosis. Apoplexy  is  often  employed  as  an  inclusive  term,  comprising 
hemorrhage  and  softening  (embolism  and  thrombosis);  but  thrombosis 
is  suggested  by  gradual  onset  of  the  paralysis  and  coma,  both  of  which 
may  be  transitory;  by  a  history  of  syphilis  or  of  another  infection  recently 
passed  through;  and  by  conditions  of  the  blood  generally  that  favor 
clotting.  Embolism  is  suggested  by  a  young  subject  and  vegetative 
endocarditis  or  other  disorder  whence  an  embolus  may  be  derived.  (2) 
Uremia.  Renal  disease  (cardiovascular-renal  disease)  is  often  pres- 
ent in  those  the  subject  of  apoplexy,  so  that  it  may  be  difficult  to 
make  a  differential  diagnosis;  but  uremia  is  suggested  by  albumin  and 
casts  in  the  urine,  convulsions,  very  high  blood  pressure,  albuminuric 
neuroretinitis,  the  absence  of  hemiplegia,  and  a  history  of  previous 
attacks  without  consecutive  paralysis.  But  now  and  then  fatal  cases  of 
hemiplegia  are  encountered  in  which  only  nephritis  and  oedema  of  the 
brain  and  meninges  are  found  at  the  necropsy.  (3)  Diabetic  coma — 
which  may  be  distinguished  by  ketonuria,  perhaps  glycosuria,  fiuity  odor 
to  the  breath,  the  characteristic  Kussmaul  dyspnoea,  and  the  absence  of 
hemiplegia.  (4)  Alcoholic  coma  (obvious  alcoholism,  alcoholic  habits, 
less  deep  coma,  and  absence  of  hemiplegia  or  other  localized  paralysis). 
(5)  Opium  poisoning  (contracted  pupils,  infrequent  respirations,  no 
convulsions,  no  paralysis). 

Prognosis. — Death  may  occur  on  the  first  attack,  but  recovery,  with 
more  or  less  permanent  incapacity,  frequently  ensues.  Succeeding  attacks 
are  likely  to  occur,  and  with  each  the  tendency  to  fatality  increases. 

Treatment. — It  is  important,  first,  to  determine  whether  the  "apo- 
plexy" is  due  to  hemorrhage  or  to  thrombosis  or  embolism.  In  hemor- 
rhage the  patient  should  be  kept  quiet,  with  the  head  high  and  the  neck 
free.  If  breathing  is  obstructed,  he  should  be  turned  on  his  side,  to 
obviate  obstruction  of  the  pharynx  by  the  paralyzed  tongue.  To  reduce 
the  blood  pressure  and  promote  stilling  the  bleeding,  ice  may  be  applied 
to  the  head  and  hot  bottles  to  the  feet,  or  a  hot  mustard  foot  bath  may 
be  given;  and  venesection  should  be  performed;  or  one  may  give 
aconite,  veratrum  viride,  or  nitroglycerin,  and  open  the  bowels  freely 
(calomel,  croton  oil,  eletarium).  But  Crile  and  Cushing  have  shown 
that  a  high  arterial  pressure  may  be  conservative,  inasnnich  as  this  tends 
to  supply  a  sufficiency  of  blood  to  the  vital  centres  in  the  medulla,  which 
otherwise — that  is,  under  the  influence  of  a  rising  intracranial  pressure — 
would  rapidly  become  anemic  and  exhausted.  Therefore,  in  cases 
with  marked  and  rising  blood  pressure  (250  mm.  Ilg. — indicative  of 
increasing  intracranial  j)ressure),  especially  if  associated  wifli  an  infre- 
quent pulse,  Cushing  recommends,  and  has  practised  with  good  results, 
trephining  the  skull  and  evacuating  the  l)lood  clot.  This  is  particularly 
indicated,  of  course,  in  meningeal  hemorrhage,  but  it  has  been  sue- 


DIFFUSE  AND  FOCAL  DISEASES  OF  THE  BRAIN 

cessfully  done  in  cerebral  hemorrhage.      In  the  ingravescent  type  of 
apoplexy  compression,  even  ligation  of  the  carotids,  has  been  practised. 

Otherwise,  the  treatment  in  the  early  days  consists  of  good  nurs- 
ing, rest  in  bed  for  ten  days  or  two  weeks,  the  prevention  of  bed 
sores,  attention  to  the  position  of  the  paralyzed  limbs  which  may  be 
enveloped  in  cotton  wool,  catheterization  if  necessary,  and  after  the 
first  day  or  two  a  light,  nutritious  diet.  Stimulants  and  heart  tonics 
should  be  avoided,  unless  cardiovascular  collapse  develops.  In  addi- 
tion, after  the  lapse  of  ten  days  or  two  weeks,  the  paralyzed  limbs  should 
be  rubbed  for  ten  to  fifteen  minutes  twice  daily,  to  maintain  nutrition 
and  lessen  contractures,  and  at  the  end  of  three  or  four  weeks  the 
faradic  current  may  be  applied — especially  to  the  extensors  and  abduc- 
tors— which  are  likely  to  be  soon  overcome  by  the  contracting  flexors 
and  adductors.  Iodide  of  potassium  is  often  given,  in  the  hope  that  it 
tends  to  promote  absorption  of  the  clot.  It  is  of  value  in  syphilitic  cases, 
and  in  the  event  of  recent  syphilis  may  be  combined  with  mercury. 
In  the  course  of  time  resort  to  surgical  intervention,  tendon  cutting  or 
transplantation,  and  nerve  transplantation,  may  be  advisable  to  overcome 
disabling  contractures. 


CEREBRAL  THROMBOSIS. 

{Cerebral  Softening.) 

Etiology. — Thrombosis  of  the  cerebral  vessels  occurs  under  conditions 
that  favor  clotting  elsewhere — the  chief  of  which  are  arteriosclerosis  and 
a  weak  or  slow  circulation.  It  most  commonly  follows  syphilitic  end- 
arteritis, and  occurs  in  middle  and  advanced  life.  It  may  develop  within 
small  or  fair-sized  aneurysmal  dilatations  of  the  cerebral  vessels,  and 
after  partial  or  complete  obstruction  by  a  clot.  It  may  occur  during  the 
course  of,  or  following,  infectious  diseases,  and  in  conditions  of  blood 
impoverishment  favoring  clotting. 

Pathology. — Thrombosis  is  most  common  in  the  middle  cerebral 
artery  (supplying  the  motor  cortex  as  well  as  the  corpus  striatum)  and 
in  the  basilar  arteries.  The  lesions  are  those  of  thrombosis  in  general, 
followed  by  an  area  of  infarction,  which  may  be  red  (or  hemorrhagic), 
but  often  is  pale  (or  anemic).  The  softened  and  necrotic  area  becomes 
replaced  by  a  scar,  or  a  cyst  ensues,  and  the  fibers  deprived  of  continuity 
with  their  nuclei,  degenerate. 

Symptoms. — The  symptoms  vary  with  the  mode  of  onset  and  the  region 
of  the  brain  involved.  Even  extensive  softening  may  be  found  without 
noteworthy  symptoms  (involvement  of  so-called  silent  areas  of  the 
brain).  In  some  cases  the  onset  is  sudden  and  quite  like  that  of  hemor- 
rhage. In  many  cases,  however,  the  onset  is  gradual,  and  may  be  pre- 
ceded by  certain  prodromes  attributable  to  temporary  anemia  of  certain 
regions  of  the  brain,  such  as  temporary  inability  to  think,  speak,  see, 
remember,  or  to   move   certain  muscles  (ptosis,  strabismus,  etc.);   or 


CEREBRAL  EMBOLISM  869 

numbness  or  tingling  in  an  arm  or  a  leg.  Out  of  these  there  may  develop 
gradually  progressing  paralysis  of  an  arm,  a  leg,  half  of  the  face  or  the 
tongue,  or  a  partial  or  complete  hemiplegia  (depending  upon  the  part 
of  the  brain  involved — small  or  large  areas  of  the  cerebral  cortex  or  the 
internal  capsule,  etc.);  and  these  may  or  may  not  be  attended  by  loss  of 
consciousness,  which,  if  it  does  ensue,  is  gradual  in  development.  Both 
the  unconsciousness  and  the  paralysis  are  likely  to  lessen  considerably, 
since,  although  usually  looked  upon  as  end  arteries,  some  considerable 
collateral  circulation  may  become  established;  but  a  permanent,  partial 
or  complete  hemiplegia  is  the  rule,  as  in  cerebral  hemorrhage.  Aphasia 
(page  840)  may  ensue  in  left-sided  lesions.  Thrombosis  of  the  basilar 
artery  and  its  branches  gives  rise  to  lesions  similar  to  those  of  hemor- 
rhage into  the  pons  (page  866).  Thrombosis  of  the  posterior  cerebral 
artery  gives  rise  to  hemianopsia  and  sensory  aphasia. 

Diagnosis. — The  diagnostic  data  are  mentioned  in  connection  with 
those  of  hemorrhage  (page  867). 

Prognosis. — The  outlook  in  general  is  rather  better  than  in  hemorrhage, 
but  the  tendency  to  thrombosis  is  likely  to  remain,  and  mental  deterio- 
ration, loss  of  memory,  etc.,  are  likely  to  ensue. 

Treatment. — The  treatment  comprises  efforts  to  ward  off  an  attack, 
the  imminence  of  which  is  suggested  by  the  prodromes  mentioned;  these 
consist  of  measures  useful  in  arteriosclerosis  (page  493)  and  syphilis  (page 
190),  and  cardiac  stimulants,  such  as  alcohol,  ammonia,  ether,  caffeine, 
strophanthus,  nitroglycerin,  and  digitalis  (in  small  doses,  and  cau- 
tiously). The  treatment  of  the  developed  attack  should  consist  of 
rest,  with  the  head  low,  and  the  aforementioned  cardiac  stimulants. 
Care  should  be  taken  not  to  depress  the  circulation  and  thus  favor 
additional  clotting.  The  general  hygienic  management  and  the  use  of 
massage  and  electricity  are  as  has  been  mentioned  in  connection  with 
cerebral  hemorrhage  (page  867). 

CEREBRAL  EMBOLISM. 

{Cerebral  Softening.) 

Etiology. — Cerebral  embolism  occurs  most  commonly  in  cases  of 
chronic  recurring  endocarditis  of  the  mitral  and  aortic  valves,  and  is 
therefore  most  common  in  young  subjects,  especially  women.  Occa- 
sionally it  occurs  in  other  conditions  in  which  emboli  gain  access  to  the 
general  circulation  (clots  from  an  aneurysm,  atheromatous  plaques, 
etc.);  and  in  conditions  of  arterial  pyemia,  but  since  these  emboli  are 
infected,  a  brain  abscess  ensues. 

Pathology. — Emboli  reach  the  brain  more  conunonly  by  the  left  tlian 
by  the  right  carotid  artery,  and  the  lesions  therefore  are  usually  left- 
sided.  They  consist  of  plugging  of  a  vessel,  usually  a  branch  of  the 
middle  cerebral  artery,  and  an  area  of  softening  analogous  to  that 
which  follows  thrombosis.  More  or  less  widespread  thrombosis  may 
follow  the  eiiibolic  plugging  of  the  vessel. 


870  DIFFUSE  AND  FOCAL  DISEASES  OF  THE  BRAIN 

Symptoms. — The  symptoms  are  sudden  in  onset,  although  they  vary 
with  the  site  of  lodging  of  the  embolus.  Usually  the  common  symptoms 
of  cerebral  hemorrhage  develop,  and  the  patient  is  soon  found  to  be 
hemiplegic  and  aphasic.  Convulsions  may  occur  in  case  the  cortex  be 
involved. 

Diagnosis. — The  diagnosis  is  to  be  based  upon  the  occurrence  of 
hemiplegia  or  other  paralysis  in  a  young  subject  with  endocarditis  or 
other  disorder  whence  an  embolus  may  be  derived.  The  differential 
diagnosis  is  like  that  of  hemorrhage  (page  867). 

Prognosis. — The  prognosis  is  rather  better  than  in  hemorrhage,  but 
the  likelihood  of  recurrence  must  be  borne  in  mind  if  the  initiating 
factor  persists. 

Treatment. — The  treatment  is  that  of  thrombosis  (page  869)  plus  the 
treatment  of  the  primary  cardiac  or  other  disorder. 


THROMBOSIS  OF  THE  CEREBRAL  SINUSES. 

Etiology. — Thrombosis  of  the  cerebral  sinuses  may  be  primary  or 
secondary.  The  primary  cases,  which  are  usually  simple  or  non- 
infected,  may  result  from  anemic  states  (chlorosis  and  severe  anemias 
in  general) ;  cachectic  states,  such  as  diarrhoeal  and  other  wasting  dis- 
eases of  children,  and  advanced  carcinoma,  Bright's  disease,  etc.,  in 
adults;  and  infections  such  as  typhoid  fever,  tuberculosis,  etc.  The 
secondary  cases,  which  are  usually  infected,  result  from  extension  of 
disease  of  contiguous  structures,  especially  middle-ear  disease,  brain 
abscess,  fracture  of  the  skull  and  subsequent  infection,  and  extension  of 
suppurative  processes  outside  the  skull  (erysipelas  and  other  pyococcic 
infections). 

Symptoms.- — Thrombosis  of  the  lateral  sinus  (usually  associated  with 
middle-ear  disease)  gives  rise  to  pain,  tenderness,  and  oedema  over  the 
mastoid,  fulness  of  the  regional  veins,  often  induration  of  the  internal 
jugular  vein  from  extension  of  the  thrombosis,  and  the  general  evi- 
dences of  septicopyemia  (chills,  fever,  sweats,  and  polynuclear  leuko- 
cytosis), and  often  delirium. 

Thrombosis  of  the  longitudinal  sinus  (which  occurs  usually  in  anemic 
and  cachectic  states,  after  typhoid  fever,  etc.)  may  not  cause  any  ob- 
trusive symptoms,  the  symptoms  of  the  primary  disease  being  predom- 
inant; but  headache,  mental  dulness,  convulsions,  and  various  paralyses, 
depending  upon  the  portion  of  the  motor  cortex  involved,  may  ensue. 
In  the  absence  of  infection  there  are  no  general  symptoms  due  to  the 
thrombosis  itself. 

Thrombosis  of  the  cavernous  sinus  (which  usually  follows  infections 
of  the  nasal  or  orbital  cavity)  may  give  rise  to  frontal  or  lateral 
headache,  oedema  of  the  orbital  tissues,  exophthalmos,  conjunctival 
ecchymosis,  ulceration  of  the  cornea,  papilloedema,  paralysis  of  the 
ocular  muscles,  etc. 


ABSCESS  OF  THE  BRAIN  871 

Treatment. — The  treatment  of  the  infective  cases  is  surgical,  and 
should  not  be  delayed.  The  treatment  of  the  anemic  and  cachectic 
cases  is  that  of  the  primary  disorder,  and  the  use  of  the  iodides,  iron, 
quinine,  strychnine*,  etc. 


ACUTE  HEMORRHAGIC  ENCEPHALITIS. 

(Acute  Hemorrhagic  Cortical  Encephalitis;  Inferior  and  Superior  Polioencephalitis; 

Cerebellar  Encephalitis.) 

Etiology. — Local  or  diffuse  inflammation  of  the  brain  substance 
occurs  under  varying  circumstances:  (1)  It  may  follow  fractures  of 
the  skull.  (2)  It  occurs,  to  a  greater  or  less  extent,  in  all  cases  of  men- 
ingitis. (3)  It  may  develop  about  foci  of  hemorrhage  and  softening 
(embolism  and  thrombosis).  (4)  It  may  follow  acute  infections,  such 
as  diphtheria,  scarlatina,  influenza,  pneumonia,  etc.  (5)  It  has  been 
attributed  to  alcoholism,  ptomaine  poisoning,  lead  poisoning,  carbon 
monoxide  poisoning,  etc.  (6)  It  may  occur  as  an  independent  disorder, 
perhaps  an  acute  infectious  disease,  involving  the  cortex  or  the  nuclei  oj 
cranial  nerves.  In  this,  the  superior  and  inferior  polioencephalitis  of 
Wernicke,  the  lesions  consist  of  acute  hemorrhagic  inflammation  of  the 
gray  matter  about  the  aqueduct  of  Sylvius;  these  have  been  described 
under  ophthalmoplegia  (page  851).  In  other  cases  the  lesions  may  be 
confined  to  the  motor  cortex,  the  acute  infantile  cerebral  palsy  of  Strum- 
pell;  a  similar  condition  may  be  found  in  adults.  In  other  cases  the 
inflammatory  process  may  be  limited  to  the  area  of  distribution  of  a 
single  arterial  branch,  or  it  may  involve  corresponding  areas  of  both 
hemispheres;  or  it  may  be  disseminated  in  the  cerebrum  and  the  cere- 
bellum. The  lesions  consist  of  foci  of  congestion,  hemorrhage,  and 
softening,  involving  especially  the  gray  matter;  in  many  respects  the 
condition  is  the  cerebral  homologue  of  acute  poliomyelitis. 

Symptoms. — The  symptoms  are  often  equivocal;  often  for  a  time 
they  are  those  of  a  general  infection  only,  with  headache,  delirium, 
coma,  fever,  etc.,  but  to  these,  focal  symptoms  are  commonly  added, 
varying  with  the  seat  of  the  lesions.  There  may  be  paralysis  of  an  arm 
or  a  leg  or  of  any  of  the  muscles  supplied  by  the  cranial  nerves,  aphasia, 
anesthesia,  .convulsions  (cortical  or  Jacksonian  in  type),  etc.  Death 
may  ensue  within  several  weeks,  or,  the  acute  symptoms  subsiding,  the 
condition  may  become  chronic  and  more  or  less  mental  deterioration 
(imbecility)  may  persist. 


ABSCESS  OF  THE  BRAIN. 

(Acute  Suppurative  Encephalitis.) 

Etiology. — Abscess  of  the  brain  is  most  common    in    young    male 
adolescents  and  adults.     The  causes  are:  (1)  Traumatism  of  the  head, 


872  DIFFUSE  AND  FOCAL  DISEASES  OF  THE  BRAIN 

usually  fracture  of  the  skull,  and  subsequent  infection.  (2)  Extension 
of  suppuration  from  adjacent  structures,  especially  middle-ear  disease, 
with  involvement  of  the  mastoid,  nasal  suppuration,  and  necrosis  of  the 
bones  of  the  skull.  (3)  Transport  of  infection  from  distant  regions, 
such  as  lung  abscess,  bronchiectasis,  empyema,  (4)  General  septico- 
pyemia. The  infectious  agents  comprise  staphylococci,  streptococci, 
pneumococci.  Bacillus  pyocyaneus.  Bacillus  influenzae.  Bacillus  tuber- 
culosis, Nocardia,  etc. 

Pathology. — There  may  be  one  or  many  abscesses.  Usually  there  is  only 
one,  which  varies  in  size  from  2  to  20  or  30  cm.  in  diameter,  and  is  most 
common  in  the  temporosphenoidal  lobe  or  the  cerebellum  (on  account 
of  the  proximity  of  the  bones  of  the  ear) ;  but  it  may  be  situated  in  the 
frontal,  parietal,  or  occiptal  lobe.  The  pus  is  often  greenish  and  has  a 
foul  odor.  In  acute  cases  there  is  likely  to  be  considerable  congestion 
and  oedema  of  the  surrounding  brain  tissue;  in  chronic  cases  there  may 
be  a  more  or  less  well-defined  area  of  limiting  neuroglial  tissue,  or  the 
surrounding  brain  tissue  may  be  rather  widely  infiltrated  with  pus. 
The  multiple  abscesses  are  usually  small,  often,  indeed,  microscopic  in 
size;  larger  ones  may  form  from  coalescence  of  smaller  ones. 

Symptoms. — Corresponding  with  the  mode  of  development  of  the 
abscess,  the  symptoms  may  come  on  acutely  or  insidiously.  The  acute 
cases  usually  follow  a  trauma  or  rapidly  progressing  middle-ear  disease. 
The  chief  symptoms  consist  of  general  nervous  phenomena,  such  as  severe 
headache,  vertigo,  vomiting,  delirium,  mental  dulness,  stupor  or  coma,  and 
often  papilloedema  and  slow  pulse;  focal  nervous  symptoms  depending 
upon  the  situation  of  the  abscess  (see  cerebrospinal  localization,  page  831); 
and  the  systemic  manifestations  of  septicopyemic  states,  such  as  chills, 
fever,  sweats,  and  polynuclear  leukocytosis.  In  the  chronic  cases  the 
abscess  may  slowly  attain  considerable  dimensions  without  occasioning 
symptoms — so-called  latent  stage,  which  is  the  more  likely  to  be  present 
if  the  abscess  develops  in  one  of  the  so-called  silent  areas.  Symptoms, 
when  they  ensue,  are  like  those  just  mentioned,  but  less  severe;  regres- 
sion and  exacerbation  of  the  symptoms  may  occur  from  time  to  time, 
and  the  exacerbations  may  be  associated  with  convulsions.  In  cases  of 
general  septicopyemic  or  of  local  suppurative  processes  elsewhere,  the 
general  and  local  symptoms  due  to  these  may  overshadow  those  due  to 
the  brain  abscess — which  may  not  be  recognized. 

Diagnosis. — The  diagnosis  depends  upon  an  etiological  factor,  the 
general  and  local  evidence  of  disease  of  the  brain,  and  the  systemic  signs 
of  pyogenic  infection.  Biain  tumor  (page  874)  and  meningitis  (page 
830)  must  be  excluded. 

Prognosis. — Unless  evacuated,  the  abscess  causes  death  by  destroying 
or  compressing  vital  regions  of  the  brain,  or  by  provoking  suppurative 
meningitis  or  general  septicopyemia. 

Treatment. — The  treatment  is  wholly  surgical,  and  consists  in  evacua- 
tion and  thorough  drainage  of  the  abscess.  This  should  be  promptly 
resorted  to,  and  is  often  followed  by  recovery. 


TUMORS  OF  THE  BRAIN  873 


TUMORS  OF  THE  BRAIN. 


Etiology. — Tumors  of  the  brain  are  more  common  in  males  than  in 
females,  and  they  occur  at  all  ages,  but,  as  a  rule,  before  rather  than 
after  the  fortieth  year;  they  are  comparatively  common  in  young  sub- 
jects and  children.  Some  cases  seem  to  follow  traumatism  to  the  head; 
but  otherwise  the  etiological  factors  are  those  of  tumors  in  general,  and  are 
as  ill  understood. 

Pathology. — Tumors  of  the  brain  may  be  primary  or  secondary,  and 
benign  or  malignant,  but  the  so-called  benign  tumors  (the  type  of  tumor 
benign  in  other  parts  of  the  body)  becomes  in  the  brain  more  or  less  malig- 
nant and  leads  to  death,  because  of  the  implication  of  vital  structures. 
The  common  tumors  are  sarcoma,  glioma  (gliosarcoma),  endothelioma, 
carcinoma,  and  fibroma;  but  to  these  one  must  add  the  tubercle  (solitary 
tubercle,  tuberculoma),  gumma,  and  cyst,  since  these  formations,  espe- 
cially tubercle  and  gumma,  are  very  common  in  the  brain,  and  there  are 
essentially  tumors  in  their  growth  and  manifestations.  The  tubercle 
(the  most  common)  is  usually  secondary  to  tuberculosis  elsewhere;  it  is 
generally  single,  but  may  be  multiple;  it  varies  in  size  up  to  that  of  a 
walnut,  or  larger;  it  occurs  especially  in  young  subjects;  and  it  develops, 
as  a  rule,  from  the  meninges  (associated  meningitis),  although  it  may 
be  found  within  the  brain  substance — near  the  cortex,  at  the  base,  or  in 
the  cerebellum.  The  gumma  is  usually  multiple;  it  develops,  as  a  rule, 
from  the  meninges;  it  is  found  most  commonly  at  the  base  of  the  brain 
or  in  the  cortex,  and  comparatively  rarely  within  the  substance  of  the 
cerebrum  or  cerebellum.  The  endothelioma  and  fibroma  develop  from 
the  meninges  or  nerve  sheaths  and  compress  the  brain.  The  glioma 
(gliosarcoma)  develops  from  the  neuroglia  and  infiltrates  the  brain  sub- 
stance. Other  sarcomas,  as  well  as  carcinomas,  may  develop  in  any 
part  of  the  brain  as  secondary  metastatic  nodules.  Cysts  may  be  par- 
asitic (rare)  or  simple  (softening  cysts),  and  occur  anywhere  in  the  brain. 
Rarer  tumors  comprise  psammoma,  cholesteatoma,  lipoma,  osteoma 
(from  the  skull),  angioma,  aneurysm,  etc. 

Symptoms. — The  symptoms  vary  with  the  variety,  situation,  and  ra- 
pidity of  growth  of  the  tumor.  Rarely,  a  tumor  is  found  after  death, 
in  the  absence  of  noteworthy  symptoms  during  life;  usually  it  has  occu- 
pied one  of  the  so-called  "silent  areas."  In  the  great  majority  of  cases, 
however,  there  are  characteristic  symptoms;  of  these,  one  group,  the 
general  symptoms,  develop  irrespective  of  the  situation  of  the  growth; 
another  group,  the  focal  symptoms,  depend  upon  the  situation  of  the 
tumor.  The  important  general  symptoms  comprise  headache,  vertigo, 
vomiting,  and  papilloedema  and  optic  atrophy.  Headache  is  almost 
always  present,  and  once  developed  rarely  disappears,  although  it 
may  vary  in  intensity  from  time  to  time.  It  may  be  dull  and  aching; 
or  a  sensation  of  fulness  and  compression;  or  it  may  be  extremely  severe 
and  paroxysmal,  especially  at  night  (syphilis).     Sometimes  it  is  localized 


874         .DIFFUSE  AND  FOCAL  DISEASES  OF  THE  BRAIN 

— which  rarely  is  of  diagnostic  significance,  although,  if  associated  with 
local  tenderness,  it  may  suggest  the  situation  of  a  gumma  and  local  menin- 
gitis. The  headache  is  variously  due  to  increased  intracranial  pressure, 
stretching  of  the  meninges,  pressure  upon  and  irritation  of  sensory  nerves 
(especially  the  fifth),  localized  meningitis,  etc.  Vertigo  is  often  an  in- 
tractable symptom,  sometimes  occurring  spontaneously,  and  often  set  up 
by  changes  in  posture.  It  may  occur  in  association  with  tumors  of  any 
part  of  the  brain,  but  is  most  common  in  tumors  of  the  base,  or  the  cere- 
bellum. Vomiting  is  common;  it  has  no  relation  to  taking  food;  it  is 
usually  unattended  with  nausea,  the  contents  of  the  stomach,  as  a  rule, 
being  suddenly  violently  ejected  without  antecedent  warning;  it  may  be 
induced  by  sudden  movements  of  the  head  (which  may  also  cause  ver- 
tigo). It  is  most  common  in  tumors  of  the  base  of  the  brain — beneath 
the  tentorium  (great  increase  in  intracranial  pressure).  Papilloedema 
(choked  disk)  in  many  respects  is  the  most  important,  and,  with  the 
other  symptoms,  the  most  trustworthy  manifestation  of  brain  tumor. 
It  occurs  in  at  least  90  per  cent,  of  the  cases,  and  is  most  common  in 
tumors  of  the  base  of  the  brain  and  cerebellum;  the  condition  is  usually 
bilateral;  in  some  cases  it  is  more  marked  on  the  side  of  the  lesion;  in 
other  cases  on  the  other  side.  The  rapidity  of  its  progress  is  sometimes 
an  evidence  of  the  rapidity  of  growth  of  the  tumor  (perhaps,  more  cor- 
rectly, of  the  rapidity  of  increase  of  intracranial  pressure);  often  there  is 
associated  neuroretinitis.     Optic  atrophy  is  the  usual  sequel. 

There  are  other  more  or  less  important  general  symptoms,  such  as 
general  irritability,  apathy,  somnolence  (sometimes  insomnia),  melan- 
cholia, even  dementia  or  mania.  General  convulsions  sometimes  occur, 
and  are  of  importance,  since  they  may  be  mistaken  for  epilepsy,  and 
thus  lead  to  overlooking  of  the  brain  tumor,  at  least  for  some  time.  If 
well  studied,  they  may  reveal  a  definite,  well-localized  onset  (Jacksonian 
or  focal  epilepsy),  of  value  in  localizing  the  tumor.  Syncopal  and  apo- 
plectiform attacks  sometimes  occur;  the  latter  may  be  due  to  hemor- 
rhage into  the  tumor.  The  pulse  is  usually  slowed,  and  may  be  irregular; 
toward  the  end  of  life  it  may  become  rapid.  The  temperature  may  be 
normal  or  subnormal;  occasionally  there  is  fever  (inflammatory  lesions 
in  the  brain  or  meninges).  Polyuria  and  glycosuria  are  sometimes 
observed  (increased  pressure  or  irritation  of  the  medulla);  and  the 
patient  may  emaciate. 

The  focal  or  localizing  signs  of  tumors  of  the  brain  are  those  men- 
tioned under  cerebrospinal  localization  (page  831). 

Diagnosis. — ^The  diagnosis  may  be  based  upon  any  two  of  the  impor- 
tant general  symptoms  (headache,  vertigo,  vomiting,  and  papilloedema) 
and  such  localizing  signs  as  may  be  detected  by  a  careful  examination. 
Since  papilloedema  may  be  present  for  some  time  and  in  notable  degree, 
with  little  or  no  impairment  of  eyesight,  the  eyegrounds  should  be  exam- 
ined in  all  cases  in  which  the  possibility  of  brain  tumor  exists.  Brain 
abscess  may  be  excluded  by  the  absence  of  the  etiological  factors  of 
abscess  (local  trauma,  middle-ear  disease,  etc.),  the  less  rapid  progress 


HYDROCEPHALUS  875 

of  the  symptoms,  and  the  absence  of  general  evidences  of  infection 
(chills,  fever,  sweats,  and  polynuclear  leukocytosis).  Meningitis  (page 
828),  cerebral  hemorrhage  (page  862),  cerebral  softening  (page  868), 
and  sometimes  uremia  (page  759)  must  also  be  excluded. 

Prognosis. — The  prognosis  depends  upon  the  nature  and  situation  of 
the  growth  and  its  amenability  to  surgical  removal.  Gummas  may  be 
absorbed  by  antisyphilitic  treatment.  In  other  tumors  the  average 
duration  of  life  is  about  two  years  or  less.  Death  may  occur  suddenly, 
in  an  apoplectiform  attack  for  instance,  or  during  general  convulsions, 
etc. 

Treatment. — The  possibility  always  exists  that  the  tumor  may  be  syph- 
ilitic; and  since  less  than  10  per  cent,  of  the  cases  are  at  any  time 
amenable  to  surgical  removal,  antisyphilitic  treatment  should  be  tried, 
especially  in  all  cases  of  doubt.  Preference  should  be  given  to  in- 
unctions of  mercury  and  the  concurrent  and  subsequent  use  of  the 
iodides  in  very  large  doses  (150  to  250  grains,  5  to  8  grams,  daily).  It  is 
useless  to  continue  the  treatment  with  mercury  if  no  improvement  occurs 
within  four  to  six  weeks.  Marked  improvement,  even  cure,  has  been 
reported  from  the  long-continued  use  of  the  iodides,  even  in  supposedly 
non-syphilitic  cases;  at  all  events,  the  headache  is  thus  often  notably 
relieved.  The  vertigo  and  vomiting  may  be  mitigated  by  the  bromides. 
Convulsions  call  for  morphine  and  atropine  hypodermicly. 

Otherwise  the  treatment  is  surgical  and  has  two  objects  in  view — the 
removal  of  the  growth  and  the  relief  of  symptoms.  The  decision  for 
surgical  intervention  should  not  be  too  long  delayed,  and  the  operation 
should  be  undertaken  if  the  focal  signs  indicate  accessibility  of  the 
tumor.  In  the  event  of  inaccessibility,  the  operation  known  as  decom- 
pression may  be  undertaken.  It  is  designed  to  relieve  intracranial 
pressure,  by  removing  a  portion  of  the  skull,  and  it  frequently  results 
in  lessening  of  the  headache,  vertigo,  vomiting,  and  papilloedema.  Some 
temporary  relief  of  the  increased  intracranial  pressure  may  also  be 
effected  by  lumbar  puncture. 

HYDROCEPHALUS. 

Hydrocephalus  is  a  condition  characterized  by  the  accumulation  of  an 
increased,  and  often  very  large,  amount  of  serous  fluid  within  the  ven- 
tricles of  the  brain.  This  condition  is  sometimes  spoken  of  as  internal 
hydrocephalus,  to  distinguish  it  from  external  hydrocephalus,  a  collection 
of  fluid  between  the  brain  and  the  dura  mater.  This  occurs  in  atrophy  of 
the  brain  (hydrocephalus  ex  vacuo),  in  advanced  life,  and  after  hemor- 
rhages, softenings,  etc. 

Internal  hydrocephalus  may  be  congenital  or  acquired.  The  con- 
genital cases  may  be  observed  at  birth,  when  the  enlarged  head  may 
interfere  with  parturition,  or  it  may  not  become  apparent  until  the  child 
is  some  months  or  a  year  old.  The  condition  may  occur  in  several  mem- 
bers of  the  same  family.     The  real  cause  is  not  known,  although  it  is 


876     DIFFUSE  AND  FOCAL  DISEASES  OP  THE  SPINAL  CORD 

likely  some  vice  of  development  or  a  foetal  meningitis  obstructing 
the  foramen  of  Majendie  and  leading  to  the  intraventricular  accumu- 
lation of  fluid.  The  acquired  cases  may  result  from  an  ependymitis 
with  marked  serous  exudation,  a  condition  which  Quincke  believes  to  be 
angioneurotic  in  nature  (Quincke's  angioneurotic  hydrocephalus);  or 
they  may  be  due  to  inflammatory  (meningitic)  or  pressure  (tumor) 
obstruction  of  the  passage  from  the  third  to  the  fourth  ventricle  or  of 
the  foramen  of  Majendie. 

In  the  congenital  cases  and  those  developing  in  early  life  the  head  may 
be  slightly  or  enormously  distended.  The  bones  of  the  skull  are  sep- 
arated and  the  fontanelles  widened;  the  forehead  overhangs  the  face, 
the  eyes  are  recessed,  and  the  bones  of  the  face  seem  small  (only  rela- 
tively small  in  comparison  with  those  of  the  skull).  The  brain  is  en- 
larged, the  ventricles  more  or  less  distended,  and  the  cortex,  as  a  rule, 
correspondingly  atrophied.  Although  rarely  considerable  intellectual 
development  occurs,  the  mentality,  as  a  rule,  is  variously  impaired  up 
to  complete  idiocy.  Death  usually  occurs  in  childhood,  but  the  patient 
may  reach  adult  life.  The  cases  developing  in  adult  life  can  scarcely 
be  recognized  with  certainty;  the  hydrocephalus  is  usually  only  an  inci- 
dent in  the  course  of  the  disease  to  which  it  is  due. 


DIFFUSE  AND  FOCAL  DISEASES  OF  THE  SPINAL  CORD. 

VASCULAR  DISORDERS  OF  THE  SPINAL  CORD. 

Hyperemia,  anemia,  and  oedema  of  the  spinal  cord,  speaking  generally, 
occur  under  circumstances  like  those  that  occasion  similar  conditions 
in  the  brain  (page  861  et  seq.).  They  often  exist  without  noteworthy 
clinical  manifestations.  The  symptoms  attributable  to  posterolateral 
or  toxic  combined  sclerosis,  which  is  rather  common  in  grave  anemias, 
are  mentioned  on  pages  375  and  858.  Embolism  and  thrombosis,  and 
consequent  softening  of  large  areas  (myelomalacia),  are  comparatively 
rare  in  the  spinal  cord;  but  thrombosis  of  fine  bloodvessels  is  quite 
common  in  the  arteriosclerosis  of  advancing  life,  and  is  found  also  in 
conditions  of  choreiform  and  athetoid  movements,  paralysis  agitans, 
etc.  Hemorrhage  into  the  spinal  membranes  (hematorrachis)  is 
mentioned  on  page  826. 

HEMORRHAGE  INTO  THE  SPINAL  CORD. 

{Hematomyelia;  Intraspinal  Hemorrhage.) 

Etiology. — Hemorrhage  into  the  spinal  cord  may  be  due  to  traumatism 
(fracture-dislocation,  acute  flexion  of  the  cervical  vertebrae  without  frac- 
ture or  dislocation),  to  severe  convulsive  diseases,  such  as  tetanus,  or  it 
may  occur  into  an  area  of  the  cord  the  seat  of  antecedent  disease,  such 
as  tumor,  myelitis,  syringomyelia,  etc. 


HEMORRHAGE  INTO  THE  SPINAL  CORD  877 

Pathology. — The  hemorrhage  may  be  very  small  (microscopic)  and 
multiple,  or  single  and  very  large,  infiltrating  a  considerable  length  'of 
the  cord.  Usually  it  occurs  into  the  gray  matter,  which  in  consequence 
is  most  destroyed;  but  more  or  less  laceration  and  secondary  disorgani- 
zation of  the  white  matter  may  also  be  found. 

Symptoms. — The  symptoms  depend  upon  the  seat  and  extent  of  the 
hemorrhage.  Usually  there  is  sudden  onset  of  paralysis,  attended  by 
more  or  less  pain.  The  hemorrhage  occurring  high  up  (in  the  cervical 
region)  may  occasion  paralysis  of  all  four  extremities,  and  may  soon 
lead  to  death  (involvement  of  the  medulla).  In  other  cases  only  the 
arms  or  the  legs  may  be  involved;  in  some  cases  there  is  a  more  or  less 
outspoken  and  typical  Brown-Sequard  paralysis  (page  838).  If  recovery 
ensues,  there  is  more  or  less  wasting  of  the  muscles  innervated  by  the 
cells  in  the  anterior  cornua  (the  usual  seat  of  the  hemorrhage)  of  the 
segment  or  segments  involved;  this  is  commonly  more  marked  on  one 
side  of  the  body  than  on  the  other,  and  is  associated  with  varying  sensory 
disturbances — usually  tactile  hyperesthesia  on  the  side  of  most  marked 
paralysis,  and  impaired  pain  and  temperature  sensibility,  with  pre- 
served tactile  sensibility,  on  the  opposite  side.  In  most  cases  there  is  also 
more  or  less  spastic  paralysis  of  one  or  both  legs  (more  marked  in  one 
than  in  the  other),  since  the  hemorrhage  usually  involves  the  pyramidal 
tracts  (upper  motor  neuron)  primarily  or  secondarily. 

Diagnosis. — The  diagnosis  is  comparatively  easy  in  traumatic  cases, 
and,  in  any  event,  if  the  symptoms  are  sudden  in  onset  (which  always 
suggests  hemorrhage).  Impaired  pain-  and  temperature  sensibility, 
with  unimpaired  tactile  sensibility,  suggests  involvement  of  the  gray 
matter  (which  is  usually  due  to  hemorrhage).  The  presence  of  ante- 
cedent disorders  (tumor,  myelitis,  syringomyelia),  to  which  the  hemor- 
rhage may  be  secondary,  must  be  determined  by  eliciting  the  signs 
significant  of  these  conditions. 

Prognosis. — The  outlook  depends  upon  the  seat  and  extent  of  the 
hemorrhage,  and  the  presence  or  absence  of  associated  lesions.  In 
uncomplicated  cases  recovery  usually  ensues,  but  more  or  less  per- 
manent paralysis  and  disability  persists. 

Treatment. — The  treatment  consists  of  enforced  rest;  perhaps  in  the 
early  days  the  application  of  an  ice-bag  to  the  spine  (of  questionable 
utility);  and  attention  to  the  general  hygienic  conditions  (feeding,  pre- 
vention of  bed  sores,  catheterization,  enemas,  etc.).  Pain  may  recjuire 
the  use  of  morphine;  general  nervousness,  the  bromides,  chloral,  etc. 
Painful  contractures  of  the  muscles  may  be  relieved  by  massage  and 
warm  applications.  The  iodides  have  been  recommended  to  promote 
absorption  of  the  clot. 

In  traumatic  cases  radiographic  examination  may  be  resorted  to  to 
determine  the  nature  of  the  lesion,  and  fixation  apparatus  may  be 
applied  if  necessary  to  maintain  a  desirable  position.  The  question  of 
operation  must  be  considered.  It  is  always  wise  to  postpone  this  until 
the  shock  has  passed;  and  in  some  cases,  even  for  a  week  or  thereabouts, 


878     DIFFUSE  AND  FOCAL  DISEASES  OF  THE  SPINAL  CORD 

to  distinguish  between  symptoms  due  to  compression  or  concussion  and 
those  due  to  permanent  damage  to  the  cord.  In  the  event  of  total 
transverse  destruction  of  the  cord  an  operation  is  useless.  But  operation 
should  not  be  too  long  delayed;  beneficial  results  are  much  more  likely 
to  follow  early  rather  than  late  operations.* 


CAISSON  DISEASE. 

(Driver's  Paralysis;  Compressed  Air  Disease;  The  "Bends.") 

Caisson  disease  is  a  form  of  paralysis  characterized  especially  by  para- 
plegia that  develops  in  persons  who  have  worked  under  increased 
atmospheric  pressure,  upon  their  return  to  the  normal  pressure  of  the 
earth's  surface. 

Etiology. — While  the  disorder  may  develop  in  perfectly  healthy  men, 
it  is  much  more  common  in  those  in  poor  health,  from  any  cause;  in 
alcoholic,  cardiac,  nephritic,  and  obese  subjects;  and  in  "green  hands" 
rather  than  in  those  who  have  worked  for  some  time  under  increased 
pressures. 

Pathology. — The  conspicuous  lesions  consist  of  air  emboli  in  the 
veins  and  capillaries  of  the  spinal  cord,  and  foci  of  hemorrhage  and 
softening.  The  disease  is  commonly  attributed  to  concentration  and 
compression,  in  the  tissues  of  the  body,  of  the  normal  gases  of  the  atmos- 
phere, caused  by  the  abnormally  great  pressures  within  the  caissons, 
etc.,  and  to  the  sudden  release  of  these  compressed  gases  upon  the  subject 
passing  rapidly  from  a  high  to  a  low  atmospheric  pressure.  The  condi- 
tion, therefore,  is  due  to  the  sudden  expansion  of  gases  in  soft  tissues, 
the  brain  and  the  cord,  contained  within  an  unyielding  bony  framework. 
McWhorter,  in  fatal  cases,  found  the  right  side  of  the  heart  filled  with 
gas,  of  which  80  per  cent,  was  nitrogen  and  20  per  cent,  carbon  dioxide; 
and  he  found  no  abnormal  gases. 

Symptoms. — The  symptoms  consist  of  the  sudden  development,  im- 
mediately or  several  hours  after  the  subject  leaves  the  caisson,  of  severe 
pain  in  the  back  and  legs,  so  that  he  is  unable  to  move,  doubles  up 
(the  "bends"),  and  falls  to  the  ground.  The  pain  is  in  the  muscles — • 
which  are  also  tender  to  palpation  and  on  passive  motion.  Pain  in  the 
joints  (knees,  ankles,  hips,  elbows,  etc.)  also  may  be  complained  of,  and 
add  considerably  to  the  patient's  disability.  In  addition,  headache, 
vertigo,  tinnitus  aurium,  deafness,  vomiting,  and  marked  prostration 
often  ensue;  or  apoplectiform  attacks,  with  hemiplegia  or  monoplegia, 
and  perhaps  aphasia,  may  develop ;  or  a  true  paraplegia  may  supervene. 
Death  may  occur  in  coma. 

Diagnosis. — The  disorder  is  readily  recognized  from  the  relationship 
of  the  symptoms  and  the  etiological  factors. 

Prognosis. — The  prognosis  is  good  in  most  cases.  Recovery  usually 
ensues  within  several  days;  but  death,  or  more  or  less  chronic  invalidism 
may  follow. 


MYELITIS  879 

Treatment. — The  disease  can  be  considerably  lessened  by  careful 
physical  examination  of  subjects  presenting  themselves  for  work  in 
caissons,  and  rejecting  only  those  in  perfect  physical  health;  and  by 
gradual  decompression — that  is,  the  use  of  air  locks  or  pneumatic 
cabinets,  in  which  the  pressure  is  gradually  reduced,  so  that  the  workers 
are  gradually  brought  from  the  greatly  increased  to  the  normal  atmos- 
pheric pressure.  The  developed  disease  is  best  treated  by  recompres- 
sion— that  is,  subjecting  the  patient  to  increased  atmospheric  pressure 
and  later  gradually  reducing  it.  Ergot  in  large  doses  has  also  been 
recommended. 

MYELITIS. 

Myelitis,  or  inflammation  of  the  spinal  cord,  may  be  a  diffuse  or  a 
circumscribed  process;  it  may  involve  only  the  gray  matter — a  disorder 
discussed  under  poliomyelitis  (page  270),  and  polioencephalitis  (pages 
850  and  851);  it  may  involve  a  narrow  vertical  area  of  both  white 
and  gray  matter — transverse  myelitis,  or  it  may  occur  in  scattered  areas 
throughout  the  cord — disseminated  myelitis. 

Etiology. — Acute  myelitis  may  be  a  primary  or  secondary  process,  but 
in  all  cases  it  must  be  ascribed  to  the  activity  of  infectious  microorgan- 
isms (or  their  toxins),  although  an  analogous  condition  of  softening 
(myomalacia)  may  result  from  interference  with  the  blood  supply 
(thrombosis  or  embolism,  or  compression).  In  some  cases  myelitis 
seems  to  be  in  itself  an  acute  infectious  disease,  but  no  specific  organism 
has  yet  been  discovered.  In  other  cases  it  follows  the  more  common 
infections,  such  as  typhoid  fever,  smallpox,  pneumonia,  dysentery,  pyo- 
coccic  and  gonococcic  infections,  syphilis,  tonsillitis,  etc.,  the  organisms 
gaining  access  to  the  cord  variously  by  way  of  the  bloodvessels  or  the 
lymphatics.  In  other  cases  myelitis  follows  meningitis  and  neuritis, 
and  tuberculosis  or  syphilis  of  the  vertebrae  and  spinal  meninges.  It  is 
said  also  to  follow  exposure  to  cold  and  damp,  traumatism  to  the  ver- 
tebrae, etc.  It  is  most  common  in  male  subjects  before  the  fortieth  year 
(susceptibility  to  the  common  exciting  causes). 

Pathology. — The  lesions  at  first  consist  of  swelling,  congestion,  oedema, 
and  softening  of  the  cord,  so  that  the  gray  and  the  white  matter  may 
be  indistinguishable  (especially  in  transverse  lesions).  Microscopicly 
there  is  vascular  congestion,  cellular  and  fluid  exudation,  minute  hem- 
orrhages, swelling  and  degeneration  of  the  axons  and  their  myelin 
sheaths,  and  vascular  and  other  degenerations  of  the  ganglion  cells  of 
the  gray  matter.  Soon  the  softened  area  may  take  on  a  yellowish  color, 
due  to  fatty  degeneration  of  the  elements  within  the  inflamed  zone. 
Ultimately,  if  the  patient  survives,  with  absorption  and  disappearance 
of  the  degenerated  tissues,  the  neuroglia  undergoes  hyperplastic,  and 
later  cicatricial,  changes,  so  that  the  zone  of  inflammation  and  softening 
becomes  replaced  by  scar  tissue.  In  transverse  lesions  secondary 
degenerations   ensue,   beginning   within    twenty-four    hours:    so-called 


DIFFUSE  AND  FOCAL  DISEASES  OF  THE  SPINAL  CORD 

descending  degeneration  in  practically  all  the  columns  of  the  cord,  but 
especially  conspicuous  in  the  crossed  and  direct  pyramidal  tract,  and 
elsewhere  in  the  anterior  and  lateral  columns  (association  fibers);  and 
ascending  degeneration  in  the  posterior  columns  of  Goll  and  Burdach, 
the  direct  cerebellar  tract,  and  the  anterolateral  ascending  tract  of 
Gowers. 

Symptoms. — The  symptoms  vary  with  the  seat  and  character  of  the 
lesion.  The  onset  may  be  abrupt  (myomalacia  from  vascular  occlusion 
or  myelitis)  or  more  insidious  (usually  myelitis).  Some  fever  is  usually 
present  in  the  inflammatory  cases.  The  symptoms  in  transverse  lesions 
consist  of  those  due  directly  to  destruction  of  a  part  of  the  cord  and  of 
secondary  manifestations  due  to  blocking  of  impulses  in  the  cord.  The 
symptoms  due  directly. to  the  lesion  (destruction  of  the  lower  motor 
neuron)  consist  of  loss  of  voluntary  muscular  control,  flaccidity,  and 
wasting,  and  the  reactions  of  degeneration  in  the  muscles  innervated 
by  the  spinal  segment  or  segments  involved;  loss  of  the  deep  reflexes 
represented  in  the  destroyed  portion  of  the  cord  (destruction  of  the  reflex 
arc);  and  anesthesia  and  paresthesia  in  the  area  of  peripheral  distri- 
bution of  the  dorsal  roots  involved  (destruction  of  the  sensory  neuron). 
The  secondary  symptoms,  those  due  to  blocking  of  motor  and  sensory 
impulses  in  the  cord,  consist  of  spastic  paralysis  of  the  muscles  below 
the  lesion  (legs),  with  rigidity,  and  ultimate  contractures  and  deformities, 
but  no  reactions  of  degeneration  and  no  atrophy,  aside  from  that  which 
follows  disuse  (disorder  of  the  upper  motor  neuron);  increased  knee- 
jerks,  ankle  clonus,  and  the  Babinski  sign;  hyperesthesia  or  anesthesia 
(protopathic,  epicritic,  and  deep  sensibility)  below  the  lesion;  loss 
of  control  of  the  vesical  and  rectal  sphincters;  and  vasomotor  and 
trophic  disturbances,  especially  coldness  and  cyanosis  of  the  extremities, 
bed  sores  at  points  of  pressure  (sacrum,  heels,  etc.),  thin,  glossy  skin,  etc. 
Just  at  and  above  the  segmental  level  of  the  lesion  there  is  usually  a  zone 
of  hyperesthesia  (irritation  of  the  dorsal  roots),  which,  together  with  the 
upper  limit  of  the  area  of  anesthesia,  form  the  best  guide  to  the  deter- 
mination of  the  level  of  the  lesion  (see  Plate  I,  page  803). 

The  symptoms  of  myelitis  occur  in  varying  combinations,  due  to 
variations  in  the  lesions.  The  following  may  be  distinguished:  (1) 
Transverse  thoracic  myelitis,  of  which  the  symptoms  are  those  just  nar- 
rated. (2)  Transverse  lumbar  myelitis,  which  difi^ers  only  in  the  fact 
that  the  cells  of  the  lower  motor  neurons  innervating  the  legs  are  likely 
to  be  involved,  so  that  instead  of  spasticity,  flaccid  paralysis,  and  atrophy 
of  the  muscles,  with  lost  knee-jerks  and  the  reactions  of  degeneration, 
ensue.  (3)  Transverse  cervical  myelitis,  in  which,  in  addition  to  the 
general  symptoms  mentioned,  there  is  likely  to  be  paralysis  and  wasting 
of  the  muscles  of  the  hand  (cervical  enlargement),  inequality  of  the 
pupils  (disorder  of  the  cervical  sympathetic),  hyperpyrexia,  and  death 
from  respiratory  failure  (involvement  of  the  cervical  roots  from  which  the 
phrenic  nerve  is  derived).  (4)  Involvement  of  the  conns  medullaris  is 
rare,  but  involvement  may  be  recognized  by  paralysis  of  the  vesical  and 


MYELITIS  881 

rectal  sphincters  and  of  the  levator  ani  muscles,  and  anesthesia  and 
other  sensory  disturbances  of  the  buttocks,  perineum,  and  external 
genitalia.  (5)  Acute  ascending  myelitis  or  paralysis  (Landry's  par- 
alysis). This  is  undoubtedly  an  acute  infection  of  the  spinal  cord, 
sometimes  of  the  spinal  cord  and  peripheral  nerves,  and  perhaps  also 
the  bulb.  It  is  characterized  by  fever  and  associated  constitutional 
disturbances,  and  by  a  rapidly  ascending  paralysis,  which,  beginning 
in  the  legs,  soon  involves  the  trunk,  the  arms,  and  the  muscles  inner- 
vated by  the  bulb  (especially  the  muscles  of  respiration),  so  that  death 
usually  results  within  a  few  days  from  respiratory  or  heart  failure,  or 
paralysis  of  the  muscles  of  deglutition.  Occasionally  a  recovery  is  re- 
ported. There  may  be  few,  if  any,  sensory  changes;  the  bladder  and 
the  rectum  may  not  be  notably  involved;  and  consciousness  is  usually 
preserved  to  the  end.  The  nature  of  the  disease  is  not  well  understood; 
all  cases  apparently  included  in  this  category  are  not  alike.  In  some 
cases  the  reverse  order  of  the  onset  and  progress  of  the  paralysis  is 
observed — a  descending  paralysis.  (6)  Disseminated  myelitis.  In  this 
varying  combinations  of  motor  paralysis  and  sensory  disturbances  may 
occur  simultaneously  or  in  succession  in  the  legs,  trunk,  and  arms;  only 
a  few  muscles  of  a  limb  may  show  atrophy  and  the  reactions  of  degener- 
ation; and  the  disturbances  of  sensibility  may  be  complete  or  incom- 
plete in  different  parts  of  the  limb. 

Acute  myelitis  may  lead  to  death  within  a  few  days  or  a  few  weeks,  or, 
if  the  lesions  are  slight,  the  initial  phenomena,  the  paralyses,  may  sub- 
side more  or  less  and  the  patient  pass  into  what  is  often  called  chronic 
myelitis  (perhaps  in  some  cases  the  symptoms  develop  so  insidiously  as 
to  merit  the  term  chronic  from  the  beginning).  There  is  spastic  para- 
plegia, muscular  rigidity,  and  consequent  deformity  of  the  legs,  lessened 
or  abolished  sensibility,  and  loss  of  control  over  the  vesical  and  rectal 
sphincters. 

Diagnosis. — The  diagnosis  should  be  readily  made  by  attention  to  the 
aforementioned  symptoms,  and  the  exclusion  of  compression  of  the  cord 
(page  882),  ataxic  paraplegia  (page  858),  subacute  combined  (toxic) 
degeneration  of  the  cord  (page  858),  disseminated  sclerosis  (page  859), 
and  meningitis  (page  828). 

Prognosis. — The  acute  cases  often  soon  lead  to  death;  this  is  almost 
inevitable  in  transverse  cervical  myelitis.  In  other  cases  more  or  less 
improvement  may  ensue,  but  the  patient  usually  becomes  permanently 
incapacitated.  Death  may  result  from  secondary  infections,  such  as 
pneumonia,  cystitis,  proctitis,  bed  sores,  etc. 

Treatment. — Rest  in  bed  is  essential,  but  the  patient  should  be  fre- 
quently moved  from  side  to  side  and  on  his  back,  and  the  most  pains- 
taking care  must  be  exercised  to  prevent  bed  sores,  cystitis,  etc.  The 
bladder  must  be  regularly  evacuated  by  catheterization,  and  the  rec- 
tum by  the  use  of  laxatives  and  enemas.  During  the  active  stage  of  the 
disease  good  results  have  been  claimed  from  the  use  of  the  salicylates, 
hexamethylenamin,  and  mercury  (by  inunction),  even  in  non-syphilitic 
56 


882     DIFFUSE  AND  FOCAL  DISEASES  OF  THE  SPINAL  CORD 

cases.  Painful  contractures  of  the  muscles  may  be  relieved  by  massage, 
hot  applications,  the  bromides,  etc.  After  the  subsidence  of  the  acute 
phenomena,  strychnine,  massage,  electricity,  warm  baths,  etc.,  are  indi- 
cated, and  orthopedic  and  other  surgical  interventions  to  prevent  and 
correct  defoimities. 


COMPRESSION  OF  THE  SPINAL  CORD. 

{Compression  Myelitis.) 

Etiology. — Compression  of  the  spinal  cord  may  result  from  caries 
of  the  vertebrae  (usually  tuberculous,  sometimes  syphilitic),  fracture- 
dislocation  or  tumor  of  the  vertebrae,  tumor  or  cyst  of  the  spinal 
meninges,  and  aneurysm  of  the  thoracic  or  abdominal  aorta. 

Pathology.^ — In  the  case  of  fracture  or  dislocation  the  compression 
may  occur  suddenly,  and  is  attended  by  varying  degrees  of  crushing  up 
to  complete  destruction  of  a  segment  or  severance  of  the  cord,  with  asso- 
ciated hemorrhage.  In  other  cases  the  compression  is  slow,  though 
usually  progressive;  the  cord  where  compressed  is  smaller  and  paler 
than  elsewhere,  and  reveals  more  or  less  secondary  degeneration  of  its 
various  tracts  and  replacement  neuroglial  fibrosis.  Various  grades 
of  meningitis  may  be  associated,  especially  in  the  tuberculous  and 
syphilitic  cases. 

Symptoms. — In  the  traumatic  cases  of  sudden  onset  the  symptoms  vary 
with  the  grade  of  compression;  they  may  be  those  of  a  total  transverse 
lesion  (page  837).  In  the  cases  of  more  insidious  onset  muscular  twitch- 
ings  and  pains,  radiating  in  the  course  of  the  nerves,  may  occur  from  irri- 
tation of  the  nerve  roots.  In  the  course  of  time  various  paralytic  and 
sensory  phenomena  develop,  varying  with  the  seat  of  the  compression; 
these  in  general  are  analogous  to  those  mentioned  in  connection  with 
myelitis  (page  880)  and  chronic  hypertrophic  pachymeningitis  (page 
828). 

Diagnosis. — The  diagnosis  depends  upon  the  symptoms  mentioned  and 
the  signs  of  the  primary  disorder  causing  the  compression.  Special 
attention  should  be  directed  to  detecting  the  early  stages  of  caries  of  the 
vertebrae,  which,  because  of  the  undefined  character  of  its  symptoms, 
often  passes  unnoticed:  persistent  pain  (lumbago,  etc.),  vertebral  ten- 
derness, muscular  rigidity  along  the  spine,  more  or  less  immobility  and 
difficulty  in  executing  vertebral  movements,  etc.,  should  not  be  over- 
looked. When  kyphosis,  skoliosis,  etc.,  have  developed,  the  diagnosis 
is  self-apparent. 

Prognosis. — The  prognosis  depends  upon  the  cause,  degree,  and  dura- 
tion of  the  compression. 

Treatment. — The  treatment  is  that  of  the  primary  cause.  In  tuber- 
culous caries  marked  benefit  and  cure  may  be  effected  by  rest,  various 
orthopedic  apparatus,  and  the  general  treatment  applicable  in  tuber- 
culosis; the  extent  of  the  improvement  in  the  nervous  symptoms  will 


TUMORS  OF  THE  SPINAL  CORD  '      883 

depend  upon  the  amount  of  permanent  damage  done  to  the  cord. 
Syphihtic  cases  require  antisyphiUtic  treatment.  Cases  due  to  fracture, 
dislocation,  or  tumor  may  be  reheved  by  surgical  measures  (laminec- 
tomy, etc.). 

TUMORS  OF  THE  SPINAL  CORD. 

Etiology. — Tumors  of  the  spinal  cord  are  more  common  in  males  than 
in  females,  and  they  may  occur  at  any  age,  although  they  are  most  com- 
mon in  young  adults.  The  etiological  factors  are  those  of  tumors  in 
general  and  are  as  ill  understood. 

Pathology. — Tumors  of  the  spinal  cord  may  be  primary  or  secondary, 
and  benign  (so-called)  or  malignant;  and  for  practical  purposes,  as  in 
the  brain,  gummas  and  large  or  solitary  tubercles  are  included  among 
the  tumors  of  the  spinal  cord.  These  spinal-cord  tumors  may  be 
divided  into:  (1)  The  medullary  or  intramedullary  growths  (those 
within  the  substance  of  the  cord).  These  comprise  not  more  than  20  to 
25  per  cent,  of  spinal  tumors;  the  most  common  are  the  gumma,  the 
tuberculoma,  and  the  glioma  (gliosarcoma).  They  give  rise  to  enlarge- 
ment and  distortion  of  the  cord  at  the  seat  of  growth,  and  to  various 
secondary  degenerations  of  the  tracts  destroyed  or  compressed.  The 
glioma  may  become  the  seat  of  secondary  softening  and  cavity  formation 
(see  syringomyelia,  page  884).  (2)  The  extramedullary  growths,  which 
develop  outside  the  cord — from  the  spinal  membranes,  intravertebral 
fibro-alveolar  tissue,  the  vertebrae,  the  intervertebral  cartilages,  etc.,  and 
comprise  endotheliomas,  sarcomas,  fibromas,  lipomas,  hydatid  and  other 
cysts,  gummas,  tubercles,  and  secondary  carcinomas.  These  compress 
the  cord  and  give  rise  to  lesions  analogous  to  those  due  to  compression 
from  other  causes  (page  882).  Tumors  in  general  may  develop  in  any 
part  of  the  cord;  they  are  more  common  on  the  dorsal  and  lateral  than 
on  the  ventral  surface. 

Symptoms. — Intramedullary  tumors  give  rise  to  initial  motor  paralysis 
and  sensory  disturbances,  varying  with  the  seat  of  development.  Occa- 
sionally there  is  an  early  localized  muscular  atrophy  (destruction  of  the 
cells  in  the  anterior  cornua);  and  this  may  be  combined  with  dissociated 
anesthesia.  In  other  cases  the  symptoms  are  those  of  a  unilateral 
lesion  (Brown-Sequard  paralysis,  page  838);  that  is,  chiefly  motor 
paralysis  on  the  side  of  and  below  the  segmental  level  of  the  lesion,  and 
anesthesia  on  the  other  side.  The  tumor  may  continue  to  grow  and 
ultimately  give  rise  to  symptoms  of  a  more  or  less  complete  transverse 
lesion  (page  837).  In  other  cases,  in  which  the  gray  matter  is  espe- 
cially involved,  the  symptoms  of  more  or  less  outspoken  syringomyelia 
ensue. 

Extramedullary  growths  give  rise  to  pain,  due  to  compression  of  the 
dorsal  roots;  generally  at  hrst  this  is  unilateral,  and  it  radiates  vaii- 
ously,  although  in  "root  distribution"  depending  upon  the  segmental 
level  of  the  lesion.     Irritation  of  the  anterior  roots  may  cause  muscular 


884     DIFFUSE  AND  FOCAL  DISEASES  OF  THE  SPINAL  CORD 

twitchings  and  rigidity.  Subsequently,  in  consequence  of  compres- 
sion of  the  cord,  various  motor  (paralytic)  and  sensory  disturbances 
ensue.  These  at  first  may  be  of  the  Brown-Sequard  type;  later,  when 
there  is  more  or  less  complete  transverse  compression  of  the  cord,  the 
symptoms  consist  chiefly  of  paralysis  and  wasting  of  the  muscles  corre- 
sponding to  the  segmental  level  of  the  growth,  and  anesthesia  corre- 
sponding to  the  dorsal  roots  compressed;  spastic  paralysis  without 
wasting  below  the  level  of  the  lesion;  and  perhaps  later  more  or  less 
complete  anesthesia  below  the  lesion  and  loss  of  control  over  the  vesical 
and  rectal  sphincters. 

Diagnosis. — ^The  diagnosis  is  often  in  doubt;  but  when  present,  pain 
radiating  in  a  root  distribution  and  progressive  paralysis  are  almost  con- 
clusive evidence  of  an  extramedullary  growth.  In  other  cases  localized 
muscular  atrophy  and  associated  anesthesia,  with  the  later  development 
of  Brown-Sequard  paralysis  or  paraplegia,  indicate  an  intramedullary 
growth.  In  most  cases,  however,  one  must  be  content  with  the  diagnosis 
of  intraspinal  tumor,  and  should  determine  the  level  of  the  growth  by 
attention  to  the  segmental  distribution  of  the  motor  and  sensory  phe- 
nomena. One  must  exclude  compression  of  the  spinal  cord  from  other 
causes  (page  882). 

Prognosis. — The  outlook  is  bad  unless  the  growth  be  a  gumma  or 
amenable  to  surgical  removal,  which,  of  course,  is  impossible  in  intra- 
medullary growths. 

Treatment. — The  treatment  is  wholly  surgical,  unless  the  growth  be 
a  gumma.  In  case  of  doubt,  therefore,  recourse  should  be  had  to  a 
course  of  antisyphilitic  treatment  for  four  to  six  weeks.  If  improve- 
ment does  not  follow,  operation  should  be  undertaken;  otherwise,  the 
treatment  is  symptomatic. 


SYRINGOMYELIA. 

{Spinal  Gliosis.) 

Syringomyelia  is  a  condition  characterized  by  neurogliomatous  new- 
growth  about  the  central  canal,  with  subsequent  cavity  formation  ex- 
tending a  variable  length  throughout  the  spinal  cord.  It  should  be 
distinguished  from  hydromyelia  or  dilatation  of  the  central  canal,  which 
may  occur,  usually  in  minor  grade,  as  a  congenital  condition  or  in  con- 
sequence of  the  pressure  of  tumors,  etc. 

Etiology. — Syringomyelia  occurs  especially  in  early  adult  life,  and  in 
both  sexes.     The  definite  etiological  factors  are  not  known. 

Pathology. — The  cavity  formation  is  most  common  in  the  cervical  and 
upper  thoracic  portion,  although  it  may  extend  throughout  more  or  less  of 
the  length  of  the  cord ;  it  varies  much  in  shape,  being  usually  more  or  less 
rounded,  but  it  may  extend  into  one  or  both  dorsal  cornua;  it  generally 
takes  the  place  of  the  central  canal,  but  it  may  develop  about  the  central 
canal,  which  may  be  found  compressed  somewhere  in  the  periphery.    The 


SYRINGOMYELIA  885 

condition  is  commonly  believed  to  be  the  result  of  primary  proliferation 
of  the  neuroglial  tissue  with  consecutive  degeneration  and  cavity  for- 
mation. Some  observers  attribute  it  to  a  congenital  defect  of  develop- 
ment, with  distention  of  the  central  canal  (hydromyelia)  and  consequent 
proliferation  of  the  surrounding  neuroglia.  Although  this  condition 
may  occur,  syringomyelia  seems  undoubtedly  to  be  a  primary  neurogliosis; 
the  epithelial  lining  of  the  cavity  found  in  some  cases  is  that  of  the 
original  central  canal. 

Symptoms. — The  symptoms  are  of  slow  and  insidious  onset  and  pro- 
gression; they  vary  with  the  position,  size,  and  direction  of  the  neu- 
rogliosis and  cavity  formation;  and  they  result  from  destruction  of  the 
spinal-cord  substance  at  different  segmental  levels,  and  from  pressure 
upon  adjacent  tracts  in  the  cord.  Since  the  gray  matter  is  primarily  and 
most  extensively  involved,  the  following  characteristic  signs  occur:  (1) 
Dissociated  anesthesia — that  is,  loss  of  the  pain  and  temperature  (pro- 
topathic)  sensibility,  with  good  or  complete  preservation  of  tactile 
(epicritic)  sensibility  in  any  part  of  the  body;  (2)  progressive  muscular 
atrophy,  with  fibrillary  twitchings,  and  ultimate  reactions  of  degenera- 
tion, usually  developing  first  and  remaining  most  marked  in  the  arms 
(destruction  of  the  cells  of  the  lower  motor  neuron);  and  (3)  trophic 
and  vasomotor  disturbances  of  the  skin,  such  as  injuries  and  burns  not 
felt  (loss  of  pain  sense),  local  hyperemias  and  anemias,  excessive  sweating 
or  dryness,  localized  atrophy,  bullae,  painless  whitlows  and  abscesses, 
gangrene,  perforating  ulcers,  etc.;  and  of  the  bones  and  joints,  such  as 
arthropathies  (considerable  effusion  into  the  joint,  thickening  of  all  the 
joint  tissues,  with  final  absorption  of  the  bone  and  atrophy  of  the  articu- 
lating surfaces);  these  resemble  the  similar  arthropathies  of  tabes  dor- 
salis,  but  are  more  common  in  the  shoulder,  elbow,  and  \\Tist  than  in  the 
knee  or  ankle.  Spontaneous  painless  fractures  also  may  occur  (due  to 
brittleness  of  the  bone).  In  addition,  there  may  be  more  or  less  spastic 
paraplegia  (involvement  of  the  pyramidal  tracts),  or  the  manifestations 
of  more  or  less  complete  transverse  myelitis  (page  880),  depending  upon 
the  extent  of  the  horizontal  involvement  of  the  cord.  Often  there  are 
symptoms  of  unilateral  (or  perhaps  bilateral)  paralysis  of  the  cervical 
sympathetic  nerves  (page  824),  from  involvement  of  the  first  thoracic 
segment  (spinal  centre  for  the  cervical  sympathetic).  Extension  of  the 
lesions  to  the  medulla  may  give  rise  to  atrophy  and  fibrillary  twitchings  of 
the  muscles  of  the  tongue  and  face  (usually,  at  first  at  least,  unilateral), 
dissociated  anesthesia  of  the  face  and  head,  oculomotor  j^araiysis  and 
nystagmus;  and  difficulty  in  speaking,  swallowing,  and  breathing,  and 
cardiac  arrhythmia  (so-called  syringol>ulbia).  Progression  of  the  lesions 
to  the  sacral  cord  may  result  in  loss  of  control  over  tlie  vesical  and 
rectal  sphincters. 

Morvaiis  disease,  a  condition  characterized  by  painless  whitlows  and 
other  trophic  or  nutritional  disorders  of  the  hands,  such  as  ulcerations, 
necroses,  falling  of  the  nails,  etc.,  is  now  believed  to  be  a  variety  of 
syringomyelia.     The  cases  studied  of  recent  years  reveal  also  muscular 


886  NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 

atrophy  and  dissociated  anesthesia,  as  well  as  cavitation  of  the  spinal 
cord  (when  studied  after  death). 

Diagnosis. — The  disease  may  be  overlooked  in  the  early  stages,  unless 
the  dissociated  anesthesia  is  carefully  sought  for;  but  this,  the  pro- 
gressive muscular  atrophy,  and  the  trophic  disorders  make  the  diag- 
nosis easy. 

Prognosis. — The  disorder,  as  a  rule,  is  slowly  progressive,  but  it  may 
last  many  years,  and  sometimes  comes  to  a  standstill ;  it  is  not  in  itself 
dangerous  to  life  unless  the  medulla  becomes  involved. 

Treatment. — The  treatment  is  purely  symptomatic — massage  and 
electricity  to  keep  up  the  nutrition  of  the  muscle,  and  perhaps  strychnine 
as  a  general  tonic. 


NERVOUS  DISEASES  OF  FUNCTIONAL  OR 
UNKNOWN  NATURE. 


MIGRAINE. 

{Hetnicrania ;  Sick  Headache;  Bilious  Headache.) 

Migraine  is  a  disorder  characterized  by  paroxysmal  attacks  of  severe 
headache,  nausea,  vomiting,  and  prostration,  and  usually  preceded  by 
certain  visual  disturbances. 

Etiology. — Migraine  is  much  more  common  in  women  than  in  men; 
it  occurs  in  neurotic  subjects;  and  it  sometimes,  but  not  always,  exhibits 
hereditary  or  familial  tendencies.  In  the  great  majority  of  cases  it  is 
a  reflex  manifestation  of  disease  of  some  organ  of  the  body,  and  is 
found  especially  related  to  errors  of  refraction,  disease  of  the  naso- 
pharynx, of  the  female  genitalia  (especially  dysmenorrhoea),  and  of  the 
gastro-intestinal  tract;  in  some  cases  it  seems  to  be  autotoxic  and  a 
manifestation  of  gastro-intestinal  auto-intoxication,  gout,  uremia,  etc.; 
it  is  perhaps  sometimes  vasomotor  in  origin — vasoconstriction  followed 
by  vasodilatation  of  the  cerebral  vessels  and  headache  (suggested  also  by 
a  primary  facial  pallor  and  blueness  and  coldness  of  the  extremities  and 
secondary  flushing  and  perhaps  sweating);  it  may  replace  an  epileptic 
attack;  in  some  cases  no  adequate  cause  can  be  assigned.  The  attacks 
may  be  induced  by  excessive  and  prolonged  eyestrain  (week-ends  in 
school  children  and  other  students),  by  general  fatigue,  dietetic  indis- 
cretions, constipation,  menstruation,  emotional  excitement,  etc. 

Symptoms. — In  the  majority  of  cases  there  are  certain  premonitory 
symptoms  (for  hours,  a  day,  or  more)  that  enable  the  patient  to  foretell 
the  advent  of  an  attack;  these  are  especially  visual — flashes  of  light, 
colored  spectra,  dimness  of  vision,  etc.;  or  the  patient  may  feel  generally 


MIGRAINE  887 

dull,  "headachy,"  and  somnolent.  The  onset  may  be  sudden,  or  there 
may  be  a  more  gradual  increment  of  the  premonitory  headache;  at  all 
events,  the  headache  becomes  severe,  and  although  usually  limited  to  one 
side  or  temple  (hemicrania),  it  may  be  bilateral  and  general.  It  is  in- 
creased by  auditory,  visual,  and  sensory  impressions  of  all  kinds.  In 
an  hour  or  thereabouts  nausea  and  vomiting  supervene;  retching  may 
be  marked,  and,  with  the  headache,  leads  to  marked  prostration.  In 
the  course  of  a  short  time  the  patient  usually  falls  asleep,  and  awakes 
several  hours  later  much  refreshed,  if  not  entirely  well;  in  some  cases, 
however,  the  attack  may  last  two  or  three  days.  Various  sensory 
phenomena  are  sometimes  associated,  such  as  numbness  and  tingling  or 
anesthesia  of  the  limbs;  sometimes  transient  muscular  weakness,  or 
vertigo,  tinnitus  aurium,  deafness,  aphasia,  etc.  The  attacks  may  occur 
at  long  or  short  intervals,  and  may  continue  throughout  life.  In  women 
they  may  cease  about  the  time  of  the  menopause,  and  at  about  the  age 
of  fifty  years  in  men. 

Diagnosis. — ^Although  migraine  is  typically  paroxysmal  and  unilateral, 
and  attended  by  visual  and  other  sensory  disturbances,  and  nausea  and 
vomiting,  all  attacks  are  not  typical;  other  causes  of  headache,  there- 
fore, must  be  inquired  into — all  possible  sources  of  reflex  irritation; 
diseases  of  metabolism,  of  the  blood,  of  the  cardiovascular  system,  of 
the  urinary  system,  and  of  the  brain  and  its  membranes  and  the  skull. 
In  neuralgia  there  are  paroxysms  of  pain,  radiating  in  the  area  of  dis- 
tribution of  a  nerve,  and  tender  spots  along  the  course  of  the  nerve;  and 
the  visual  signs  and  the  nausea  and  vomiting  of  migraine  do  not  occur. 

Prognosis. — The  prognosis  is  the  better  the  earlier  the  patient  is  thor- 
oughly studied  and  all  possible  sources  of  reflex  irritation  eliminated. 
The  outlook  is  bad  for  cure  in  cases  of  long  standing,  but  in  even  the 
most  intractable  cases  much  relief  can  be  afforded  the  patient. 

Treatment. — The  most  essential  part  of  the  treatment  is  to  prevent  the 
attacks.  In  the  great  majoiity  of  cases  this  can  be  done  by  the  proper 
correction  of  errors  of  refraction — even  slight  errors;  in  other  cases, 
other  sources  of  reflex  irritation  must  be  sought  and  adequately  treated; 
the  diet  should  be  regulated  (purin-free  diet),  the  bowels  opened  thor- 
oughly daily,  a  hygienic  mode  of  life  insisted  upon,  and  all  factors  that 
in  any  way  tend  in  the  individual  patient  to  provoke  an  attack  corrected. 
Bromides,  salicylates,  sodium  benzoate,  and  potassium  acetate  (and  other 
alkalies)  also  are  serviceable  in  preventing  attacks;  as  are  also  the  saline 
cathartics  taken  daily  before  breakfast.  During  the  attack  the  patient 
should  go  to  bed  in  a  quiet,  darkened  room,  and  abstain  from  food.  If 
retching  continues,  it  may  be  best  relieved  by  lavage;  local  hot  applica- 
tions, bismuth,  cerium  oxalate,  cocaine,  etc.,  may  also  be  tried.  The 
bowels  should  be  opened  by  calomel  or  blue  mass  and  a  saline  cathartic. 
Acetphenetidin,  acetanilide,  and  similar  drugs  are  often  necessary  for  the 
headache;  or  one  may  give  caffeine,  sodium  benzoate,  or  nitroglycerin 
(in  the  event  of  high  blood  pressure),  or  gelsemium  or  cannabis  indica. 


NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 


EPILEPSY. 

Epilepsy  is  a  disorder  of  the  nervous  system,  characterized  by  recur- 
ring attacks  of  loss  of  consciousness,  attended  or  not  by  convulsions. 
The  attacks  of  momentary  loss  of  consciousness  unattended  by  convul- 
sions are  know  as  petit  mal,  or  slight  attacks;  those  in  which  there  is  loss 
of  consciousness  and  general  convulsions  are  known  as  grand  mal,  or 
severe  attacks;  and  those  in  which  the  convulsive  seizures  remain  local- 
ized to  a  certain  definite  area  or  group  of  muscles,  or  at  least  always  begin 
therein,  and  are  often  unattended  by  loss  of  consciousness,  are  known  as 
Jacksonian  epilepsy. 

Etiology. — In  a  majority  of  the  cases  epilepsy  begins  before  puberty, 
and  it  involves  the  sexes  equally.  It  rarely  develops  de  novo  after  the 
twentieth  year,  the  cases  observed  thereafter  being  usually  either  recur- 
rences of  attacks  occurring  for  the  first  time  during  childhood,  or  Jack- 
sonian epilepsy  due  to  a  local  cortical  lesion.  In  the  so-called  idiopathic 
epilepsy  no  definite  cause  can  be  assigned,  although  etiological  impor- 
tance is  attributed  to  certain  hereditary  influences,  such  as  epilepsy,  in- 
sanity, hysteria  and  other  neurotic  conditions,  syphilis,  and  chronic 
alcoholism  in  one  or  both  parents.  In  other  cases  the  disease,  or  at  least 
epileptiform  convulsions,  may  be  due  to:  (1)  Injuries  to  the  head  re- 
ceived during  birth,  or  vascular  (hemorrhagic)  disorders  suffered  soon 
thereafter  and  followed  by  persisting  residual  lesions  (cerebral  paralyses 
of  infants  and  children).  (2)  Toxemias,  such  as  infectious  diseases  (in 
infants  and  children),  alcoholism  (especially  common  in  middle-aged  and 
elderly  chronic  alcoholic  subjects),  plumbism,  uremia,  intestinal  auto- 
intoxication (especially  in  infants  and  children).  (3)  Reflex  factors, 
such  as  dentition,  an  adherent  prepuce,  intestinal  worms,  a  foreign  body 
in  the  auditory  canal  or  the  nose,  errors  of  refraction,  the  irritation  pro- 
duced by  a  cicatrix,  onset  of  puberty,  menstruation,  etc.  (4)  Cardio- 
vascular disease,  such  as  arteriosclerosis,  which  sometimes  causes  con- 
vulsive seizures  in  elderly  subjects,  and  if  associated  with  disorder  of  the 
bundle  of  His  may  lead  to  Adams-Stokes  disease  (page  420).  (5)  Organic 
disease  of  the  brain,  especially  fracture  of  the  skull  and  resulting  irrita- 
tion of  the  brain  by  a  spicule  of  bone,  local  meningitis,  etc.;  brain 
tumor;  brain  abscess;  syphilis,  etc.  Many  of  these  conditions  can 
scarcely  be  classed  as  epilepsy  in  a  true  sense,  although  the  convulsive 
seizure  may  be  indistinguishable  from  that  of  true  epilepsy;  some  of 
them  are  promptly  cured  by  the  removal  of  the  exciting  cause  of  the 
attack,  such  as  a  foreign  body  in  the  auditory  canal,  an  adherent  prepuce, 
a  spicule  of  bone  irritating  the  cerebral  cortex,  etc. ;  but  in  some  of  these 
cases  the  "epileptic  habit"  may  have  become  acquired,  and  the  convul- 
sive seizures  may  not  subside  for  some  time. 

Pathology. — In  the  idiopathic  cases  there  is  no  recognizable  lesion. 
In  the  other  cases  there  are  the  various  lesions  peculiar  to  the  disorders 
mentioned. 


EPILEPSY  889 

The  epileptic  fit  may  be  looked  upon  as  a  sudden  discharge  of  nervous 
energy,  provoked  by  influences  which  may  be:  (1)  Toxic  in  nature,  such 
as  the  poison  of  uremia;  the  products  of  perverted  metabolism,  such  as 
ammonium  carbamate,  etc. ;  (2)  irritative,  such  as  the  various  organic 
disorders  of  the  brain  mentioned;  or  (3)  vascular;  and  these  various 
toxic  and  other  stimuli  may,  if  sufficiently  active,  provoke  the  discharge 
of  nervous  energy  (the  convulsion)  by  acting  upon  normal  nerve  cells; 
but,  as  is  likely  more  common,  being  not  excessively  active,  they  unduly 
stimulate  subnormal  or  highly  sensitive  cells  and  provoke  an  altogether 
disproportionate  discharge  of  nervous  energy. 

Symptoms. — Grand  Mal. — ^A  typical  attack  of  grand  mat  consists  of 
an  aura,  a  convulsive  seizure  with  loss  of  consciousness,  and  certain  after- 
effects. The  attack  apparently  may  originate  in  any  part  of  the  cerebral 
cortex,  and  the  aura  or  premonitory  sensations  vary  accordingly.  These 
may  be  psychical  in  nature  (a  vague,  dreamy,  or  terrified  state) ;  associ- 
ated with  the  special  senses — visual  (occiptal  lobe),  auditory  (temporo- 
sphenoidal  lobe),  olfactory  or  gustatory;  related  to  the  abdomen  and 
the  viscera  (sensations  of  epigastric  "sinking"  or  distress,  or  palpitation 
or  other  sensations  related  to  the  heart — pneumogastric  aura);  or  there 
may  be  a  sensation  of  numbness  or  other  paresthesia  in  a  finger  or  a 
hand  (sensory  aura),  or  localized  twitching  (motor  aura).  These  aurse 
may  be  absent;  when  present,  they  are  usually  of  momentary  duration 
— a  few  seconds  to  perhaps  a  minute  or  thereabouts.  Very  soon  the 
patient  emits  a  loud  scream  or  yell  (epileptic  cry),  falls  to  the  ground 
without  any  conscious  effort  to  protect  himself  from  injury,  and  is  imme- 
diately in  a  convulsive  seizure  and  unconscious.  The  spasms,  which  may 
begin  anywhere,  soon  become  generalized,  although  not  everywhere 
equally  marked.  At  first  they  are  tonic,  and  involving  the  muscles  of 
respiration,  lead  to  cyanosis  and  venous  distention;  in  a  few  seconds  they 
become  clonic,  intermittent,  jerky,  and  often  violent,  provoking  marked 
tossing  about  of  the  patient's  limbs  and  body;  the  eyelids  open  and  close, 
the  eyes  move  about  in  varying  directions,  the  face  is  intermittently  dis- 
torted and  relaxed,  and  the  jaws  open  and  close  violently,  in  consequence 
of  which  the  tongue  is  usually  lacerated  and  blood-stained  saliva  issues 
from  the  mouth.  The  uiine  often  and  the  feces  sometimes  are  dis- 
charged involuntarily;  and  petechial  hemorrhages  may  occur  into  the 
skin  and  conjunctivae.  As  a  rule,  in  the  course  of  one  or  two,  rarely 
three  or  more,  minutes  the  convulsive  movements  gradually  cease  and 
the  patient,  fully  relaxed,  falls  into  a  profound  coma.  In  some  cases  he 
can  be  more  or  less  aroused  after  a  short  time,  but  he  may  sleep  for  hours 
and  awake  mentally  confused  and  complaining  of  headache  and  muscular 
soreness;  and  there  may  be  other  after-eft'ects,  such  as  a  trance-like  state, 
loss  of  memory,  aphasia,  monoplegia,  hemiplegia,  mania,  etc. — all  of 
which  soon  subside,  as  a  rule.  Or  he  may  become  subject  to  post- 
epileptic automatism,  and  perform  apparently  purposeful  acts,  such  as 
walking,  riding,  journeying,  criminal  acts,  etc.,  without  subsequent  recol- 
lection thereof.     In  some  cases  the  period  of  sleep  is  very  short — rarely 


890  NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 

perhaps  absent — so  that  soon  after  even  a  rather  severe  convulsion  the 
patient  may  return  to  his  former  occupation.  Attacks  may  occur  once  or 
more  frequently  daily,  or  at  longer  intervals — weeks,  months,  years.  In 
some  cases  a  number  of  convulsive  seizures  follow  in  rapid  succession, 
the  patient  meanwhile  remaining  entirely  unconscious;  this,  so-called  status 
epilepticus,  may  continue  for  hours  or  a  day  or  more;  it  is  often  attended 
by  fever  and  rapid  pulse,  and  may  soon  lead  to  death  from  exhaustion. 

Petit  Mal. — ^Attacks  of  petit  mal  consist  of  momentary  loss  of  con- 
sciousness, perhaps  also  vertigo  and  faintness,  but  no  convulsions. 
The  patient  may  suddenly  stop  talking  or  perfoiming  some  act,  drop 
what  he  may  hold  in  his  hand,  or  take  up  some  new  act,  and  almost 
immediately  revert  to  his  former  activity.  The  attack  may  pass  almost, 
if  not  quite,  unnoticed  by  the  patient's  associates,  or  they  may  observe  a 
transient  pallor  of  the  face  or  twitching  of  a  muscle.  In  other  cases  the 
patient  may  experience  only  the  aura  of  the  more  severe  grand  mal. 
These  slight  attacks  may  occur  alone  at  long  or  short  intervals,  or  they 
may  alternate  with  severe  seizures. 

Jacksonian  (Cortical,  Partial)  Epilepsy. — Jacksonian  epilepsy  is 
characterized  by  convulsive  seizures  that  begin  and  usually  remain 
localized  in  a  certain  definite  group  of  muscles,  and  are  often  unattended 
by  loss  of  consciousness;  but  in  some  cases  the  convulsions  become  more 
widespread,  and  consciousness  may  finally  become  lost.  A  study  of  the 
beginning  of  the  convulsive  seizures,  commonly  in  the  finger,  hand,  toe, 
or  face,  may  lead  to  an  accurate  localization  of  the  lesion,  which  is  com- 
monly an  irritative  lesion  of  the  motor  or  sensory  cortex. 

Diagnosis. — Grand  mal  is  usually  readily  recognized  by  the  aura,  the 
epileptic  cry,  the  sudden  loss  of  consciousness,  tonic  and  later  clonic 
spasms,  laceration  of  the  tongue,  involuntary  voiding  of  the  urine,  the 
postconvulsive  sleep,  and  other  after-effects.  Attacks  often  occur  at 
night,  and,  if  unobserved  by  others,  may  be  recognized  by  the  involun- 
tary voiding  of  urine,  laceration  of  the  tongue,  and  a  rather  common 
mental  confusion  and  headache  in  the  morning.  Hysterical  attacks  may 
be  distinguished  by  associated  emotional  disturbances  and  hysterical 
stigmas;  usually  a  gradual  onset  and  rarely  an  injury  when  falling;  crying, 
talking,  or  screaming  during  the  attack;  absence  of  complete  uncon- 
sciousness, and  of  lacerations  of  the  tongue  and  voiding  the  urine 
during  the  attack;  longer  duration  of  the  attack,  and  the  frequent 
possibility  of  stopping  it  by  procedures  such  as  throwing  water  in  the 
patient's  face,  etc.  Attacks  of  vetit  mal  may  be  distinguished  from  vertigo 
due  to  other  causes  and  syncope  by  the  occurrence  of  actual,  although 
momentary,  loss  of  consciousness,  and  the  absence  of  the  ordinary  causes 
of  vertigo  and  syncope  (heart  disease,  Meniere's  disease,  etc.).  Jack- 
sonian epilepsy  is  in  itself  characteristic.  The  epileptiform  convulsions 
due  to  other  mentioned  etiological  factors  should  be  recognized  by  deter- 
mining the  presence  of  those  causes  in  the  individual  case. 

Prognosis. — The  prognosis  varies,  and  depends  upon  the  age  when  the 
disease  developed,  its  severity,  and  the  possibility  of  removing  exciting 


EPILEPSY  891 

causes  of  the  attack.  In  a  considerable  proportion  of  the  cases  cessation 
of  the  attacks  or  cure  can  be  effected,  but  a  tendency  sometimes  per- 
sists for  the  attacks  to  recur  in  later  life.  The  prognosis  is  poor  in  the 
cases  beginning  in  children  and  after  the  thirty-fifth  year  (many  syph- 
ilitic); it  is  relatively  good  in  those  developing  about  puberty.  In  many 
cases,  especially  in  cases  of  frequently  recurring  attacks,  the  mentality 
gradually  becomes  impaired. 

Treatment. — In  all  cases,  upon  the  development  of  fits  the  most  pains- 
taking care  must  be  exercised  to  discover  any  possible  source  of  irritation, 
since  in  the  early  stages  removal  of  local  irritations  may  lead  to  mitiga- 
tion if  not  cure  of  the  disease.  The  best  possible  hygienic  conditions 
must  be  secured.  The  child  should  not  be  forced  to  keep  up  in  studies 
with  others  better  endowed.  Excellent  results  have  been  achieved  at 
epileptic  colonies  where  the  patients  are  taught  some  interesting  and  use- 
ful manual  occupation.  The  diet  should  be  light,  nutritious,  and  non- 
stimulating;  recent  studies  suggest  the  wisdom  of  reducing  foods  con- 
taining purin  bodies  (meat,  fish,  tea,  coffee,  etc.),  and  some  observers 
believe  in  the  desirability  of  reducing  the  sodium  chloride  intake.  The 
bowels  should  be  opened  regularly  and  thoroughly;  colonic  flushings 
seem  sometimes  to  be  of  service  (lessening  intestinal  auto-intoxication?). 

The  epileptic  seizure  requires  no  special  treatment,  aside  from  care  to 
prevent  the  patient's  injuring  himself;  a  mouth  gag  or  similar  contrivance 
between  the  teeth  to  prevent  his  biting  his  tongue  (usually  impossible, 
on  account  of  the  brevity  of  the  attack);  and  loosening  the  clothing  to 
facilitate  breathing. 

On  the  whole  the  best  medicinal  treatment  still  seems  to  consist  of  the 
use  of  the  bromides,  despite  some  opinions  to  the  contrary.  Any  of  the 
bromides  may  be  given,  although  perhaps  the  mixed  bromides  secure  the 
best  results.  They  may  be  combined  with  antipyrin  (5  grains,  0.3  gram, 
thrice  daily — H.  C.  Wood);  or,  to  counteract  the  tendency  to  produce 
acne,  they  may  be  given  as  follows : 

I^ — Potassium  bromide 4  drams  16  0 

Sodium  bromide, 

Ammonium  bromide,  of  each 2  drams  8|0 

Solution  of  potassium  arsenite 45  minims  3  0 

Camphor  water,  sufficient  to  make 8  ounces  250l0 — M. 

S. — Two  teaspoonfuls  (10  c.o.)  in  water  three  times  daily. 

Strontium  bromide  also  may  be  used;  and  the  dose  of  the  bromides  in 
general  may  be  varied  to  suit  the  individual  patient;  more  than  40  to  50 
grains  (2.5  to  3.25  grams)  daily  is  rarely  required.  The  cases  not  bene- 
fited by  these  doses  are  not  likely  to  be  benefited  by  larger  doses,  and 
large  doses  not  only  produce  acne,  but  almost  certainly  cause  mental 
depression  (bromism),  and  sometimes  ultimate  mental  deterioration. 
Belladonna,  atropine,  sodium  borate,  nitroglycerin,  thyroid  extract,  and 
other  drugs,  alone  or  in  combination  with  the  bromides,  have  also  been 
recommended.  In  status  epilepticus  the  bromides,  chloral,  morphine, 
hyoscine,  etc.,  are  indicated,  and  stimulants  if  the  patient  goes  into 


892  NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 

collapse.  In  Jacksonian  epilepsy  operation  is  often  of  the  greatest  utility; 
it  should  be  undertaken  if  the  focal  symptoms  are  definite  and  referable 
to  an  accessible  region  of  the  brain,  especially  if  there  is  a  history  of 
injury  to,  or  a  depression  of,  the  skull. 


HYSTERIA, 

Hysteria  is  one  of  the  so-called  functional  disorders  of  the  nervous  sys- 
tem, consisting  of  a  permanent  abnormal  psychic  state  (hysterical  tem- 
perament), abnormal  suggestibility,  and  divers  transient  motor,  sensory, 
vasomotor,  trophic,  and  other  neurotic  phenomena. 

Etiology. — Hysteria  is  very  common  in  females,  but  it  occurs  also  in 
males — more  commonly  than  is  generally  supposed — and  it  is  not  un- 
common in  children.  Its  manifestations  may  become  obtrusive  at  any 
age,  but  they  are  most  common  at  or  soon  after  puberty  or  in  early  adult 
life.  Heredity — hysteria,  epilepsy,  insanity,  neurotic  instability,  etc.,  in 
one  or  both  parents — is  of  predisposing  influence;  almost  equally  impor- 
tant is  bad  early  training  and  education.  The  exciting  causes  of  the 
initial  manifestations  comprise  traumas,  shocks  of  various  kinds,  emo- 
tional disturbances,  etc. 

Pathology. — No  definite  lesions  are  known;  the  disease,  therefore,  is 
called  functional,  although  doubtless  there  is  some  lesion  which  still 
eludes  detection.  Hysterical  phenomena,  of  course,  may  accompany 
organic  disorders. 

Symptoms. — The  basis  of  hysteria  is  the  permanent  hysterical  tempera- 
ment, which  is  said  by  Starr  to  be  manifested  "by  an  abnormally  keen 
sensibility  to  all  external  impressions  and  sensations,  by  a  high  grade  of 
imaginative  power,  by  a  susceptibility  to  suggestions,  by  an  unusual 
desire  for  attention  and  notice,  by  variations  in  mood  not  due  to  apparent 
causes,  by  a  lack  of  judgment,  by  a  manifest  incapacity  to  exercise  con- 
trol over  thought,  emotion,  and  action,  and  by  a  tendency  to  act  on  sud- 
den impulses." 

The  motor  phenomena  consist  of  convulsive  attacks,  paralyses,  spasms, 
and  tremors.  The  convulsive  attacks  (hysteria  major),  which  are  rather 
uncommon,  bear  some  resemblance  to  epilepsy,  which  has  suggested  the 
term  hystero-epilepsy — a  misnomer.  They  are  usually  preceded  by 
emotional  disturbances,  globus  hystericus  (a  sensation  of  a  lump  or 
obstruction  in  the  throat  and  consequent  suffocation),  etc.  The  onset 
is  usually  rather  gradual,  although  it  may  be  sudden;  consciousness  is 
not  wholly  lost;  a  tonic  stage  is  followed  by  clonic  movements  and  the 
adoption  of  various  more  or  less  grotesque  attitudes.  The  attack  often 
lasts  upward  of  a  half  hour  or  more,  and  may  be  succeeded  by  a  period  of 
mental  aberration — pseudomania,  a  dreamy  state,  lethargy,  trance,  etc. 
Incomplete  or  abortive  attacks  (hysteria  minor)  may  occur;  they  are  un- 
associated  with  convulsive  seizures  and  may  consist  of  attacks  of  causeless 
laughing  and  crying,  grotesque  attitudes,  passionate  attitudes  (ecstasy), 


HYSTERIA  893 

catalepsy,  somnambulism,  etc.  Hysterical  paralysis  may  be  mono- 
plegic,  hemiplegic,  paraplegic  (most  common),  or  affect  any  or  all  the 
limbs  variously,  or  only  groups  of  muscles.  The  paralyses  may  come  on 
slowly  or  suddenly  and  they  may  disappear  as  they  came;  they  may  be 
partial  or  complete,  and  they  are  often  preceded  by  more  or  less  muscular 
weakness  (hysterical  myasthenia).  Some  muscular  atrophy  may  follow 
(from  disuse),  but  there  are  no  reactions  of  degeneration;  the  knee-jerk 
may  be  normal  or  exaggerated  (never  absent);  an  imperfect  ankle  clonus 
is  said  to  be  occasionally  observed,  but  the  Babinski  sign  is  never  elicited. 
The  superficial  reflexes  may  be  abolished,  especially  when  sensory 
changes  are  associated.  Control  over  the  vesical  and  rectal  sphincters 
is  maintained,  but  retention  of  the  urine,  with  overflow,  may  occur. 
Partial  or  complete  aphonia  may  ensue  from  paralysis  of  the  laryngeal 
muscles,  usually  the  adductors.  In  some  cases  of  paraplegia  the  loss  of 
power  is  apparent,  not  in  the  reclining  or  sitting  posture,  but  only  w^hen 
the  patient  attempts  to  stand  (astasia)  or  walk  (abasia);  in  these  cases 
there  is  usually  no  ataxia  and  no  disturbances  of  sensation ;  most,  if  not 
all,  of  the  cases  are  hysterical.  There  may  be  also  involvement  of  the 
pharyngeal  and  other  muscles  supplied  by  the  cranial  nerves.  Muscular 
spasms  often  occur;  involving  the  arm,  leg,  or  neck,  they  give  rise  to 
various  contractures  and  deformities  (which  may  relax  during  sleep  or 
anesthetization);  involving  the  muscles  supplied  by  the  cranial  nerves, 
they  may  cause  spasmodic  ptosis,  strabismus,  deviation  of  the  tongue, 
spasmodic  oesophageal  obstruction,  etc.  Sometimes  peculiar  dancing 
movements  occur  (a  form  of  saltatory  spasm).  Tremors  are  very  com- 
mon; they  may  be  fine  or  coarse,  rhythmic  or  arrhythmic,  choreiform; 
and  they  may  involve  any  part  of  the  body,  especially  the  eyelids,  mouth, 
tongue,  fingers,  shouldeis,  legs,  etc. 

The  sensory  phenomena  consist  of  anesthesia,  hyperesthesia,  and 
paresthesia.  Anesthesia  is  the  most  common;  it  is  usually  a  hemi- 
anesthesia (skin  and  mucous  membranes),  which  may  be  partial  or 
complete  for  all  types  of  sensibility,  or  the  sensibility  may  be  dissociated; 
in  other  cases  it  is  limited  to  a  distal  portion  of  a  limb  (glove  or  stocking 
form),  or  a  segment  (cuff  form);  or  it  may  occur  in  variously  shaped 
patches,  which  may  change  from  time  to  time.  Hyperesthesia  is  a  sig- 
nificant symptom,  the  basis  of  so-called  hysterogenetic  zones;  these 
are  most  common  over  the  ovaries,  beneath  the  breasts,  just  below  the 
ribs,  and  over  the  vertebrae  (see  F'ig.  15,  page  804).  Pressure  over  these 
tender  spots  may  induce  hysteiical  "attacks,"  and  promote  their  cessa- 
tion when  they  have  developed.  Paresthesic  phenomena  of  various  kinds 
(sensations  of  heat  and  cold,  numbness,  tingling,  etc.)  may  be  observed 
variously  in  different  cases.  Sensory  phenomena  referable  to  the  special 
senses,  especially  the  eyes  and  ears,  are  common  and  significant.  The 
most  important  consists  of  concentric  contraction  of  the  field  of  vision, 
usually  bilateral,  but  often  more  marked  on  the  side  of  hemianesthesia 
(crossed  aml)lyopia);  perversion  of  color  perception  (dyschromatopsia), 
consisting  usually  of  the  recognition  first  of  red  or  green,  instead  of  the 


894  NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 

normal  sequence  of  blue,  yellow,  red,  green,  and  violet;  sometimes  all 
color  perception  is  lost,  everything  appearing  dull  or  grayish  (achroma- 
topsia). Hysterical  deafness  may  occur,  and  the  sense  of  smell  and  of 
taste  may  be  impaired  or  lost,  usually  only  or  more  markedly  on  the 
side  of  hemianesthesia ;  and  there  may  be  also  a  nervous  hysterical 
anorexia,  vomiting,  constipation,  etc. 

Vasomotor  and  trophic  phenomena  are  often  observed  in  varying  com- 
binations with  the  other  phenomena;  they  consist  of  erythematous  erup- 
tions, oedema,  urticaria,  dermographism,  cutaneous  gangrene  (neurotic 
or  hysterical  dermatitis),  etc.  Fever  (doubtless  of  artificial  production) 
may  be  observed;  and  disorders  of  metabolism  and  of  the  secretions  and 
excretions  may  occur. 

Diagnosis. — Hysteria  may  simulate  almost,  if  not  quite,  all  other  ner- 
vous diseases;  but,  as  a  rule,  it  can  be  more  or  less  readily  distinguished, 
because  the  clinical  picture  is  not  typical  of  the  simulated  disease,  and 
because,  in  addition,  hysteria  itself  manifests  certain  characteristic  phe- 
nomena. Hysterical  phenomena  are  characterized  by  their  frequent  sud- 
den onset,  variability  from  day  to  day,  and  frequent  sudden  cessation; 
by  the  character  of  the  motor  paralyses,  and  their  association  with  the 
anesthetic  and  other  so-called  stigmas  of  hysteria;  and  by  their  occur- 
rence in  a  person  of  hysterical  temperament.  The  differentiation  of  the 
attacks  of  major  hysteria  from  epilepsy  is  mentioned  on  page  890. 

Prognosis. — The  prognosis  is  good;  many  patients  recover  entirely 
spontaneously,  and  others  under  well-directed  management.  Many, 
however,  may  readily  be  made  worse  by  a  tactless  physician;  indeed, 
Babinski  and  other  observers  believe  that  almost,  if  not  quite,  the  whole 
complex  of  hysteria  (the  motor,  sensory,  and  other  phenomena)  results 
from  suggestion  to  a  susceptible  subject  by  a  maladroit  or  unskilful 
physician  or  other  person :  assuredly  an  extreme  and  not  proved  view. 

Treatment. — ^The  treatment  should  consist  in  improvement  in  the  gen- 
eral health,  the  eradication  of  any  functional  defects  aside  from  the  purely 
hysterical,  good  food,  fresh  air,  etc.  In  addition,  the  hysterical  tempera- 
ment and  the  abnormal  suggestibility  of  the  patient  must  be  borne  in 
mind — its  potentialities  for  good  as  well  as  evil.  The  successful  physician 
will  exercise  a  firm,  although  tactful,  control  over  the  life  and  activities 
of  the  patient— for  a  time  at  least,  regulating  and  commanding  the  daily 
life  and  diet  of  one;  preventing  introspection  in  another  by  enlisting  her 
interest  in  some  useful  and  absorbing  occupation,  charitable  work,  out- 
door exercise,  etc. ;  prescribing  a  modified,  complete  or  incomplete  Weir 
Mitchell  rest  cure  in  another,  or  a  work  cure  in  another,  or  a  course  of 
massage,  electricity,  or  hydrotherapy.  A  resourceful  psychotherapy 
finds  here  a  special  field  of  usefulness.  In  addition,  tonics,  such  as  iron 
and  arsenic,  and  nervines,  such  as  valerian  and  asafoetida,  are  useful 
from  time  to  time.  Hypnotism  is  rarely  if  ever  indicated,  and  assuredly 
never  in  inexpert  hands;  it  is  a  two-edged  sword,  and  often  cuts  in  the 
adverse  direction. 


NEURASTHENIA   AND  PSYCHASTHENIA  895 

NEURASTHENIA  AND  PSYCHASTHENIA. 

(Nervous  Debility  or  Disability;  Nervous  Exhaustion;  Nervous  Prostration.) 

Neurasthenia  is  a  disorder  of  the  nervous  system,  unassociated  with 
demonstrable  anatomical  lesions,  and  manifested  clinically  by  marked 
mental  and  bodily  fatigue,  which  upon  effort  develop  rapidly  and  dispro- 
portionately to  the  exciting  cause;  by  undue  irritability  and  response  to 
external  stimuli;  and  often  by  disturbances  of  the  emotional  and  psychic 
functions.  Psychasthenia  nowadays  is  sometimes  used  as  a  synonym 
for  neurasthenia,  and  it  is  sometimes  restricted  to  that  type  of  neuras- 
thenia in  which  the  symptoms  are  mental  rather  than  spinal. 

Etiology. — Neurasthenia  may  occur  in  men  and  in  women.  In  a  great 
majority  of  the  cases  there  is  a  predisposing  congenital  factor — a  ner- 
vous system  ill  adapted  to  the  stress  and  stain  (mental,  physical,  emo- 
tional) of  modern  life — well  borne  by  the  majority  of  mankind.  One  or 
both  parents  of  neurasthenic  or  psychasthenic  subjects  are  often  found  to 
have  been  neurasthenic,  epileptic,  hysterical,  excessively  emotional,  alco- 
holic, insane,  etc.,  and  they  transmit  an  unstable  nervous  system.  De- 
termining factors  of  the  nervous  breakdown  comprise  overwork  (physical 
and  mental),  worry,  misdirected  education,  shocks,  anxiety,  insomnia, 
excessive  alcoholism  and  venery ;  infections,  such  as  typhoid  fever,  syphilis, 
etc.;  auto-intoxications,  such  as  chronic  gastric  and  intestinal  derange- 
ments, gout,  diabetes,  nephritis,  etc.;  exogenous  intoxications,  such  as 
ptomaine  poisoning,  plumbism,  mercurial  poisoning,  etc.;  disease  of 
various  organs  of  the  body,  such  as  the  female  genitalia,  the  kidney 
(nephroptosis),  stomach  (gastroptosis),  eyes  (eyestrain),  etc.;  prolonged 
residence  in  the  tropics;  and  trauma.  Most  of  these  determining  factors 
do  not  cause  neurasthenia  in  the  absence  of  the  congenitally  weak  or 
unstable  nervous  system — the  primary  factor. 

Symptoms. — The  symptoms  differ  in  different  cases,  and  they  comprise 
a  variable  congeries  of  mental,  motor,  sensory,  vasomotor,  somatic,  and 
sexual  symptoms.  The  mental  symptoms  are  almost  always  present  and 
usually  dominate  the  clinical  picture  (psychasthenia);  they  consist  of 
general  "nervousness,"  inability  to  concentrate  the  attention  or  to  persist 
in  mental  effort,  which  of  itself  may  induce  headache,  vertigo,  and  mental 
confusion;  imperfect  reception  and  retention  of  perceptions,  and  conse- 
quent loss  memory;  loss  of  confidence  in  one's  ability,  delay  and  dis- 
inclination in  coming  to  conclusions,  and  impaired  judgment;  morbid 
fears  (agoraphobia,  cleithrophobia),  and  more  or  less  compulsory 
ideas  (which,  however,  verge  upon,  if  they  do  not  constitute,  insanity); 
irritability  of  temper  and  exaggerated  reaction  to  external  impressions 
— of  sensibility,  sight  (retinal  hyperesthesia),  hearing  (auditory 
hyperesthesia),  smell,  etc.;  and  emotional  disturbances.  The  eyes 
are  readily  tired  by  reading  or  other  "close  work"  (refractive  errors 
should  be  searched  for);  the  visual  fields  may  be  contracted,  or  may  be- 
come contracted  under  examination  (fatigue  contraction).     The  motor 


896  NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 

symptoms  consist  of  muscular  fatigue,  readily  induced  and  dispropor- 
tionate to  the  exertion;  tremors,  especially  of  the  hands,  and  twitchings 
or  habit  spasms,  especially  of  the  face;  and  usually  normal  or  exaggerated 
tendon  reflexes,  which  readily  become  exhausted.  The  sensory  symp- 
toms consist  of  a  feeling  of  malaise,  irregular,  fugitive  pains  (in  the  head, 
the  back,  the  legs,  along  the  vertebrae),  paresthesias  (numbness,  tingling, 
sensations  of  heat  and  cold),  areas  of  hyperesthesia,  especially  about  the 
head,  along  the  vertebrae,  etc.  Vasomotor  symptoms  consist  of  readily 
induced  pallor  or  flushing  of  the  face,  blueness  and  coldness  of  the 
extremities,  excessive  perspiration,  dermographism,  etc.  The  somatic 
symptoms  comprise  various  symptoms  referable  to  the  heart  (palpita- 
tion, vertigo,  distressing  pulsation  of  the  arteries,  etc.),  of  the  gastro- 
intestinal tract  (gastric  neurasthenia,  page  621),  of  the  kidneys  (lessening 
or  increase  in  the  amount  of  urine,  phosphaturia),  etc.  The  sexual  symp- 
toms (sexual  neurasthenia)  comprise  various  paresthetic  phenomena, 
nocturnal  emissions,  spermatorrhoea,  imperfect  erection,  premature  ejac- 
ulation, etc.,  in  the  male,  and  hyperesthetic  and  paresthetic  phenomena 
unassociated  with  organic  disease,  frigidity,  nocturnal  involuntary  or- 
ganisms, etc.,  in  the  female.  The  importance  of  these  is  often  unduly 
exaggerated. 

Diagnosis. — The  diagnosis  rests  upon  the  generally  inherited  neuro- 
pathic basis  and  the  activity  of  some  one  of  the  many  determining  causes. 
But  many  organic  diseases  of  the  nervous  system  and  of  other  organs 
may  begin  with  "neurasthenic"  symptoms,  so  that  careful  and  repeated 
physical  examination  and  prolonged  observation  may  be  required  to 
exclude  other  disorders. 

Traumatic  neurasthenia  (the  traumatic  neuroses  and  psychoses)  is  a 
disorder  of  the  nervous  system  that  follow  injuries  and  shocks,  and  is 
unassociated  with  gross  lesions  of  the  nervous  system  and  the  enclosing 
bony  framework;  it  is  often  spoken  of  as  "railway  brain"  and  "railway 
spine."  The  condition  is  more  common  after  accidents  in  which  the 
patient  may  not  be  notably  injured,  but  suffers  a  "mental  shock"  in  con- 
sequence of  the  suddenness  of  the  accident  or  disquieting  attending  cir- 
cumstances (railway  wrecks,  etc.),  than  it  is  after  accidents  in  which  the 
patient  may  be  more  or  less  severely  injured.  The  nature  of  the  disorder 
is  not  known:  it  has  been  attributed  to  cerebral  and  spinal  concussion;  to 
organic  lesions  of  the  brain  so  slight  as  to  elude  detectioa;  to  disturb- 
ances in  the  intimate  make-up  of  the  cerebral  cells;  to  psychic  as  distin- 
guished from  cerebral  disorder;  and  to  malingering  pure  and  simple. 
The  symptoms  in  general  do  not  differ  from  those  of  neurasthenia 
caused  by  other  factors;  only  from  the  history  of  an  injury  can  the  phy- 
sician distinguish  definitely  the  traumatic  from  the  non-traumatic  cases. 
The  traumatic  cases,  however,  as  a  rule,  are  rather  more  acute  in  onset, 
although  they  may  not  develop  for  days  or  weeks  after  the  injury;  mental 
symptoms  are  markedly  in  the  foreground;  hysterical  manifestations  are 
often  associated,  especially  paralyses  (monoplegic,  hemiplegic,  para- 
plegic)  and   anesthesias;  and   traumatic   lumbago   (due   doubtless   to 


OCCUPATION  NEUROSES  897 

twisting  or  torsion  of  the  vertebrae  or  stretching  or  laceration  of  the  lum- 
bar muscle  and  ligaments)  may  also  be  present.  The  condition  may  last 
a  long  time,  and  may  suddenly  clear  up  entirely  (sometimes  very  soon 
after  the  successful  issue  of  a  lawsuit);  but  mental  deterioration,  melan- 
cholia, etc.,  may  ensue. 

Prognosis. — The  prognosis  should  be  guarded,  since  neurasthenia  usu- 
ally occurs  in  a  person  with  a  more  or  less  subnormal  nervous  system;  the 
breakdown  may  be  entirely  recovered  from,  but  the  predisposition  to 
a  relapse  is  always  present;  so  that,  following  recovery,  the  patient's 
life  and  work  must  be  ordered  well  within  his  capabilities. 

Treatment. — ^As  in  the  treatment  of  hysteria,  so  also  in  neurasthenia, 
success  depends  largely  upon  the  physician,  the  confidence  that  he  in- 
spires in  the  patient  (psychotherapy),  and  the  attention  that  he  gives  to 
detail.  All  possibilities  of  organic  disease  should  be  excluded  by  examina- 
tion and  reexamination  of  the  patient  and  assuring  him  that  none  exists; 
if  found,  it  should,  of  course,  be  treated  appropriately.  All  the  func- 
tions of  the  body,  the  secretions  and  excretions,  the  diet,  the  daily  life, 
must  be  regulated  in  accordance  with  the  exigencies  of  each  patient; 
and  all  the  possible  factors  determining  the  breakdown  must  be 
carefully  sought  and  rigidly  excluded  from  activity.  Errors  of 
refraction  should  be  corrected;  a  modified,  partial,  or  complete  Weir 
Mitchell  rest  cure  is  of  much  benefit  in  selected  cases;  others  are  better 
adapted  to  a  work  cure,  a  change  of  scene  and  occupation,  a  prolonged 
sea  voyage,  etc.  Hydrotherapy  is  one  of  the  best  therapeutic  measures 
at  our  command.  Electricity  may  form  part  of  the  exaggerated  psycho- 
therapy, the  practice  of  which  is  now  fashionable  in  certain  C][uarters. 
The  bromides  for  a  short  time  are  often  serviceable,  or  one  may  use 
valerian,  asafoetida,  etc.  Tonics,  such  as  iron,  quinine,  nux  vomica, 
arsenic,  etc.,  are  useful  as  occasion  may  demand. 

OCCUPATION  NEUROSES. 

(Professional  Neurosis;  Occupation  or  Professional  Cramps.) 

The  occupation  neuroses  comprise  a  series  of  disorders  characterized 
by  cramps  of  muscles  or  groups  of  muscles  concerned  in  the  frequent  or 
prolonged  execution  of  certain  voluntary  coordinated  movements. 

Etiology. — The  occupation  neuroses  are  more  common  in  men  than  in 
women;  most  of  the  subjects  are  "neurotic,"  endowed  with  a  nervous 
system  ill  adapted  to  the  prolonged  strain  to  which  it  is  subjected.  The 
cramps  occur  most  commonly  in  writers  (writer's  cramp  or  palsy),  but 
also  in  telegraphers,  typewriters,  seamstresses,  pianists,  and  others;  the 
movements  ultimately  leading  to  the  cramp  may  be  fine  and  compli- 
cated (such  as  writing),  or  coarse  and  more  or  less  simple. 

Pathology. — The  nature  of  the  disorder  is  not  known;  it  has  been 

variously  ascribed  to  disorder  of  the  muscles,  the  peripheral  nerves,  and 

the  cerebral  cortex;  it  is  likely  that  much  of  the  disorder  emanates  from 

the  cells  of  the  cerebral  cortex,  which  perhaps  become  exhausted  from 

57 


898  NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 

the  necessarily  prolonged  effort  to  innervate  the  muscles;  but  whether 
this  is  the  whole  process  is  doubtful. 

Symptoms. — The  symptoms  consist  of  the  development  of  spasms  in 
groups  of  muscles  concerned  in  the  special  occupational  activity;  the 
spasms,  as  a  rule,  are  tonic;  occasionally  there  is  a  clonic  or  jerky  move- 
ment. The  spasms  develop  only  when  the  special  occupational  activity 
is  undertaken,  the  same  muscles  or  group  of  muscles  contracting  nor- 
mally when  acting  independently  or  in  other  associations  (in  executing 
other  movements).  In  writer's  cramp  there  is  a  progressive  disability; 
the  movements  of  writing  are  performed  with  increasing  effort  and  slow- 
ness; perhaps  there  is  some  associated  tingling  and  aching  in  the  muscles 
of  the  hand  and  the  forearm,  until  finally  writing  becomes  almost,  if  not 
quite,  impossible  from  tonic  spasm  of  the  muscles;  occasionally  there 
may  be  a  jerky  clonic  spasm  (separation  of  the  fingers,  for  instance),  or 
tremors,  or  paresis.  In  a  few  cases  some  muscular  atrophy,  especially 
of  the  thenar,  hypothenar,  and  interossei  muscles,  occurs  (peripheral 
nerve  disorder?).  Similar  phenomena,  involving,  however,  other  groups 
of  muscles,  occur  in  other  circumstances,  depending  upon  the  occupation 
of  the  subject. 

Diagnosis. — The  disorder  is  readily  recognized  from  the  occurrence  of 
the  spasms  only  upon  the  patient  attempting  certain  special  acts,  and 
from  the  ability  to  perform  other  acts  involving  the  same  muscles.  Neu- 
ritis may  be  excluded  by  the  absence  of  pain  and  tenderness  along  the 
course  of  the  nerves  and  of  muscular  atrophy.  In  the  event  of  tremor, 
other  disorders  attended  by  tremor,  especially  multiple  sclerosis,  paralysis 
agitans,  and  progressive  paresis  of  the  insane,  must  be  excluded. 

Prognosis. — Recovery  may  ensue  if  the  patient  discontinues  the  pro- 
voking occupation — at  least  for  some  time. 

Treatment. — The  first  essential  is  discontinuance  of  the  special  ac- 
tivities that  provoke  the  spasms.  The  muscles  involved  should  also  be 
protected  from  such  fatigue  as  may  follow  prolonged  muscular  movements 
of  other  sorts.  Locally,  hydrotherapy  and  massage  are  often  serviceable; 
perhaps  also  galvanism.  Attention  should  also  be  paid  to  improving  the 
general  health,  as  in  neurasthenia. 

PARALYSIS  AGITANS. 

(Shaking  Palsy;  Parkinson's  Disease.) 

Paralysis  agitans  is  a  disease  of  the  nervous  system,  unassociated  with 
definite  or  constant  anatomical  lesions,  and  characterized  clinically  by 
muscular  weakness,  rigidity,  and  tremor,  and  a  consequent  characteristic 
facial  expression,  attitude,  and  gait. 

Etiology. — Paralysis  agitans  usually  begins  after  middle  life  and  is  twice 
as  conimon  in  men  as  in  women.  The  onset  is  variously  attributed  to 
mental  shock,  worry,  trauma,  etc.,  but  their  real  significance  is  undeter- 
minate. 

Pathology. — There  are  no  definite  or  constant  anatomical  lesions. 
Changes  have  been  found  in  the  cortical  nerve  cells  of  the  cerebrum;  in  the 


PARALYSIS  AGITANS  899 

bloodvessels  of  the  spinal  cord  (changes  of  an  arteriosclerotic  nature,  and 
associated  atrophic  and  sclerotic  alterations  in  the  gray  and  white  matter 
of  the  cord);  and  in  the  muscles  (especially  in  the  muscle  spindles).  The 
disorder  has  been  looked  upon  as  a  manifestation  of  senescence  of  the 
nervous  system;  as  a  toxemia;  as  the  result  of  some  disturbance  of  the 
parathyroid  bodies,  etc. 

Symptoms. — The  onset  of  the  disease  is  insidious,  although  the  first 
symptoms  are  sometimes  referred  to  a  shock  or  injury.     The  chief  mani- 
festation consists  of  a  slowly  progressive  weakness  and  rigidity  of  the 
muscles,  usually  (but  not  always  at  first)  associated  with  tremors.     The 
tremors,  which  develop  in  at  least  two-thirds  of  the  cases,  are  commonly 
first  observed  in  the  hands.     In  the  beginning  they  may  be  slight  and 
escape  observation,  but  soon  the  forefinger  and  thumb  (of  one,  but  soon 
of   both  hands)  are  seen   to  be  the  seat  of  a  so-called  "pill-rolling"  or 
"cigarette-rolling"    movement;  gradually   ail    the    fingers  become    in- 
volved; and  ultimately  the  muscles  of  the  arm,  leg,  trunk,  and  face  may 
share  in  the  tremor.     The  tremors  are  fine  (four  to  seven  to  the  second); 
they  are  present  during  rest  and  quiescence;  they  are  diminished,  some- 
times abolished,  at  least  temporarily,  by  voluntary  movements;  they  usu- 
ally cease  during  sleep,  and  they  are  increased  by  excitement.     The 
really  characteristic  manifestation  of  the  disease  is  the  muscular  rigidity, 
which  develops  insidiously  and  becomes  universal.     It  gives  rise  to  the 
characteristic  fixed  and  expressionless  facial  features  (Parkinson's  mask); 
to  the  dull  and  monotonous  voice  (rigidity  of  the  muscles  of  the  lips, 
tongue,  and  larynx);  to  a  characteristic  attitude — arching  of  the  head 
and  body  forward  (stooping  posture),  and  flexion  of  the  arms  and  hands 
(general  overcoming  of  the  extensors  and  adductors  by  the  flexors  and 
abductors);  to  the  characteristic  gait — steps  at  first  slow  and  shuffling, 
but  soon  becoming  short  and  rather  rapid  (festination),  due  to  forward 
propulsion  of  the  body  and  advance  of,  and  the  patient's  effort  to  catch 
up  with,  his  centre  of  gravity;  in  consequence  of  this  the  patient  may 
ultimately  fall   forward;    if   suddenly  started  or  pushed   backward  or 
laterally,    a    corresponding    retropulsion    or   lateral    pulsion    may    be 
observed.      This  muscular  rigidity  also  results   in  delay  in   initiating 
voluntary  movements,  and  in  resistance  to  passive  movements;    mus- 
cular spasms  also  may  occur.    Muscular  power  is  usually  relatively  well 
maintained  for  a  considerable  time.     The  tendon  reflexes  may  be  normal 
or  exaggerated.     Subjective  sensations  of  heat,  sometimes  of  cold,  and 
dull  aching  in  the  legs  or  arms  may  be  complained  of,  but  objective  sen- 
sory changes  do  not  occur.     Vasomotor  disorders,  such  as  a  dry  skin, 
sweating  or  flushing,  and  increased  surface  temperature,  are  occasionally 
observed.     The  patient  is  often  apathetic,  but  when  interested  his  men- 
tal faculties  are  usually  found  normal;  he  perhaps  does  not  think  as 
slowly  as  he  must  express  himself. 

Diagnosis. — The  disease  is  usually  readily  recognized;  one  must  not 
overlook  the  cases  without  tremor.  Multiple  sclerosis  is  easily  differ- 
entiated by  the  cessation  of  the  tremor  on  voluntary  movement  (as 


900  NERVOUS  DISEASES   OF  FUNCTIONAL  NATURE 

contrasted  with  the  volitional  tremor),  and  by  the  other  characteristic  signs 
(page  859).  With  advancing  age,  but  usually  not  much  before  the  seven- 
tieth year,  a  fine  tremor  often  develops  (senile  tremor) ;  it  usually  involves 
the  hands,  and  sometimes  the  neck  and  head  (causing  a  slight  nodding 
movement)  and  the  legs;  but  it  is  not  associated  with  the  other  signs  of 
paralysis  agitans. 

Prognosis. — The  disease  is  incurable,  although  of  itself  it  does  not 
shorten  life  or  lead  directly  to  death. 

Treatment. — The  treatment  comprises  a  quiet  life,  freedom  from  worry 
and  distress,  and  the  best  hygienic  and  dietetic  regimen.  Hyoscine 
hydrobromate,  duboisine,  codeine  and  other  preparations  of  opium, 
belladonna,  cannabis  indica,  and  extract  of  the  parathyroid  bodies  have 
been  recommended  to  control  the  tremors.  Some  benefit  attends  massage, 
hydrotherapy  (hot  baths),  active  and  passive  movements,  and  the  use 
of  tonics,  such  as  arsenic,  quinine,  etc. 


ACUTE  CHOREA. 

(Sydenhain's  Chorea;  Chorea  Minor;  Infectious  or  Rheumatic  Chorea; 
St.  Vitus'  Dance.) 

Acute  chorea  is  a  disease  almost  certainly  infectious,  involving  chiefly 
the  nervous  system,  and  characterized  clinically  by  involuntary,  irregular, 
jerky  muscular  contractions  and  purposeless  movements,  and  frequently 
associated  with  endocarditis  and  various  psychic  disturbances. 

Etiology. — Acute  chorea  is  a  disease  of  childhood,  occurring  especially 
between  the  fifth  and  the  fifteenth  year,  and  twice  or  thrice  as  commonly 
in  girls  as  in  boys.  An  inherited  unstable  nervous  system  (epilepsy,  hys- 
teria, insanity,  and  other  neuropathic  taints  in  one  or  both  parents)  seems 
to  be  a  predisposing  factor.  The  exciting  cause  appears  to  be  an  infec- 
tious agent,  as  yet  undiscovered,  but  allied  to,  if  not  identical  with,  that  of 
rheumatic  fever;  a  history  of  rheumatism  may  be  elicited  in  from  25  to 
50  per  cent,  of  cases  of  chorea,  and  cardiac  murmurs  are  very  commonly 
found  clinically.  Perhaps  other  infectious  processes  may  be  active  etio- 
logically;  but  in  some  cases  a  history  or  evidence  of  infection  cannot  be 
obtained.  Fright,  shocks,  and  divers  forms  of  reflex  irritation  (worms, 
errors  of  refraction,  the  harass  of  too  strenuous  education,  etc.),  are  often 
put  down  as  exciting  causes,  but  their  influence  is  unquestionably  over- 
estimated. 

Pathology. — No  constant  or  characteristic  lesions  have  been  described. 
The  disease  is  rarely  fatal;  but  congestion,  swelling,  and  degeneration  of 
the  cerebral  cortical  cells  have  been  reported,  and  Diplococcus  rheu- 
maticus  (Poynton  and  Payne)  has  been  isolated  from  the  meninges.  The 
lesions  of  endocarditis  are  commonly  associated. 

Symptoms. — The  onset  of  the  disease  is,  as  a  rule,  gradual.  During 
what  may  be  called  a  prodromal  period,  of  a  week  or  more,  the  child 
may  be  listless,  inattentive,  generally  nervous,  restless,  and  unable  to 


ACUTE  CHOREA  901 

remain  quiet.  Soon,  or  in  some  cases,  following  a  fright  or  emotional  dis- 
turbance, the  child  is  observed  to  be  very  nervous  and  to  exliibit  involun- 
tary, irregular,  jerky,  and  purposeless  movements.  These  may  involve 
one  or  both  arms  (most  commonly  the  fingers),  or  the  legs,  the  face,  one- 
half  of  the  body,  or  the  whole  body;  they  vary  much  in  degree  from  those 
that  are  slight  and  may  almost  pass  unobserved,  to  those  that  preclude  the 
possibility  of  the  child's  remaining  still,  and  if  involving  the  facial  muscles, 
result  in  characteristic  grotesque  grimaces;  they  are  increased  by  ex- 
citement, and  may  be  augmented  in  the  hands  and  arm,  for  instance,  by 
getting  the  child  to  attempt  to  grasp  some  object  (associated  incoordi- 
nation); and  they  usually  disappear  during  sleep.  Involvement  of  the 
muscles  of  articulation  results  in  defective  speech,  and  sometimes  various 
explosive  (laryngeal)  sounds;  of  the  muscles  of  deglutition,  in  difficult 
swallowing;  of  the  diaphragm  and  other  muscles  of  respiration,  in  em- 
barrassed, irregular,  or  spasmodic  breathing;  and  the  cardiac  action 
may  become  irregular.  There  is  usually  at  least  some  muscular  weak- 
ness; at  times  this  may  become  marked  in  one  or  more  limbs  (paretic 
chorea).  The  tendon  jerks,  usually  difficult  to  determine,  are  normal  or 
slightly  exaggerated.  Cardiac  murmurs  and  other  evidences  of  acute 
endocarditis  (usually  mitral)  are  present  in  more  than  one-half  of  the 
cases,  and  often  persist  after  recovery  from  the  chorea;  perhaps  in  some 
cases  the  murmur  is  due  to  incoordinated  action  of  the  papillary  muscles 
rather  than  endocarditis.  Other  rheumatic  manifestations,  such  as  joint 
disorders,  erythema  nodosum,  subcutaneous  rheumatic  (sometimes 
called  fibrous)  nodules,  etc.,  may  be  present.  The  child,  as  a  rule, 
is  fretful  and  unruly;  sometimes  more  marked  psychic  symptoms,  such 
as  mental  dulness  or  depression,  hallucinations,  delirium,  mania,  etc., 
may  occur.  At  the  end  of  two  to  four  weeks  the  more  acute  symptoms 
usually  tend  to  subside,  but  the  attack  commonly  lasts  from  one  to  three 
months,  and  recurrences  are  not  uncommon. 

In  some  cases,  however,  the  symptoms  increase  in  intensity,  or  they 
may  be  very  severe  from  the  beginning — so-called  malignant  chorea 
(chorea  insa^iiens).  This  is  most  common  in  early  adult  life  and  during 
pregnancy  (toxic  or  infectious  cases).  The  spasms  are  severe,  general, 
and  almost  if  not  quite  constant;  they  interfere  with  sleep  and  induce 
exhaustion;  fever,  delirium,  and  mania  often  ensue,  and  death  usually 
results. 

Diagnosis. — ^The  diagnosis,  as  a  rule,  is  easy.  One  must  differentiate 
habit  chorea  (habit  spasm;  one  type  of  convulsive  tic),  a  disorder  of  chil- 
dren, especially  neurotic  girls,  which  may  or  may  not  develop  out  of  the 
frequent  repetition  of  volitional  acts  (mimicry),  and  which  consists  of 
rapid  coordinated  acts,  usually  of  a  purposeful  nature,  and  partly  or  com- 
pletely under  the  control  of  the  patient's  will.  The  movements  are  most 
commonly  facial,  such  as  winking,  wrinkling  the  forehead,  or  drawing  the 
mouth  to  one  side,  or  they  may  consist  of  rapid  shaking  of  the  head, 
shrugging  the  shoulders,  etc.  The  movements  difi'er  from  those  of  acute 
chorea  in  their  generally  purposeful  nature  and  in  being  confined  to  one 


902  NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 

muscle  or  group  of  muscles  (frequent  repetition  of  the  same  movement). 
One  must  also  exclude  the  athetoid  and  choreiform  movements  of  the 
cerebral  paralysis  of  children  (history  of  the  case,  permanent  paralyses, 
arrested  mental  development,  etc.);  hysteria  (more  regular  movements 
and  other  stigmas  of  hysteria);  and  paramyoclonus  multiplex  (shock- 
like, often  symmetrical  muscular  movements,  frequently  involving  the 
trunk). 

Prognosis. — The  outlook  is  good,  except  in  the  so-called  malignant 
cases.     Recurrences,  however,  are  common  even  in  the  mild  cases. 

Treatment. — The  child  must  be  removed  from  school,  all  disturbing 
and  exciting  influences  must  be  guarded  against,  and  all  possible  sources 
of  reflex  irritation  must  be  inquired  into,  and,  if  found,  corrected.  The 
best  results  follow  confinement  to  bed  for  some  time,  or  at  least  to  the 
quietude  of  a  sunny,  pleasant  room.  The  diet  should  be  nutritious  and 
not  stimulating;  coffee  and  tea  must  be  prohibited.  Hydrotherapeutic 
measures  (warm  baths,  cold  packs,  etc.,)  and  massage  are  often  of  the 
greatest  service.  Arsenic  (solution  of  potassium  arsenite)  is  of  distinct 
value  in  most  cases;  it  should  be  given  in  doses  of  2  to  3  minims  (0.12  to 
0.2  c.c.)  three  times  daily,  and  gradually  increased  to  6  to  10  minims 
(0.4  to  0.6  c.c);  larger  doses  should  be  avoided.  Salicyl  preparations, 
belladonna,  cimicifuga,  and  other  drugs  have  been  recommended. 
Quinine,  bitter  tonics,  cod-liver  oil,  are  often  useful  adjuvants.  The 
severe  cases  require  the  use  of  sedatives,  such  as  the  bromides,  chloral, 
chloretone,  hyoscine,  cannabis  indica,  valerian,  etc.  The  cardiac  com- 
plications are  to  be  treated  as  are  similar  conditions  developing  under 
other  circumstances. 


HEREDITARY  CHOREA. 

(Huntington's  Chorea;  Chronic  Progressive  Chorea.) 

Huntington's  chorea  is  a  chronic  hereditary  disease  of  the  nervous 
system  characterized  clinically  by  choreiform  and  ataxic  movements,  a 
staggering,  ataxic  gait,  disorders  of  speech,  and  progressive  mental  deterio- 
ration. The  disease  bears  no  relationship  whatever  to  acute  (Syden- 
ham's) chorea.  Its  nature  has  not  been  definitely  determined;  in  the 
few  cases  that  have  come  to  necropsy  chronic  meningo-encephalitis,  with 
atrophy  of  the  cerebral  cortex,  especially  of  the  frontal  and  parietal  con- 
volutions, has  been  found;  in  other  cases,  lesions  analogous  to  hemor- 
rhagic pachymeningitis.  Some  observers  postulate  a  congenital  defect 
or  maldevelopment  of  the  nervous  system.  The  disease  begins  usually 
in  adult  life,  after  the  thirty-fifth  year,  occurs  in  succeeding  generations, 
and  affects  several  members  of  the  family — the  males  more  frequently 
than  the  females.  The  movements  begin  in  the  hands  and  feet  and 
finally  involve  the  entire  body,  including  the  trunk;  they  resemble  those 
of  acute  chorea  in  being  jerky  and  purposeless,  but  they  are  usually 
slower    and   more   incoordinate   (ataxic),    and   they   are   likely  to   be 


CONVULSIVE  TICS  903 

bilaterally  symmetrical.  The  gait  becomes  ataxic  and  staggering,  some- 
times jerky;  speech  becomes  slow  and  is  sometimes  varied  by  explosive 
sounds  (involvement  of  the  muscles  of  articulation).  There  is  gradual 
mental  deterioration,  with  loss  of  memory,  delusions,  etc.,  and  final 
dementia.  The  disease  lasts  for  years  and  is  irremediable.  It  is  readily 
recognized  from  its  hereditary  transmission,  development  in  adult  life, 
choreiform  and   ataxic  movements,  and  progressive  dementia. 

CONVULSIVE  TICS. 

{Tic  Convulsif;  Impulsive  Tic;  Gilles  de  la  Tourette's  Disease.) 

The  convulsive  tics  comprise  a  group  of  disorders  characterized  by 
the  more  or  less  frequent  repetition  of  involuntary  spasmodic  muscular 
movements  of  a  generally  purposeful  nature.  These  tics  are  of  cortical 
origin,  and  represent,  therefore,  a  psychosis;  they  are,  in  many  respects, 
hysterical  in  nature,  and  may  be  associated  with  other  hysterical  phe- 
nomena; they  occur  in  neuropathic  subjects,  and  usually  develop  in 
childhood,  although  they  may  come  on  in  later  life.  Sometimes  they 
develop  out  of  habit  spasms  (page  901)  and  mimicry;  in  some  cases  they 
are  perhaps  of  reflex  nature,  having  developed  in  consequence  of  errors 
of  refraction  (blinking),  of  disease  of  the  nose,  mouth,  etc.  The  dis- 
order usually  consists  of  involuntary,  rapid,  often  lightning-like  move- 
ments of  the  muscles  of  the  face,  such  as  blinking,  wrinkling  the  fore- 
head, twitching  about  the  mouth,  etc.;  or  there  may  be  only  fibrillary 
twitchings  of  certain  muscles,  such  as  of  the  eyelids  (simple  tics).  In 
other  cases  the  movements  are  more  complicated,  such  as  shrugging  the 
shoulders,  or  convulsive  movements  of  more  or  less  of  the  body  (complex 
tics).  Sometimes  the  tics  involving  the  laryngeal  and  associated  muscles 
result  in  explosive  cries  or  utterances;  or  words  or  names  may  be  fre- 
quently repeated  (echolalia),  or  obscene  language  used  (coprolalia),  or 
actions  mimicked  (echokinesis) — indicating  the  cortical  nature  of  the 
disorder.  A  common  psychic  element  in  many  cases  is  shown  in  the 
recurrence  of  a  melody  or  harmony  (mental  equivalent  of  the  muscular 
tic),  in  an  almost  irresistible  impulse  to  touch  objects  (delire  de  toucher), 
to  repeat  words  (onomatomania),  to  count  before  acting  (arithmomania), 
in  morbid  fears  (agoraphobia,  cleithrophobia),  doubts  (folic  de  doute), 
etc.  The  disorder  is  usually  readily  recognized.  In  children  it  may  be 
distinguished  from  chorea  by  the  generally  purposeful  nature  of  the 
movements,  their  explosive,  lightning-like  character,  their  restriction  to 
a  group  of  muscles  (the  repetition  of  the  same  movement),  the  periods  of 
freedom,  and  the  associated  psychic  phenomena.  Tic  douloureux  (page 
808)  and  other  reflex  tics  are  of  an  altogether  different  nature.  The 
outlook  is  not  especially  good,  although  recovery  may  ensue,  especially 
in  children.  In  the  treatment,  special  attention  should  be  paid  to  all 
possible  sources  of  irritation  and  to  the  general  health.  Benefit  attends 
proper  educational  procedures  and  exercises,  and  attention  to  the  under- 
lying neurotic  condition. 


904  NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 


'    CHOREIFORM  DISORDERS. 

Acute  (Sydenham's)  chorea,  chronic  hereditary  (Huntington's)  chorea, 
the  habit  spasms,  the  convulsive  tics,  and  paramyoclonus  multiplex  are 
characterized  by  movements  that  more  or  less  resemble  one  another  and 
sometimes  lead  to  diagnostic  difficulties,  but  they  should  be  readily  dif- 
ferentiated, as  already  pointed  out.  In  addition,  there  are  the  following 
choreiform  affections-  (1)  Senile  chorea,  a  disorder  that  occasionally 
develops  in  late  middle  life  and  much  resembles  Huntington's  chorea, 
but  differs  in  the  absence  of  hereditary  characteristics.  (2)  Duhini's 
electrical  chorea,  a  rare  disorder,  characterized  by  rapid,  violent,  electric- 
like  movements  of  the  extremities,  and  sometimes  also  of  the  head  and 
face;  fever  (perhaps  infectious),  ultimate  atrophy  of  the  muscles,  and 
epileptiform  convulsions  are  usually  associated,  and  death  supervenes 
after  weeks  or  months.  (3)  Henoch's  hysterical  chorea,  a  rare  disorder  of 
adults,  characterized  by  sudden  rhythmic  electric-like  contractions  of 
the  muscles  of  the  shoulder  girdle,  of  the  neck,  of  the  abdomen  (Salaam 
convulsion),  or  of  the  psoas  muscles,  etc.  It  is  likely  hysterical  in  nature, 
and  may  be  associated  with  other  hysterical  stigmas.  (4)  Saltatory 
spasm  (latah,  myriachit,  jumpers),  a  disorder  characterized  by  the  occur- 
rence, when  the  subject  attempts  to  stand,  of  strong  contractions  of  the 
muscles  of  the  legs  and  a  consequent  jumping  or  springing  movement. 
It  is  most  common  in  neurotic  men,  and  may  occur  endemically:  in 
Maine  and  Canada  (jumpers),  in  Russia  (myriachit),  in  Java  and  its 
neighborhood  (latah). 


FAMILY  PERIODICAL  PARALYSIS. 

Family  periodical  paralysis  is  a  rare  disorder  that  occurs  in  families, 
is  transmitted  from  one  generation  to  another,  involves  both  sexes,  and 
is  characterized  by  paralysis  of  all  the  muscles  suppl:2d  by  the  spinal 
nerves.  The  nature  of  the  disease  is  not  understood;  it  is  believed  to  be 
toxic,  since  attacks  may  be  induced  by  fatigue,  constipation,  infections, 
etc.;  but  they  often  come  on  without  definite  cause.  Mitchell,  Edsall, 
and  others  have  found  a  lessened  creatinin  excretion  for  several  days 
before  the  attacks,  and  a  normal  excretion  after  the  attacks.  The  symp- 
toms develop  rather  insidiously,  and  consist  of  increasing  lassitude  and 
somnolence,  and  gradually  progressing  paralysis;  this  begins  in  the  legs, 
and  then  involves  the  trunk  and  arms,  and  is  usually  complete  at  the  end 
of  twenty-four  hours;  the  muscles  innervated  by  the  cranial  nerves  often 
escape  entirely,  but  they  may  exhibit  slight  paresis.  The  paralysis  is  of 
the  flaccid  type;  the  tendon  reflexes  are  lessened  or  lost;  the  superficial 
reflexes  are  diminished;  and  the  electrical  excitability  of  the  nerves  and 
muscles,  especially  to  the  faradic  current,  is  diminished  or  lost.  The 
heart  may  be  dilated  during  the  attack.     Sensation  and  consciousness  are 


HEAT  STROKE  905 

unimpaired.  At  the  end  of  twenty-four  hours  or  thereabouts,  the  par- 
alysis begins  to  disappear,  reversely  compared  to  its  development;  re- 
covery may  be  complete  at  the  end  of  forty-eight  hours.  The  attacks 
may  recur  at  irregular  intervals — days,  weeks,  etc.,  and  they  may  dis- 
appear permanently  in  advanced  adult  life.  The  prognosis  is  good, 
although  rarely  death  has  occurred  during  an  attack.  Potassium  citrate 
has  sometimes  shortened  or  aborted  an  attack;  otherwise  the  treatment 
is  symptomatic, 

HEAT  STROKE. 

{Sunstroke;  Thermic  Fever;  Siriasis;  Heat    Exhaustion   or   Prostration;  Insolation; 

Heat  Cramps.) 

In  consequence  of  exposure  to  excessive  heat,  one  of  three  conditions 
may  ensue — heat  stroke,  heat  exhaustion,  or  heat  cramps. 

Heat  stroke  (sunstroke,  siriasis,  thermic  fever)  is  a  condition  that  occurs 
after  exposure  to  the  sun's  rays,  and  develops  especially  in  persons  who 
at  the  same  time  are  engaged  in  hard  manual  work,  such  as  railway  and 
other  laborers,  soldiers  on  the  march,  etc.  There  are  no  constant  or 
characteristic  lesions;  congestion  of  the  brain,  parenchymatous  degen- 
eration of  the  solid  viscera,  undue  fluidity  of  the  blood,  etc.,  have  been 
found  in  fatal  cases.  The  disorder  is  attributable  to  (toxic?)  paralysis 
of  the  vasomotor  centre  in  the  medulla,  provoked  by  the  extreme  or  pro- 
longed heat;  some  observers  look  upon  it  as  an  infection.  The  onset 
of  the  disorder  is  sudden.  There  may  be  premonitory  headache,  vertigo, 
nausea,  vomiting,  malaise,  etc.,  but  often  the  subject  suddenly  drops  to 
the  ground,  becomes  unconscious,  goes  into  deep  coma,  and  soon  dies 
from  vasomotor  paralysis  and  heart  failure;  or  he  may  be  found  in 
deep  coma,  with  high  fever  (108°  to  111°  F.,  or  more),  hot  skin,  flushed 
face,  rapid  pulse,  labored,  stertorous,  or  Cheyne-Stokes  breathing,  and 
complete  muscular  relaxation;  occasionally  fibrillary  twitchings  of  the 
muscles  or  convulsions  occur.  Subcutaneous  petechia  may  be  found, 
the  pupils  are  usually  contracted  (although  at  first  they  may  be,  and 
sometimes  they  continue  to  be,  dilated).  Death  may  ensue  within  twenty- 
four  hours;  or  the  temperature  may  fall,  coma  disappear,  and  recovery 
ensue.  Often,  however,  the  patient  thereafter  is  unable  to  withstand  the 
effects  of  high  temperature;  and  occasionally  mental  deterioration,  with 
loss  of  memory,  etc.,  may  ensue. 

Heat  exhaustion,  or  ^prostration,  is  a  condition  that  follows  prolonged 
exposure  to  high  temperatures  (the  sun's  rays  as  well  as  indoor  tempera- 
ture), and  it  occurs  especially  in  those  doing  hard  manual  labor,  such 
as  workers  in  iron  foundries,  stokers  in  steamships  (among  whom  poor 
ventilation  is  doubtless  a  factor),  soldiers  on  the  march,  etc.  The 
condition  is  attributable  to  excessive  sweating  and  insufficient  water- 
drinking  and  consequent  augmented  specific  gravity  of  the  blood  and 
inspissation  of  the  tissues;  a  certain  number  of  the  cases,  especially 
some,  at  least,  of  those  occurring  in  the  tropics,  appear  to  be  due  in 


906  NERVOUS  DISEASES  OF  FUNCTIONAL  NATURE 

part  at  least  to  long-continued  exposure  to  excessive  light  (the  actinic 
rays  of  the  sun),  whence  they  may  be  termed  "light  exhaustion  or 
prostration."  The  symptoms  consist  of  initial  headache,  restlessness 
and  vertigo;  and  profuse  sweating,  subnormal  temperature  (96°  F.  or 
less),  muscular  cramps,  prostration,  and  collapse.  The  surface  of  the 
body  is  cool,  as  well  as  bathed  in  perspiration;  the  pulse  is  small  and 
rapid,  and  the  breathing  rapid  and  shallow;  consciousness,  aside  from 
its  obscuration  by  the  general  prostration,  may  be  maintained,  but 
delirium  may  supervene  (whence  the  not  uncommon  suicidal  tendencies 
and  sudden  jumping  into  the  water  of  stokers  of  ocean  steam- 
ships). 

Heat  cramps  is  a  condition  that  develops  in  those  who  at  the  same 
time  are  exposed  to  great  artificial  heat  and  do  much  muscular  work, 
especially  workers  in  iron  foundries,  stokers  on  steamships,  etc.  It  is 
described  by  Edsall  as  consisting  of  continuous  fibrillary  contractions 
of  the  muscles,  especially  those  of  the  calves,  and  paroxysms  of  severe  and 
painful,  tonic  spasms  of  the  muscles,  notably  of  the  forearms  and  legs, 
but  also  of  the  abdomen,  etc.  The  spasms  occur  spontaneously,  and 
are  provoked  by  efforts  of  voluntary  movement  and  by  mechanical, 
electrical,  and  other  stimuli;  and  they  last  from  one-half  to  one  minute. 
An  attack  lasts,  as  a  rule,  not  more  than  twenty-four  hours,  and  is  fol- 
lowed only  by  slight  exhaustion  and  muscular  soreness.  Edsall  attrib- 
utes the  condition  to  an  acute  degenerative  process  in  the  muscles. 

Diagnosis. — The  sudden  onset  of  coma  in  those  exposed  to  high  tem- 
perature, and  the  high  fever,  serve,  as  a  rule,  to  differentiate  heat  stroke 
from  apoplexy  and  coma  due  to  other  causes;  but  one  thus  exposed,  of 
course,  may  suffer  an  apoplexy  or  go  into  uremic  or  other  coma,  so  that 
these  must  be  excluded  in  all  doubtful  cases.  Heat  stroke,  heat  exhaus- 
tion, and  heat  cramps  each  is  so  distinctive  that  no  difficulty  should  be 
experienced  in  differentiating  them. 

Prognosis. — The  outlook  in  heat  stroke  is  good  if  the  patient  is  brought 
promptly  under  treatment;  but  in  some  cases  death  ensues  almost  imme- 
diately, or  within  twenty-four  hours.  The  prognosis  in  heat  exhaustion 
and  heat  cramps  is  good. 

Treatment. — In  heat  stroke  the  bodily  temperature  should  be  reduced 
as  promptly  as  possible — by  cold-water  or  ice-water  bathing,  not  forget- 
ting to  apply  cold  to  the  head;  cold- or  ice-water  enemas  also  may  be 
employed.  Venesection  is  valuable  in  markedly  asphyxiated  subjects, 
and  chloroform  in  the  event  of  continued  convulsions.  Stimulants,  such 
as  strychnine,  camphor,  ammonia,  whiskey,  etc.,  should  be  employed 
in  case  of  marked  prostration.  These,  as  well  as  external  heat,  are 
necessary  in  heat  exhaustion.  Enteroclysis  and  hypodermoclysis,  with 
physiological  saline  solution,  are  valuable  in  all  toxic  states,  including  the 
cases  of  heat  exhaustion  and  heat  cram.ps,  in  which  there  has  been 
much  sweating  and  comparatively  little  water  drinking.  Morphine  or 
apomorphine  may  be  resorted  to  if  necessary  to  control  the  painful 
myospasms. 


ERYTHROMELALGIA  907 

VASOMOTOR  AND  TROPHIC  DISORDERS. 


ANGIONEUROTIC   OEDEMA. 

{Quincke's  Disease.) 

Angioneurotic  oedema  is  a  disorder  characterized  by  the  occurrence 
of  localized  transient  oedematous  swellings  of  the  skin  and  mucous  mem- 
branes. It  may  be  hereditary,  and  is  believed  by  Quincke  to  be  a  vaso- 
motor neurosis  leading  to  increased  permeability  of  the  bloodvessels. 
Some  attacks  seem  to  be  precipitated  by  articles  poisonous  to  the  indi- 
vidual, such  as  shellfish,  certain  berries,  etc.;  by  ptomaines;  by  gouty, 
gastro-intestinal,  or  other  autotoxic  states,  etc.  The  face,  the  limbs,  the 
trunk,  may  be  the  seat  of  these  swellings,  which  cause  local  redness,  dis- 
comfort, pain,  and  itching;  in  the  mouth  and  pharynx  they  may  impede 
swallowing;  in  the  larynx  they  may  cause  dyspnoea,  stridor,  and  more 
or  less  asphyxiation ;  and  in  the  gastro-intestinal  tract  they  may  give  rise 
to  more  or  less  severe  colicky  pain,  nausea,  vomiting,  and  diarrhoea. 
They  may  be  associated  with  erythema,  urticaria,  purpura,  etc.  (page  389). 
The  attack  may  last  only  a  few  hours,  or  a  day  or  two,  and  it  may  recur 
at  regular  or  irregular  intervals.  The  treatment  is  not  very  satisfactory. 
The  intestinal  tract  should  be  thoroughly  cleared  by  means  of  blue  mass 
or  calomel  and  saline  cathartics;  inquiry  should  be  made  into  all  possible 
exciting  causes,  especially  articles  of  diet  (which  may  be  toxic  to  the 
individual  and  not  to  others);  and  nervines,  tonics,  such  as  strychnine, 
and  so-called  intestinal  antiseptics,  may  be  prescribed. 


ERYTHROMELALGIA. 

(Red  Neuralgia;  Weir  Mitchell's  Disease.) 

r  Erythromelalgia  is  a  disorder  characterized  by  pain,  tenderness,  con- 
gestion, and  increased  temperature  of  the  feet  and  sometimes  of  the 
hands,  which  develop  especially  when  the  parts  are  dependent.  The 
disorder  may  apparently  occur  as  an  independent  disorder — a  so-called 
vasomotor  neurosis;  but  similar  phenomena  may  be  associated  with 
arteriosclerosis,  multiple  neuritis,  etc.  The  symptoms  begin  with  pain 
(usually  burning  in  character)  and  tenderness  in  the  feet,  especially  the 
soles;  soon  capillary  distention  supervenes  and  the  feet  become  at  first 
dusky  red  (often  patchy,  rather  than  uniformly);  the  arteries  may  pul- 
sate visibly,  the  veins  become  dilated,  and  the  local  temperature  become 
increased;  but  after  some  time  the  foot  becomes  purplish  red,  or  of  a 
pallid  cyanotic  hue,  and  cold.  The  hands  are  occasionally  involved. 
The  phenomena  are  aggravated  by  the  dependent  position,  exercise,  and 
warmth;  they  may  be  induced  in  susceptible  subjects  by  long  standing. 


908  VASOMOTOR  AXD  TROPHIC  DISORDERS 

They  may  occur  parox}'smally  or  become  more  or  less  permanent.  A 
non-dependent  position  of  the  limbs,  cool  applications,  massage,  and 
electricity  are  of  more  or  less  avail,  but  the  disease  is  usually  quite  in- 
tractable. 

ACROPARESTHESIA. 

Acroparesthesia  is  a  painful  disorder  of  the  fingers  and  hands  that 
occurs  especially  in  women  who  do  considerable  washing  (long  immersion 
of  the  hands  in  hot  water),  and  sometimes  in  men  as  well  as  women  who 
use  the  hands  a  great  deal.  It  is  often  associated  with  general  ill  health 
and  impaired  nutrition.  It  is  perhaps  sometimes  of  vasomotor  origin, 
but  it  may  also  be  neurotic,  neuralgiform,  or  arteriosclerotic.  The  chief 
complaint  is  of  numbness  and  tingling  of  the  fingers  and  hand,  which  are 
likely  to  occur  after  prolonged  immersion  in  hot  water  (therefore,  toward 
night),  or  upon  exposure  to  the  heat  of  a  fire,  etc.  Occasionally  there  is 
slight  motor  weakness  and  difficulty  in  executing  fine  movements  (gen- 
eral involvement  of  the  nerve).  The  symptoms  vary  in  severity  and 
duration.  Usually  they  cease  with  cessation  of  the  provoking  cause,  and 
they  may  be  ameliorated  by  massage  and  electricity. 


RAYNAUD'S  DISEASE. 

(Local  Syncope;  Local  Asphyxia;  Symmetrical  Gangrene.) 

Raynaud's  disease  is  a  disorder  characterized  variously  by  symmet- 
rical S}Ticope,  asph>Tda,  or  gangrene.  In  the  early  stage  (local  sjmcope) 
the  fingers  or  toes,  or  both,  and  occasionally  the  ear  tips  or  the  nose, 
appear  pale  and  cold — the  so-called  "dead"  fingers  and  toes  of  the  laity. 
This  is  analogous  to  the  condition  (chilblains)  that  may  be  produced  by 
great  cold  (the  low  temperature  of  winter),  and  is  attributed  to  spasm 
and  incomplete  obstruction  of  the  peripheral  arterioles.  It  may  last  for 
several  hours  or  more  and  then  subside,  but  in  many  cases  a  reaction 
ensues  and  the  affected  part  becomes  red  or  purplish,  burning,  tingling, 
and  swollen  (local  asph^'xia);  sometimes  exquisitely  painful  and  more 
or  less  anesthetic.  This  is  attributed  to  complete  spasmodic  obstruction 
of  the  arterioles  and  stagnation  of  the  venous  circulation;  all  fingers  or 
toes  may  not  become  thus  affected  at  once;  one  may  remain  pale  and 
cold  and  its  neighbor  become  cvanotic.  In  some  cases  the  disorder  con- 
sists  of  recurring  attacks  of  such  pallor  and  succeeding  asphyxia  of  the 
fingers  and  toes;  and  the  attacks  may  be  set  up  by  exposure  to  cold 
(worse,  therefore,  in  winter),  by  emotional  disturbances,  by  gastro- 
intestinal disorders  (toxic?),  etc.  In  other  cases  the  lesions  progress  to 
local  gangrene  and  sphacelation  of  the  finger-  and  toe-tips;  rarely,  to  more 
extensive  loss  of  tissue,  or  multiple  foci  of  gangrene  in  other  parts  of  the 
body.  In  some  cases  there  has  been  a  curious  association  of  these 
phenomena   of   Raynaud's   disease   and   paroxysmal    hemoglobinemia 


RAYNAUD'S  DISEASE  909 

(vasomotor  disturbance  in  the  kidneys?);  these  have  occurred  together, 
and  in  other  cases  the  hemoglobinemia  apparently  has  replaced  the  attack 
of  the  more  familiar  phenomena.  The  cause  of  the  arterial  spasm  is  not 
definitely  known:  Raynaud  believed  it  to  be  of  central  origin;  others 
attribute  it  to  reflex  or  toxic  causes;  and  others  look  upon  it  as  syphilitic 
or  as  a  phenomenon  of  arteriosclerosis  and  thrombo-angiitis.  The  diag- 
nosis is  readily  made,  and  should  exclude  the  cases  due  to  manifest 
cardiac  and  arterial  disease,  ergotism,  etc.  The  treatment  should  consist 
of  a  horizontal  position  of  the  limbs,  wrapping  the  affected  fingers 
and  toes  in  cotton  wool,  and  warm  local  applications.  Nitroglycerin 
and  other  vasodilators,  massage,  and  galvanism  (the  positive  pole  to 
the  affected  limb  immersed  in  saline  solution)  are  often  of  service.  The 
pain  may  require  the  use  of  morphine  or  other  narcotics  and  sedatives. 


SECTION   XL 
DISEASES  OF  THE  MUSCLES. 


MUSCULAR  RHEUMATISM. 

(Myalgia.) 

Muscular  rheumatism,  or  myalgia,  is  a  disorder  of  the  voluntary 
muscles  and  the  related  fasciae,  characterized  by  pain  which  is  markedly 
aggravated  by  motion. 

Etiology. — Muscular  rheumatism  is  more  common  in  men  than  in 
women;  it  occurs  especially  in  those  exposed  to  wet  and  damp,  or  di- 
rectly to  a  draught  of  cold  air  (open  window^,  etc.)  and  sudden  cooling, 
particularly  after  exercise  sufficient  to  induce  sweating.  In  many  re- 
spects it  is  analogous  etiologically  to,  and  may  be  the  muscular  equivalent 
of,  rheumatic  fever;  at  all  events,  it  occurs  in  "rheumatic"  and  "gouty" 
subjects. 

Pathology. — The  nature  of  the  disease  is  not  definitely  known.  It  is 
probably  an  inflammation  of  the  fibrous  investment  of  the  muscular 
fibers  and  of  the  related  fasciae  and  periosteal  attachments  of  the  muscles; 
but  some  observers  look  upon  it  as  a  disorder  of  the  sensory  nerve  endings 
in  the  muscles. 

Symptoms. — The  symptoms  may  come  on  suddenly  or  insidiously,  and 
continue  either  a  short  or  a  long  time  (several  hours  to  several  weeks). 
The  chief  and  often  the  only  complaint  is  pain  in  and  about  a  muscle 
or  muscles;  there  is  sometimes  a  little  fever,  but  rarely  any  other  general 
disturbance.  The  pain  may  be  dull  and  aching,  or  sharp  and  cramp- 
like; it  is  markedly  aggravated  by  any  movement  that  involves  the 
affected  muscles,  and  it  often,  therefore,  effectually  prevents  motion  and 
leads  to  more  or  less  contracture  and  malposition.  Common  types  of 
the  disorder  are:  (1)  Lumbago,  involvement  of  the  lumbar  muscles, 
which  is  usually  very  painful  and  often  completely  incapacitates  the 
patient.  One  should  exclude  disease  of  the  vertebrffi,  sacro-iliac  joint, 
etc.  (2)  Pleurodynia,  involvement  of  the  intercostal  muscles,  and  some- 
times the  pectorals  or  the  serratus  magnus.  It  is  usually  very  painful, 
on  account  of  the  necessary  respiratory  movements  of  the  chest.  There 
may  be  circumscribed  tenderness  over  the  involved  and  contracted 
muscles.     Pleuritis  can  be  excluded  by  the  absence  of  friction  sounds; 


912  DISEASES  OF  THE  MUSCLES 

and  intercostal  neuraliga,  by  the  absence  of  pain  following  the  course  of 
the  nerves,  of  acute  unprovoked  exacerbations  of  pain,  and  of  the  painful 
or  tender  spots  (page  809).  (3)  Torticollis  (wry-neck),  involvement  of  the 
sternomastoid  muscle  and  sometimes  of  other  regional  muscles  (back  of 
the  neck  especially).  The  sternomastoid  muscle  stands  out  as  a  tense, 
painful,  and  tender  cord,  and  causes  rotation  of  the  head  and  chin  toward 
the  unaffected  side. 

Treatment. — In  many  cases  prompt  relief  follows  the  use  of  remedies 
advised  for  rheumatic  fever  (page  256).  In  addition,  rest  to  the  disabled 
muscle  or  muscles  is  of  the  greatest  importance.  Pleurodynia  is  usually 
markedly  benefited  by  strapping  the  side,  or  by  a  light  application  of  the 
Paquelin  cautery — which  is  also  of  the  greatest  service  in  lumbago.  Hot 
applications,  chloroform  and  other  liniments,  belladonna  plasters, 
massage,  galvanism,  etc.,  afford  relief  in  other  cases.  A  hot  or  Turkish 
bath  may  cause  almost  immediate  cessation  of  •  the  pain.  In  obstinate 
chronic  cases  the  iodides,  mercury,  belladonna,  and  iodine  ointment, 
and  attention  to  the  dietary  (antigout  diet)  are  usually  efficacious. 


MYOSITIS. 

Inflammation  of  the  muscles  is  a  rare  disorder;  but  it  may  occur  as  a 
secondary,  and  apparently  also  as  a  primary,  process.  Secondary  myo- 
sitis may  be:  (1)  Suppurative,  in  which  case  it  is  usually  part  of  a  gen- 
eral pyococcic  process  (page  61)),  with  multiple  muscular  foci,  although 
rarely  perhaps  there  may  be  only  a  single  muscular  focus.  The  involved 
muscle  is  at  first  swollen  and  painful,  and  gradually  goes  on  to  abscess 
formation;  the  abscess,  if  not  evacuated,  may  lead  to  or  increase  the 
general  pyococcic  process.  (2)  Syphilitic.  Early  in  the  infection  there 
may  be  a  cellular  myositis;  late  gummatous  formation  may  occur.  The 
gumma  being  absorbed  gives  rise  to  more  or  less  loss  of  muscular  sub- 
stance and  consecutive  fibrosis.  Primary  myositis  is  very  rare;  occa- 
sionally it  is  observed  as  part  of  a  dermatomyositis,  a  condition  in  which 
dermatitis  and  multiple  involvement  of  the  muscles  and  oedema  occur. 
The  muscles  become  tense,  firm,  and  oedematous,  and  later  degenerated 
and  atrophic.  In  some  cases  hemorrhage  may  occur  into  the  involved 
muscles  (hemorrhagic  polymyositis).  The  condition  resembles  trichi- 
nosis, but  may  be  differentiated  by  the  absence  of  eosinophilia  and  of  the 
parasite  in  a  piece  of  excised  muscle. 


PROGRESSIVE  MUSCULAR  DYSTROPHY. 

(The  Aluscular  Dystrophies;  Primary  Myopathy;  Pseudohypertrophic  Muscular 

Paralysis.) 

Progressive  muscular  dystrophy  is  a  primary  disorder  of  the  muscles 
characterized  clinically  by  progressive  muscular  wasting. 


PROGRESSIVE  MUSCULAR  DYSTROPHY  913 

Etiology. — Progressive  muscular  dystrophy  is  more  common  in  males 
than  in  females.  In  most  cases  the  disease  is  hereditary,  being  trans- 
mitted, as  a  rule,  by  the  females  to  the  males;  in  other  cases  it  is  familial, 
several  members  of  the  same  generation  being  affected;  some  cases,  how- 
ever, exhibit  neither  hereditary  nor  familial  characteristics.  Infections, 
injuries,  shocks,  etc.,  have  been  variously  looked  upon  as  exciting  causes, 
but  at  most  these  are  of  only  secondary  significance,  the  predisposition, 
the  primary  myopathy,  being  present. 

Pathology. — The  chief  lesions  consist  of  atrophy  (which  may  be  pre- 
ceded by  hypertrophy)  of  the  muscular  fibers,  replacement  fibrosis,  and 
the  deposition  in  the  connective  tissue  of  fat.  The  process  may  progress 
to  complete  atrophy  of  the  muscular  fibers,  although  the  muscle 
spindles  are  likely  to  remain  intact,  and  the  deposition  of  fat  may  be  so 
marked  as  to  cause  notable  enlargement  of  the  part  (pseudohypertrophy; 
hypertrophic  lipomatosis;  pseudohypertrophic  muscular  paralysis).  The 
nervous  system  usually  exhibits  no  lesions;  rarely,  degenerated  changes 
have  been  seen  in  the  cells  of  the  anterior  cornua  of  the  spinal  cord,  and 
functional  or  other  changes  beyond  our  present  means  of  detection  have 
been  postulated.  The  disorder  appears  to  be  unquestionably  a  primary 
myopathy — a  muscular  abiotrophy;  the  individual  is  born  with  a  muscular 
system  ill  adapted  to  the  exigencies  of  life,  so  that  sooner  or  later  it 
begins  to  succumb  and  atrophy. 

Erb  has  classified  the  cases  into  (1)  those  that  begin  in  infancy  and 
childhood,  and  (2)  those  that  develop  in  adolescence  or  early  adult  life 
(between  which  there  is  no  essential  difference);  and  he  has  also  classi- 
fied them  into  (1)  those  in  which  there  is  a  true  hypertrophy  of  the  mus- 
cular tissue,  or  a  pseudohypertrophy  (hypertrophic  lipomatosis)  of  the 
part,  and  (2)  those  in  which  there  is  progressive  atrophy  of  the  muscle 
without  the  accumulation  of  fat ;  but  between  these  cases  there  is  also  no 
essential  difference,  although  the  distinction  is  convenient  clinically. 

Symptoms. — The  disease  usually  begins  before  puberty,  but  may  be 
delayed  until  adolescence  or  early  adult  life  (before  the  twenty-fifth  year). 
The  onset  is  insidious,  the  first  symptoms  being  muscular  weakness  and 
disability,  with  or  without  increase  in  the  volume  of  the  muscles  of  the 
part.  Depending  upon  the  muscles  involved,  several  clinical  types  of 
the  disease  are  distinguished,  although  there  is  no  sharp  line  of  demarca- 
tion between  them:  (1)  The  pseudohypertrophic  form  of  Duchenne. 
This  usually  develops  before  the  tenth  year  and  in  males.  It  involves 
especially  the  muscles  of  the  calves — which  become  much  enlarged.  The 
child  in  w^alking  readily  grows  tired,  stumbles,  or  drags  the  legs  (in 
marked  contrast  to  the  healthy  looking  calves);  and,  to  aid  progression, 
soon  begins  to  bring  the  pelvis  into  play,  and  develops  a  waddling  gait. 
The  muscles  of  the  thigh,  buttocks,  and  back  soon  become  involved ;  the 
child  experiences  increasing  difficulty  in  arising  from  a  lying  to  a  standing 
posture,  and  characteristically  aids  himself  by  "climbing  up  on  his  legs 
with  his  hands."  When  erect,  he  stands  with  his  legs  apart,  his  shoulders 
thrown  back  (in  an  effort  to  compensate  the  forward  curvature  of  the 
58 


914  DISEASES  OF  THE  MUSCLES 

spine,  due  to  atrophy  of  the  lumbar  muscles),  and  the  abdomen  protruded. 
The  common  enlargement  of  the  muscles  of  the  calves  and  of  the  anterior 
aspect  of  the  thighs  and  the  atrophy  of  the  glutei  muscles  accentuate 
this  attitude.  Later,  the  muscles  of  the  shoulder  girdle  may  become  in- 
volved. Muscles  originally  hypertrophied  become  atrophic,  and  con- 
tractures may  ensue.  Cases  unassociated  with  the  pseudohypertrophy 
are  sometimes  spoken  of  as  the  Leyden-Mobius  form.  (2)  The  scapulo- 
humeral form  of  Erb  (Erb's  juvenile  form).  This  begins,  as  a  rule,  be- 
tween the  ages  of  twelve  and  sixteen  years,  and  involves  first  the  muscles 
of  the  shoulder  girdle,  and  then  those  of  the  upper  arm  and  the  anterior 
chest,  and  finally  those  of  the  back.  In  advanced  cases  the  muscles  of 
the  thigh  and  calf  become  involved,  so  that  the  condition  much  resembles 
the  pseudohypertrophic  form  of  the  disease.  (3)  The  facioscapulo- 
humeral type  of  Landouzy  and  Dejerine.  This  begins  in  early  childhood, 
in  the  third  or  fourth  year,  as  a  rule,  and  is  especially  characterized  by 
atrophy  of  the  muscles  of  the  face,  as  well  as  of  the  muscles  of  the  shoulder 
girdle  and  the  upper  arm  (Erb's  infantile  form) ;  the  pseudohypertrophic 
type  of  Duchenne  also  may  be  associated.  The  lips  protrude  and  can- 
not be  closed,  and  their  finer  movements  (articulation,  puckering,  re- 
taining fluid  and  food)  are  interfered  with,  although  mastication  and 
deglutition  may  be  unimpaired.  The  ocular  and  palpebral  muscles 
often  escape. 

Diagnosis. — The  different  forms  of  muscular  dystrophy  are  readily  dis- 
tinguished by  their  hereditary  or  familial  occurrence,  their  usual  onset  in 
early  life,  involvement  of  the  muscles  near  to  the  trunk  (rather  than  the 
small  muscles  of  the  hands  and  feet,  as  in  progressive  muscular  atrophy), 
and  the  occurrence  of  pseudohypertrophy  of  certain  muscles,  especially 
the  calves;  by  gradual  reduction  in  the  deep  reflexes  and  electrical  excita- 
bility of  the  muscles — depending  upon  the  gradual  muscular  atrophy 
(the  muscular  fibers  remaining  continuing  to  respond);  and  by  the 
absence  of  the  reactions  of  degeneration,  of  fibrillary  twitchings,  and  of 
sensory  changes.  These  serve  to  exclude  chronic  poliomyelitis,  progres- 
sive muscular  atrophy,  and  multiple  neuritis. 

Prognosis. — Muscular  dystrophy  is  slowly  progressive,  but  it  may  last 
twenty  or  thirty  years,  and  does  not  lead  directly  to  death. 

Treatment. — It  is  at  least  doubtful  whether  any  treatment  is  really 
efficacious.  Regulated  exercises,  passive  movements,  massage,  elec- 
tricity, hydrotherapeutic  measures,  and  tonics  are  serviceable  in  some 
cases. 

MYOCLONUS. 

(Paramyoclonus  Multiplex,  Friedreich.) 

Myoclonus  is  a  disorder  characterized  by  clonic,  constant  or  paroxys- 
mal, contractions  of  the  muscles,  chiefly  of  the  legs.  The  disease  is 
sometimes  hereditary;  it  may  affect  several  members  of  the  same  family; 
it  occurs  especially  in  males,  and  it  may  be  found  in  epileptic  subjects. 


CONGENITAL  MYOTONIA  915 

Its  cause  is  not  known;  it  is  said  to  follow  fright,  shock,  and  general  ill 
health.  Its  nature  has  not  been  determined;  some  observers  believe  it 
to  be  allied  to  the  convulsive  tics,  electric  chorea,  etc.  The  characteristic 
symptoms  consist  of  sudden  electric-like,  clonic  contractions  of  the 
muscles,  especially  of  the  legs,  sometimes  of  the  trunk,  and  rarely  of  the 
face.  The  spasms,  as  a  rule,  are  bilateral  and  rhythmic;  they  vary  from 
50  to  150  per  minute,  and  may  be  so  violent  as  to  cause  motion  of  the 
entire  limb,  or  even  tossing  about  of  the  patient.  They  are  often  lessened 
by  voluntary  movement,  and  they  usually  cease  during  sleep.  In  the 
paroxysmal  cases  tremors  of  the  muscles  may  occur  during  the  intervals. 
The  reflexes  are  usually  exaggerated,  the  nutrition  of  the  muscles  is  well 
maintained,  and  there  are  no  reactions  of  degenerations,  sensory  changes, 
or  psychic  disturbances.  The  disorder  may  be  distinguished  from 
acute  chorea  by  the  sudden  electric-like  quickness  of  the  movements  and 
their  occurrence  especially  in  the  legs,  and  from  the  convulsive  tics,  the 
movements  of  which  are  purposeful  and  usually  unilateral.  The  dis- 
order lasts  a  variable  time,  and  may  cease  spontaneously.  The  treatment 
consists  of  the  use  of  sedatives,  such  as  the  bromides,  valerian,  hyoscine, 
etc. 

CONGENITAL  MYOTONIA. 

{Thovisen's  Disease.) 

Congenital  myotonia  is  a  disease  characterized  by  rigidity  or  tonic  con- 
tractions of  the  muscles  upon  attempting  voluntary  movements  after  a 
period  of  rest.  It  is  usually  hereditary;  it  may  affect  several  members 
of  the  same  generation;  it  is  almost  ten  times  as  common  in  males  as  in 
females,  and  it  usually  develops  during  childhood.  The  nature  of  the 
disorder  is  not  known;  it  has  been  attributed  to  changes  in  the  muscle 
fibers,  to  an  auto-intoxication  involving  especially  the  muscles,  etc.  The 
nervous  system  shows  no  lesions.  The  symptorns  consist  of  the  occur- 
rence of  tonic  spasms  of  the  muscles  upon  attempting  voluntary  move- 
ments—such as  arising  from  a  chair,  walking,  grasping  an  object,  closing 
the  eyelids,  etc.;  that  is,  the  patient  experiences  difficulty  and  delay  in 
initiating  the  movement,  but,  once  begun,  persistence  in  the  movement 
results  in  relaxation  of  the  contracted  muscle;  but  a  period  of  rest  is  fol- 
lowed by  recurrence  of  the  phenomena.  This  incapacitates  the  child 
more  or  less  and  prevents  his  engaging  in  children's  plays  and  games. 
The  muscles  are  usually  well  developed  and  may  even  appear  hyper- 
trophied,  but  some  muscular  weakness  is  common,  although  there  is 
no  atrophy.  The  mechanical  excitability  of  the  muscles  is  increased — a 
blow,  for  instance,  causing  a  quick  and  lasting  contraction  (ten  to 
twenty  seconds).  The  electrical  excitability  also  is  increased  and  occasions 
the  so-called  myotonic  reaction:  undue  excitability  to  mild  faradic  and 
galvanic  currents;  rather  slow  maximum  response  to  the  current  and  slow 
relaxation;  under  the  influence  of  the  galvanic  current  the  anode-closing 
contraction  (ACC)  becomes  equal  to  or  greater  than  the  cathode-closing 


916  DISEASES  OF  THE  MUSCLES 

contraction  (CCC);  and  if  a  continuous  galvanic  current  is  passed  through 
the  muscle,  rhythmic,  vermicular  contractions  pass  from  the  cathode  to 
the  anode.     No  efficacious  treatment  is  known. 


CONGENITAL  AMYOTONIA. 

(Congenital  Myatonia;  General  or  Localized  Hypotonia  of  the  Muscles  of  Children; 
Congential  Hypotonic  or  Atonic  Pseudoparalysis;  Oppenheitn's  Disease.) 

Congenital  amyotonia  is  a  disease  characterized  by  diminished  tone 
(hypotonia)  of  the  voluntary  muscles.  The  disorder  is  undoubtedly 
congenital,  and  becomes  manifest  during  childhood;  infections  are 
sometimes  said  to  act  as  exciting  causes.  The  nature  of  the  condition  is 
not  known;  changes  in  the  muscles  analogous  to  those  of  the  muscular 
dystrophies  have  been  found.  The  symptoms  consist  of  flaccidity  and 
loss  of  tone  and  power  of  the  voluntary  muscles,  but  there  is  no  absolute 
paralysis  and  no  wasting  of  the  muscles.  The  condition  is  usually  most 
marked  in  the  limbs,  and  is  often  associated  with  relaxation  of  the  joints, 
so  that  the  limbs  may  be  readily  placed  in  grotesque  positions  and  luxa- 
tions may  ensue;  but  the  muscles  of  the  trunk  and  of  the  face  may  be 
involved.  The  deep  reflexes  are  lessened  or  lost ;  the  electrical  excitability 
is  diminished,  and  currents  much  stronger  than  in  health  can  be  borne 
with  equanimity.  The  disorder  may  be  distinguished  from  the  muscular 
dystrophies  by  its  being  congenital  (but  not  hereditary)  and  non-familial, 
and  by  the  marked  hypotonia  and  absence  of  wasting  of  the  muscles.  It 
should  be  readily  differentiated  from  acute  poliomyelitis,  rickets,  etc.  The 
prognosis  is  good,  since  the  condition  tends  to  lessen  and  finally  to  disap- 
pear as  the  child  grows  older,  but  contractures  may  occasionally  occur. 
The  treatment  consists  of  hygienic  and  dietetic  regulations  designed  to 
improve  the  general  health  and  nutrition  of  the  child,  and  of  massage, 
electricity,  and  hydropathic  measures  to  increase  the  tone  of  the  muscles. 


SECTION  XII. 
DISEASES  OF  THE  BONES  AND  JOINTS. 


ACUTE  ARTHRITIS. 

Etiology. — Acute  arthritis,  aside  from,  and  often  including,  the  cases 
that  follow  local  injury,  is  always  due  to  bacterial  infection  or  intoxica- 
tion. It  may  occur  as  a  primary  disorder,  of  which  the  joint  manifesta- 
tions are  the  conspicuous  feature— rheumatic  fever  (page  253);  or  it  may 
occur  in  the  course  of  or  following  any  of  the  well-known  pyococcic, 
pneumococcic,  gonococcic  (page  91),  influenzal,  and  other  infections. 
Special  importance  attaches  to  unsuspected,  masked,  and  more  or  less 
obsolete  infections,  such  as  tonsillitis,  pyorrhoea  alveolaris,  chronic  gono- 
coccic infection  with  involvement  of  the  seminal  vesicles  and  the  pros- 
tate, other  infections  of  the  urinary  tract,  of  the  gastro-intestinal  tract,  etc. 

Pathology. — One  or  several  joints  may  be  involved.  In  the  mild  cases 
the  lesions  consist  of  congestion,  swelling,  and  oedema  of  synovial  tissues, 
and  the  outpouring  into  the  cavity  of  the  joint  of  a  more  or  less  turbid 
albuminous  fluid  containing  a  few  flakes  of  fibrin  and  leukocytes.  In 
more  severe  cases  the  synovial  and  fibrous  capsules  of  the  joints  are 
swollen,  oedematous,  and  adherent,  and  the  cavity  of  the  joint  is  filled 
up,  perhaps  obliterated,  by  more  or  less  thick,  fibrinous,  fibrinopurulent, 
or  distinctly  purulent  exudate;  the  articulating  cartilaginous  surfaces 
may  reveal  erosions  with  thickened  infiltrated  borders.  In  less  severe 
and  more  chronic  cases  there  may  be  more  or  less  villous  pi'oliferation 
of  the  synovial  tissue.  The  infecting  microorganisms  may  sometimes  be 
isolated  from  the  articular  fluid  or  tissues,  but  often  having  initiated  the 
lesions  they  die  out;  or  the  lesions  may  be  set  up  by  bacterial  toxins  alone. 

Symptoms. — The  onset  of  the  disorder  may  be  abrupt  or  more  or  less 
insidious,  depending  upon  the  severity  of  the  infection.  The  chief 
symptoms  consist  of  pain,  tenderness,  swelling,  increased  temperature, 
and  disability  of  the  joint  or  joints.  On  palpation  the  joint  is  soft  and 
boggy — in  consequence  of  more  or  less  intra-articular  fluid,  swelling  of 
the  synovial  tissues,  and  periarticular  oedema.  In  addition,  there  are  the 
general  evidences  of  infection — due  in  part  to  the  primary  disorder,  but 
perhaps  aggravated  by  the  local  joint  condition — fever,  rapid  pulse,  and 
leukocytosis;  in  the  event  of  suppuration,  also  chills  or  chilliness  and 
sweats. 


918  DISEASES  OF  THE  BONES  AND  JOINTS 

Diagnosis. — The  diagnosis  is  quite  apparent  from  the  local  conditions. 
Efforts  should  be  made  to  determine  the  nature  of  the  infection — by 
searching  for  sources  of  infection  and  cultivating  therefrom  the  infecting 
microorganism,  or,  when  the  conditions  appear  to  warrant  it,  aspirating 
the  joint  and  studying  the  fluid  bacteriologically  and  cytologically. 

Prognosis. — The  prognosis  depends  upon  the  severity  of  the  in- 
fection and  the  nature  of  the  ensuing  lesions.  There  is  always  a  ten- 
dency for  the  condition  to  become  polyarthritic,  even  in  originally  mon- 
arthritic  cases,  and  in  all  but  the  mildest  cases  more  or  less  permanent 
disability  is  likely  to  ensue. 

Treatment. — Ml  possible  local  sources  of  infection  anywhere  in  the 
body  must  be  eradicated,  since  the  joint  symptoms  may  be  kept  active 
by  bacterial  toxemia  without  local  joint  infection.  The  best  treatment 
comprises  rest  and  fixation  of  the  joint  and  the  local  remedies  mentioned 
on  page  257.  The  rest  should  not  be  too  long  continued,  passive  move- 
ments being  substituted  as  soon  as  possible.  Good  results  also  may 
attend  the  use  of  specific  bacterins.  In  cases  of  severe  and  progressive 
infections,  resort  should  be  had  to  surgical  procedures — opening  and 
irrigating  and  draining  the  joint. 


CHRONIC  ATROPHIC  ARTHRITIS. 

{Arthritis  Deformans;   Rheumatoid  Arthritis;   Chronic  Polyarthritis  of  the  Atrophic 

Type  of  Goldthwait.) 

Etiology. — The  form  of  chronic  polyarthritis  known  as  deforming  or 
rheumatoid  arthritis  (the  atrophic  type  of  Goldthwait),  is  a  disease  of 
adult  life,  and  is  more  common  in  women  than  in  men.  Goldthwait 
discounts  the  likelihood  of  an  infectious  cause  in  these  cases,  emphasizing 
the  etiological  significance  of  poverty,  wear  and  tear  of  life,  grief,  fear, 
severe  nervous  shock,  and  great  physical  and  mental  strain.  These  are 
undoubtedly  present  in  many  cases,  and  of  unquestionable  causative  im- 
portance; but  in  many  cases  also,  and  in  increasing  numbers  as  the  cases 
are  the  more  carefully  studied,  some  chronic  unsuspected,  masked,  or 
concealed  infection  is  found — in  the  tonsils,  about  the  teeth,  gleet, 
chronic  gastro-intestinal  infections,  etc.;  some  cases  represent  an 
advanced  stage  of  a  disorder  developed  acutely  and  undoubtedly  infec- 
tious; and  Still  has  described  a  type  of  the  disorder  occurring  in  children, 
and  characterized  by  enlargement  of  the  lymph  nodes  and  the  spleen,  in 
addition  to  the  joint  lesions.  In  some  cases  gastro-intestinal  and  other 
metabolic  poisons  may  be  an  active  factor. 

Pathology. — The  lesions  involve  all  the  articular  structures — the  syn- 
ovial membrane  and  fluid,  the  cartilages,  and  the  bone.  The  earliest 
changes  consist  of  inflammatory  and  hypertrophic  alteration  of  the  syno- 
vial tissue,  with  the  production  of  a  condition  called  villous  arthritis,  and 
thickening,  swelling,  and  infiltration  of  the  peri-articular  tissues.  Grad- 
ually the  inflammatory  lesions  of  the  synovial  tissue  subside,  and  cicatri- 


CHRONIC  ATROPHIC  ARTHRITIS  919 

zation  and  atrophy  ensue.  In  the  course  of  time  the  cartilage  becomes 
opaque,  striated,  and  atrophied,  so  that  large  or  small  erosions  of  the 
articular  surfaces  develop;  opposed  surfaces  of  exposed  bone  being 
brought  into  contact,  give  rise  to  rough,  grating  impressions;  the  bone 
trabeculse  become  reduced  in  size  and  number,  and  other  atrophic  and 
rarefying  changes  ensue.  The  synovial  fluid  may  be  present  in  excess  in 
the  early  stages,  but  late  it  is  usually  normal  in  amount,  the  increase  in 
the  size  of  the  joint  being  due  to  thickening  of  the  soft  periarticular 
tissues.     Osseous  spurs  may  sometimes  be  seen  (attempt  at  repair). 

Symptoms. — Chronic  atrophic  arthritis  is  a  poly  arthritic  disorder  that 
begins  insidiously  in  the  small  joints  of  the  hands — not  always  at  the 
same  time  in  both  hands,  but  both  soon  become  involved;  later,  the 
small  joints  of  the  feet,  and  the  wrists,  elbows,  ankles,  knees,  shoulders, 
and  other  joints,  even  all  the  joints  of  the  body,  may  become  affected. 
A  single  joint  is  rarely  involved  alone.  The  patient  at  first  experiences 
pain  or  difficulty  in  executing  fine  and  complicated  movements  involving 
the  hands;  the  phalangeal  and  metacarpophalangeal  joints  soon  become 
swollen — due  to  periarticular  oedema  and  infiltration,  in  part  sometimes 
to  increase  of  the  synovial  fluid.  Deformities  gradually  ensue,  which 
result  in  part  from  the  swelling,  in  part  from  gradual  atrophy  of  the 
articular  tissues,  and  in  part  from  subluxation  and  flexion  (the  stronger 
flexors  overcoming  the  weaker  extensors);  lateral  deformities  also  may 
ensue,  notably  ulnar  deviation  of  the  hands  and  knock-knees.  Crepita- 
tion occurs  on  flexing  and  extending  the  joints  (due  to  the  rubbing  of 
villi  or  erosions),  and  more  or  less  fixation  may  result  from  the  contrac- 
tion of  muscles  or  bony  ankylosis.  The  muscles  about  the  joints  usually 
atrophy.  Fluctuation  in  the  severity  of  the  lesions  occurs  from  time  to 
time;  and  the  condition  may  even  abate  or  become  quiescent.  There 
are,  as  a  rule,  few  general  symptoms  aside  from  general  malnutrition  and 
anemia. 

Diagnosis. — The  symptoms  are  sufficiently  distinctive  to  enable  one  to 
recognize  the  disorder.  The  lesions  may  be  well  studied  by  radiographic 
examination. 

Prognosis. — The  outlook  is  not  promising,  although  considerable  ameli- 
oration of  the  condition  may  be  brought  about  in  the  early  stages. 

Treatment. — Sources  of  infection  must  be  searched  for  and  eradicated; 
and  attention  must  be  given  to  improving  the  general  nutrition  of  the 
patient  by  good  food,  good  air,  rest,  and  freedom  from  distress  and  worry. 
Internally,  syrup  of  iron  iodide,  cod-liver  oil,  arsenic,  and  thyroid  extract 
are  sometimes  efficacious.  Locally,  belladonna,  mercury,  and  iodine 
ointment,  massage,  electricity,  passive  movements,  hydrotherapeutic 
measures,  exposure  to  superheated  air  ("baking"  the  joints)  render  ser- 
vice. If  there  is  much  and  persistent  accumulation  of  fluid,  it  may  be 
withdrawn.  Care  must  be  taken  that  flexions,  subluxations,  and  other 
deformities  do  not  ensue,  and  if  ankylosis  seems  inevita])le,  that  it  occurs 
while  the  joints  are  in  a  position  to  permit  of  their  being  useful.  Per- 
sistent and  disabling  deformities  may  be  corrected  by  surgical  methods. 


920  DISEASES  OF  THE  BONES  AND  JOINTS 

CHRONIC  HYPERTROPHIC  OSTEO-ARTHRITIS. 

{Arthritis  Deformans  of  the  Hypertrophic  Type  of  Goldthwait.) 

Etiology. — Goldthwait  applies  the  term  chronic  hypertrophic  arthritis 
to  a  "chronic  constitutional  disease  with  local  joint  manifestations, 
which  may  or  may  not  be  polyarticular."  The  disorder  is  more  common 
in  men  than  in  women,  and  occurs  in  middle  life  and  old  age.  The  etio- 
logical factors  are  not  well  understood;  some  significance  is  attached  to 
exposure;  to  injuries,  which  maybe  single  and  severe  and,  involving  one 
of  the  large  joints,  may  apparently  soon  lead  to  the  disease,  or  which  may 
be  slight,  inconsequential,  but  frequently  repeated  and  related  to  the 
patient's  occupation;  to  gastro-intestinal  derangements  and  consequent 
auto-intoxication;  and  to  the  changes  of  senility. 

Pathology. — The  joints  most  commonly  involved  are  the  fingers,  knees, 
vertebra?,  hips,  and  feet.  The  chief  lesions  consist  of  slight  localized  vil- 
lous hypertrophy  of  the  synovial  tissue  and  of  the  related  cartilage;  and 
of  hypertrophy  of  the  cartilage  along  the  outer  margin  of  the  joint  and 
that  associated  with  the  ligaments  (so-called  lipping).  This  hypertrophy 
consists  of  fairly  normal  cartilage  (in  contrast  with  the  changes  in  the 
cartilage  in  the  atrophic  form  of  the  disease) ;  it  is  quite  irregular  in  de- 
gree, and  soon  becomes  ossified — that  is,  into  it  osteophytes  develop 
(so-called  Haygarth's  nodosities  at  the  knuckles);  sometimes  there  is  an 
associated  bony  spur  formation  or  hyperplasia  at  the  point  of  attach- 
ment of  the  ligaments  and  tendons.  These  together  produce  more  or  less 
joint  disability  and  fixation.  Erosions  occur,  but  they  result  from  the 
action  of  the  osteophytes  or  from  pressure,  and  they  differ  from  those  of 
the  atrophic  type  of  the  disease  in  showing  at  their  bottom  eburnated 
cartilage  and  not  exposed  bone. 

Symptoms. — The  onset  of  the  disorder  is  slow,  and  considerable  progress 
may  be  made  before  noteworthy  symptoms  supervene.  The  usual  com- 
plaint is  of  articular  discomfort  and  pain  and  more  or  less  disability,  all 
of  which  are  increased  on  activity  and  improved  on  resting.  From  time 
to  time  the  symptoms  disappear,  perhaps  entirely,  and  leave  no  symptoms 
except  the  bony  deformities.  The  condition  is  quite  common  in  the 
hands,  occurring  as  small,  hard  knobs  of  hypertrophied  cartilage  and 
bone  at  the  dorsal  or  dorsolateral  margin  of  the  articulating  surfaces  of 
the  terminal  phalanges  (Heberden's  nodes).  Flexion  or  lateral  devia- 
tion of  the  terminal  phalanges  occurs  from  pressure  atrophy  on  the  side 
toward  which  the  nodes  push.  The  condition  is  incurable,  but  it  brings 
with  it  the  happy  reflection  that  its  subjects  rarely  become  affected  with 
disease  of  the  larger  joints.  In  the  knees,  considerable  enlargement,  of 
the  femur,  the  tibia,  and  the  patella,  with  subluxation  and  fixation  of  the 
joint  (osteophyte  formation)  ensue,  and  the  patient  is  often  permanently 
disabled.  In  the  hip  (morbus  coxae  senilis)  the  changes  involve  the  head 
of  the  femur  and  the  acetabulum;  the  acetabulum  becomes  broadened 
and  the  upper  lip  grows  over  and  may  completely  surround  the  neck  of 


OSTEOMALACIA  921 

the  femur,  effectually  limiting  motion.  In  the  vertebrae  the  lesions  often 
involve  several  adjacent  vertebrae;  the  cartilaginous  proliferation  may 
extend  to  several  neighboring  bones,  and  the  osteophytic  proliferation 
may  invade  not  only  this  but  also  the  intervertebral  cartilages,  and  may 
extend  down  the  anterior  and  anterolateral  aspects  of  the  vertebrae, 
effectually  ankylosing  them  (so-called  spondylose  rhizomelique).  The 
condition  is  most  common  in  the  thoracicolumbar  and  the  cervical  ver- 
tebrae. It  gives  rise  to  more  or  less,  often  marked,  rigidity  of  the  ver- 
tebrae, and  local  pain;  the  pain  often  radiates  (unusually  unilaterally) 
to  the  area  of  distribution  of  the  sensory  roots  that  enter  the  vertebral 
column  amidst  the  lesions. 

Diagnosis. — The  disease  is  readily  recognized.  The  articular  lesions 
can  be  well  studied  by  radiographic  examination. 

Prognosis. — The  outlook  as  to  cure  is  not  good.  Once  established 
the  disease  is  irremediable,  but  some  amelioration  can  be  effected  in  the 
early  stages. 

Treatment. — The  treatment  is  that  recommended  for  the  atrophic  form 
of  the  disease.  Care  should  be  taken  to  prevent  deformities;  if  they 
develop  they  may  be  corrected  by  surgical  methods. 


OSTEOMALACIA. 

(MolUties  Ossium;  Fragilitas  Ossium.) 

Osteomalacia  is  a  chronic  disorder  of  nutrition  characterized  by  decal- 
cification and  progressive  softening  of  developed  and  ossified  bones, 
leading  to  bending  or  fracture  and  more  or  less  deformity. 

Etiology. — The  disorder  is  rare,  but  occurs,  especially  in  adult  life  and 
in  women  (10  to  1  man).  It  is  commoner  among  the  poor  than  the 
well-to-do,  and  seems  to  be  epidemic  in  certain  regions  (in  Europe).  It 
occurs  most  frequently  in  pregnant  and  nursing  women,  especially  mul- 
tipara, but  also  in  virgins  (relation  to  ovulation  ?) ;  pregnancy  may  merely 
cause  an  exacerbation  of  the  disease  already  existent. 

Pathology. — The  bones  most  commonly  affected  are  the  pelvic  bones, 
the  vertebrae,  and  the  ribs;  the  long  bones  usually  are  affected  late.  The 
lesions  consist  in  decalcification  of  the  compact  and  spongy  parts  of  the 
bone  and  their  replacement  by  a  soft,  vascular,  gelatinous,  sometimes 
hemorrhagic  or  cystic,  tissue;  the  periosteum  may  be  involved  or  thick- 
ened and  hyperemic.  The  bones  in  consequence  become  softened  or 
brittle,  and,  yielding  to  divers  influences,  become  bent,  distorted,  and 
may  be  readily  fractured.  The  nature  of  the  disease  is  not  known;  a 
relationship  between  the  osteomalacia  (decalcification)  of  pregnancy  and 
lactation  and  the  need  of  the  growing  foetus  and  child  for  lime  and  phos- 
phorus has  been  postulated.  An  influence  of  the  ductless  glands  also  has 
been  suggested;  the  parathyroids  are  known  to  have  an  influence  on 
calcium  metabolism  (deficiency  provoking  tetany);  the  ovaries  perhaps 
influence  the  absorption  of  calcium  (and  some  cases  of  osteomalacia 


922  DISEASES  OF  THE  BONES  AND  JOINTS 

have  been  cured  by  oophorectomy);  the  thyroids  also  have  been  impli- 
cated— but  the  exact  interrelationship,  if  any,  is  not  well  understood. 

Symptoms, — The  onset  of  the  disease  is  insidious,  and  it  may  be  far 
advanced  when  first  recognized  (as,  for  instance,  vaginal  examination  at 
impending  parturition).  The  earliest  symptom  usually  is  pain  (misin- 
terpreted as  rheumatic)  in  the  pelvis,  vertebrae,  thorax,  legs,  etc.,  perhaps 
associated  with  difficulty  in  locomotion  (hobbling  or  wobbling  gait). 
Gradually  deformities  develop;  the  sacral  promontory  and  the  acetabula 
approach  one  another  (osteomalacic  pelvis);  lordosis,  kyphosis,  or  sko- 
liosis  ensues;  the  bones  of  the  legs  become  curved  (the  patient  often  is  obvi- 
ously growing  shorter),  and  fractures  may  occur  spontaneously  or  on  very 
slight  provocation.  The  cranium  usually  is  not  much,  if  at  all,  involved. 
The  patient  may  become  bedridden.  The  muscles  are  usually  flaccid 
and  atrophic  (rarely  spastic),  and  may  exhibit  fibrillary  twitchings, 
intention  tremors,  etc.  The  urine  contains  an  excess  of  calcium  and 
phosphorus. 

Diagnosis. — ^The  diagnosis  often  is  not  made  until  the  disease  is  well 
advanced — when  it  presents  no  difficulties.  In  the  early  stage,  muscular 
rheumatism  and  divers  diseases  of  the  bones  and  of  the  nervous  system 
must  be  excluded.  Attention  to  the  possibility  of  the  disease  in  a  pregnant 
or  nursing  woman,  examination  especially  of  the  pelvic  bones  for  defor- 
mities, radiographic  examination  (for  decalcification),  and  a  study  of 
the  calcium  output  in  the  urine  should  enable  the  diagnosis  to  be  made 
early  in  many  cases. 

Prognosis. — The  disease  is  usually  progressive,  running  a  course  of  five 
or  ten  years  or  more;  sometimes  the  course  is  rapid — less  than  a  year; 
sometimes  it  becomes  arrested,  and  perhaps  made  worse  by  a  subsequent 
pregnancy.  Death  usually  ensues  from  progressive  weakness  or  inter- 
current infection. 

Treatment. — The  treatment  is  largely  symptomatic:  good  food, 
good  hygiene,  and  the  avoidance  of  etiological  factors — nursing  in  those 
already  affected,  as  well  as  subsequent  pregnancy.  Calcium  and  phos- 
phorus (cod-liver  oil  and  other  phosphorus-bearing  oils  and  foods)  often 
are  markedly  beneficial.  Improvement  has  followed  the  use  of  adrenalin 
to  the  point  of  toleration.  Ovariotomy  has  led  to  improvement  in  ad- 
vanced cases  in  women. 


OSTEITIS  DEFORMANS. 

{Paget's  Disease.) 

Osteitis  deformans  is  a  rare  disorder,  characterized  by  "enlargement 
and  forward  projection  of  the  head,  dorsocervical  kyphosis,  prominence 
of  the  clavicles,  spreading  of  the  base  of  the  thorax,  a  diamond-shaped 
abdomen  crossed  by  a  deep  sulcus,  a  relative  increase  in  the  width  of 
the  hips,  and  an  outward  and  forward  bowing  of  the  legs"  (Packard, 
Steele,  and  Kirkbride).     The  subjects  become  notably  reduced  in  height. 


FACIAL  HEMIATROPHY  023 

The  cause  of  the  disease  is  not  known;  it  is  believed  to  be  related  to 
osteomalacia,  and  perhaps  to  disorders  of  the  pituitary  body  and  the 
other  ductless  glands.  The  lesions  consist  of  a  rarefying  and  formative 
osteitis.  The  diagnosis  is  apparent  at  a  glance.  Treatment  seems  to 
be  inefficacious. 


HYPERTROPHIC  PULMONARY  OSTEO-ARTHROPATHY. 

Hypertrophic  pulmonary  osteo-arthropathy  is  a  rare  disorder,  charac- 
terized by  enlargement  of  the  ends  of  the  bones  of  the  hands  and  feet, 
especially  the  terminal  phalanges,  and  sometimes  also  of  the  distal  ends 
of  the  long  bones  of  the  forearm  and  legs.  The  ends  of  the  fingers 
become  characteristically  bulbous  and  the  finger  nails  elongated  and 
curved  about  them.  The  nature  of  the  disease  is  not  known.  Most  of  the 
cases  are  associated  with  long-standing  (usually  suppurative)  disorders 
of  the  lungs  or  pleura,  and  it  has  been  supposed  (Marie)  that  the  toxins  of 
the  pulmonary  disorder,  reaching  the  bones  by  way  of  the  circulation, 
set  up  an  ossifying  periostitis.  A  somewhat  similar  condition  sometimes 
occurs  in  chronic  heart  disease,  syphilis,  tuberculosis;  or  it  may  develop 
from  unknown  causes.  Freedom  from  involvement  of  the  bones  of  the 
skull  and  face  readily  excludes  akromegaly. 

OSTEOGENESIS  IMPERFECTA. 

Osteogenesis  imperfecta  is  a  rare  disorder,  characterized  by  imperfect 
development  of  the  bones,  especially  of  the  skull  and  the  extremities. 
The  bones  are  exceedingly  fragile,  so  that  intra-uterine  and  extra-uterine 
fractures  are  common.  Should  the  child  survive,  ossification  ultimately 
may  become  normal,  although  the  bones  may  be  more  or  less  deformed. 

ACHONDROPLASIA. 

{Chondrodystropkia  Foetalis.) 

Achondroplasia  is  a  disorder  due  to  perverted  development  (dys- 
trophy) of  the  epiphyseal  cartilages  (connective-tissue  invasion  from  the 
periosteum),  in  consequence  of  which  the  epiphyses  and  diaphyses  become 
prematurely  united  and  the  normal  growth  of  the  long  bones  does  not 
occur.  The  subjects  are  dwarfs,  usually  with  normal  heads  and  trunks, 
and  short,  stumpy  extremities. 

FACIAL  HEMIATROPHY. 

Facial  hemiatrophy  is  a  rare  disorder,  characterized  by  atrophy  of  the 
bones  and  soft  tissues  of  one-half  of  the  face.     The  nature  of  the  disorder 


924  DISEASES  OF  THE  BONES  AND  JOINTS 

is  not  well  understood;  interstitial  neuritis  of  the  entire  trigeminal  nerve 
has  been  found.  The  disorder  begins  usually  in  childhood,  although  it 
may  come  on  later;  and  it  may  follow  an  injury  or  infection.  There  is 
gradual  wasting  of  all  the  tissues,  skin,  subcutaneous  connective  tissues, 
and  the  bone,  and  to  some  extent  also  the  muscles.  The  skin  becomes 
pale,  the  hair  whitens  and  may  fall,  and  the  teeth  may  drop  out.  There 
may  be  some  associated  sensory  changes.  The  condition  is  readily 
recognized. 

LEONTIASIS  OSSEA. 

Leontiasis  ossea  is  a  rare  disorder,  characterized  by  enlargement  of  the 
cranial,  and  sometimes  the  facial,  bones — occasioning  a  so-called  leontine 
expression.     The  nature  of  the  disease  is  unknown. 


INDEX. 


Abasia,  893 
Abdominal  angina,  492 

typhus,  32 
Abducens  nerve,  816 
Abnormal  intestinal  contents,  677 
Abscess  of  brain,  871 

of  Uver,  707 

of  lung,  559 

peritonsillar,  599 

retropharyngeal,  604 

of  spleen,  406 

subphrenic,  749 
Acanthocephaliasis,  221 
Acariasis,  224 
AchoUa,  688 

Achondroplasia,  329,  923 
Achjdia  gastrica,  619,  620 
Acidosis  and  acid  intoxications,  304 
Acroparesthesia,  908 
Actinomycosis,  169 
Activators,  338 
Adams-Stokes  syndrome,  421 
Addison's  anemia,  573 

disease,  353 

incomplete,  352 
Adenie,  397 

Adenoid  vegetations,  601 
Adenohpomatosis,  symmetrical,  328 
Adenoma,  349 
Adhesive  pericarditis,  485 
Adiposis  cerebralis,  328 

dolorosa,  327 

tuberosa,  328 
Adrenal  glycosuria,  338 

inadequacy,  353 

insufficiency,  352 
Adrenals,  diseases  of,  351 
African  blood  fluke,  213 

lethargy,  194 

tick  fever,  178,  224 
Agglutinins,  21 
Aggressins,  22 
Agoraphobia,  895,  903 
Agraphia,  842 
Ague,  197 
Ainhum,  287 
Air  and  gas  in  pericardium,  488 

disease,  compressed,  878 

-hunger,  508 
Akoria,  617 


Akromegaly,  355 
Albuminuria,  764 

accidental,  764 

adolescent,  765 

extrarenal,  764 

factitious,  764 

functional,  765 

physiological,  765 

spurious,  764 
Albumosuria,  767 
AlcohoUsm,  289 
Alexia,  841 
Alexin,  21 
Alkaptonuria,  758 
Amaurotic  family  idiocy,  847 
Amblyopia,  hj'sterical,  815 
Amboceptors,  21 
Amnesia,  844 
Amoebiasis,  175 
Amoebic  colitis,  175 

dysentery,  175 
Amyloid  disease,  334 
Amyloidosis,  334 
Amyotonia,  congenital,  916 
Amyotrophic  lateral  sclerosis,  852 
Anakhre,  287 
Anaphylaxis,  29 
Anemia,  361 

acute  secondary,  365 

aplastic,  377 

chronic  secondary,  367 

in  children,  409 

infantum   pseudoleukaemica   of   von 
Jaksch,  409 

miiners',  218 

of  brain,  861 

pernicious,  373 

splenic,  407,  408 
Aneurysm,  497 

diagnosis  of,  501 

of  heart,  443 

physical  signs  of,  500 

symptoms  of,  498 

treatment  of,  502 
Angina,  598 

abdominal,  492 

Ludovici,  597 

pectoris,  493 
Angioneurotic  oedema,  907 
Angiosclerosis,  489 
Ankylostomiasis,  218 
Anopheles,  198 


926 


INDEX 


Anorexia,  617 
Anosmia,  814 
Anthracosis,  554 
Anthrax,  161 

oedema,  malignant,  162 
Antibodies.  20 

specific,  21 
Antigen,  20,  21 
Antilysin,  21 
Anuria,  763 
Aortic  insufficiency,  462 

stenosis,  466 
Aortitis,  acute,  489 
Aphasia,  840 

types  of,  841 
Aphemia,  642 
Aphthae  of  palate,  591 
Aphthous  fever,  273 
Aplastic  anemia,  377 
Apneumatosis,  547 
Apoplexy,  862 

pulmonary,  545 
Appendicitis,  668 
Apraxia,  843 
Aprosexia,  601 
Aptyalism,  596 
Arithmomania,  903 
Arrhythmia,  cardiac,  416 
Arrhythmic  breathing,  509 
Arsenical  poisoning,  296 
Arteries,  diseases  of,  489 
Arterio-capillary  fibrosis,  489 
Arteriosclerosis,  489 

hypertrophy  of  heart  in,  439 

nodose,  489 

senile,  490 

syphiUtic,  490 
Arteriosclerotic  kidney,  783 
Arthritis,  acute,  917 

chronic  atrophic,  918 
hypertrophic,  920 

deformans,  918 

gonococcic,  91 
Ascariasis,  219 
Ascites,  746 
Asiatic  blood  fluke,  213 

opisthorchiasis,  211 
Aspergillosis,  pulmonary,  171 
Asphyxia,  510 

local,  908 
Astasia,  893 
Astereognosis,  844 
Asthenia,  cardiac,  424 
Asthma,  bronchial,  534 

cardiac,  413 

Kopp's,  404 

Millar's,  404 

spasmodic,  534 

thymic,  403 
Ataxic  paraplegia,  858 
Atelectasis  of  lung,  547 
Atehosis,  336 
Atheroma,  489 
Atherosclerosis,  489 


Athlete's  heart,  427 
Athyrea,  339 

Atypical  actinomycosis,  171 
Auditory  nerve,  819 

vertigo,  819 
Aura  asthmatica,  535 

epileptica,  889 
Auricles,  hypertrophy  of,  442 
Auricular  extrasy stoles,  417 
Auriculo ventricular  extrasystoles,  418 
Auto-intoxication,  acid,  304 

duodenal,  304 

gastro-intestinal,  303 

retention,  305 
Autumnal  catarrh,  515 
A  virulent  diphtheria,  135 
Azotorrhoea,  737 


B 


Baccelli's  sign  in  pleuritis,  569 
Bacillary  dysentery,  145 
Bacteremia,  22,  61 

gonococcic,  90 

typhoid  fever,  34 
Bacteria,  pathogenic,  20 
Bacterial  infection,  32 

intoxication,  22 

protein,  21 

vaccines,  32 
Bacterins,  32 
Bacteriolysins,  21 

Bamberger's  sign  in  pericarditis,  481 
Banti's  disease,  408 
Barlow's  disease,  333 
Bartender's  paralysis,  823 
Basedow's  disease,  342 
Basophilia,  364 
Bed-bugs,  225 
Bednar's  aphthte,  591 
Beef  tapeworm,  216 
Bell's  palsy,  818 

Bence- Jones  albumosuria,  401,  767 
Bends,  the,  878 
Beriberi,  275 
Biermer's  anemia,  373 
Big  jaw,  169 
Bigeminal  pulse,  418 
Bilharziosis,  213 
Biliary  ducts,  diseases  of,  721 

obstruction  of,  732 

fistula,  733 
Birth  palsies,  846 
Black  tongue,  595 
Blackwater  fever,  208 
Bladder,  inflammation  of,  788 

tuberculosis  of,  121 

tumors  of,  799 
Blastomycetic  dermatitis,  172 
Blastomycosis,  172 
Blood  and  hemopoietic  system,  diseases 

of,  359 
Blood-fluke  disease,  213 


INDEX 


927 


Bolt's  breathing,  509 

Bone  marrow,  tuberculosis  of,  102 

Bones  and  joints,  diseases  of,  917 

tuberculosis  of,  124 
Boulimia,  611,  617 
Brachial  plexus,  821 
Bradycardia,  422 
Brain,  832 

abscess  of,  871 

anemia  of,  861 

diffuse  and  focal  diseases  of,  861 

hyperemia  of,  861 

localization  of  disease,  831 

non-system  diseases  of,  859 

oedema  of,  862 

system  diseases  of,  845 

tumors  of,  873 
Break-bone  fever,  265 
Breast-pang,  493 
Bridal  paralysis,  823 
Bright's  disease,  acute,  773 
chronic,  780,  783 
Brissaud's  type  of  infantilism,  336 
Broadbent's  sign  in  diseases  of  pericar- 
dium, 486 
Bromatotoxism,  299 
Bronchi,  diseases  of,  524 
Bronchial  asthma,  534 

catarrh,  acute,  524 
chronic,  527 
Bronchiectasis,  532 
Bronchiolectasis,  533 
Bronchiohtis  exudativa  of  Curschmann, 

535 
Bronchitis,  acute,  524 

capillary,  549 

chronic,  527 

fetid,  528 

fibrinous,  529 

gouty,  528 

putrid,  528 

with  emphysema,  chronic,  528 
Bronchocele,  340 
Bronchopneumonia,  549 
Bronchopulmonary  hemorrhage,  539 
Bronchorrhoea,  529 
Brown-Sequard  paralysis,  838 
Bruit  d'airain  of  Trousseau,  582 

de  diable,  368,  371 

de  drapeau,  532 

de  rappel,  461 
Bubo,  parotid,  596 

tropical,  283 
Bubonic  plague,  156,  157 
Bulbar  palsy,  acute,  850 
asthenic,  851 
chronic,  850 
Buhl's  disease,  387 


Cachexia,  chronic  malarial,  203,  209 
lead,  295 
parastrumipriva,  349 


Cachexia,  tropical,  195 

Caisson  disease,  878 
Calabar  swelUngs,  224 
CalcuU,  biliary,  728 

pancreatic,  745 

renal,  794 

salivary,  597 
Calmette's  conjunctival  test,  126 
Camp  fever,  237 
de  la  Camp's  sign  in  tuberculosis  of  lymph 

nodes,  101 
Cancrum  oris,  593 
Capillary  bronchitis,  549 
Carcinoma   of    gall-bladder    and    biliary 
ducts,  736 

of  intestine,  676 

of  larynx,  523 

of  liver,  719 

of  oesophagus,  607 

of  pancreas,  744 

of  peritoneum,  747 

of  stomach,  638 

of  thyroid,  349 
Cardarelli's  sign  in  aneurysm,  499 
Cardia,  spasm  of,  615 
Cardiac  asthenia,  424 

asthma,  413 

cirrhosis,  710 

pain,  415 

strain,  427 

type  of  infantilism,  336 
Cardialgia,  617 
Cardio-renal  disease,  783 
Cardiovascular  changes  in  nephritis,  760 
Catarrh,  autumnal,  515 

dry  chronic,  528 

sec,  528 
Catarrhal  bronchitis,  527 

cholangitis,  acute,  722 
chronic,  725 

fever,  epidemic,  143 

gastritis,  acute,  622 
chronic,  626 

jaundice,  722 

laryngitis,  517 

tonsillitis,  599 
Cellulocutaneous  plague,  158 
Central  ovale,  lesions  of,  834 
Cephalic  tetanus  of  Rose,  151 
Cerebello-pontine  angle,  tumors  of,  837 
Cerebellum,  lesions  of,  837 
Cerebral  disorders,  832 

embolism,  869 

hemorrhage,  862 

meningeal  hemorrhage,  825 

meninges,  tuberculosis  of,  122 

palsies  of  children,  846 

softening,  868,  869 

thrombosis,  868 
Cerebrospinal  fever,  86 

localization,  831 

meninges,  diseases  of,  825 

meningitis,  epidemic,  86 
Cervical  myelitis,  transverse,  880 


928 


INDEX 


Cervical  plexus,  821 

rib,  822 

sympathetic  nerves,  diseases  of,  824 
Cervicooccipital  neuralgia,  821 
Cestode  infection,  214 
Chalicosis,  554 
Chancre,  hard,  181 

Hunterian,  182 
Charbon,  161 

Charcot-Leyden  octahedral  crystals,  535 
Charcot's  disease,  852 
Chattering  teeth,  817 
Cheek,  gangrene  of,  593 
Cheese  poisoning,  299 
Cheyne-Stokes  breathing,  413,  509 
Chicken-pox,  235 
Chills  in  typhoid  fever.  40 
Chloranemia,  369 

Chloroform  poisoning,  delayed,  699 
Chloroma,  383 
Chlorosis,  369 

Egyptian,  218 
Choked  disk,  815 
Cholangitis,  acute  catarrhal,  722 

chronic  catarrhal,  725 

suppurative,  724 
Cholecystitis,  acute,  726 

chronic,  728 
Cholehthiasis,  728 

complications  and  sequels  of,  733 

diagnosis  of,  733 

etiology  of,  728 

pathology  of,  729 

prognosis  of,  734 

symptoms  of,  730 

treatment  of,  735 
Cholemia,  688,  694 
Cholera,  153 

Asiatic,  153 

infantum,  661 

morbus,  657 

nostras,  155,  657 

sicca,  155 
Cholerine,  155 
Choluria,  758 

Chondrodystrophia  foetaUs,  925 
Chorea,  acute,  900 

chronic  progressive,  902 

habit,  901 

hereditarj^  902 

insaniens,  901 

malignant,  901 

minor,  900 

senile,  904 
Choreiform  disorders,  904 
Chromaffin  system,  351 
Chvostek's  sign  in  tetany,  351 
Chylopericardium,  488 
Chylothorax,  583 
Chylous  ascites,  223 

diarrhoea,  223 
Chyluria,  758 

Circulatory  system,  diseases  of,  411 
tuberculosis  of,  106 


Cirrhosis,  atrophic,  710 

bihary,  710,  717 

capsular,  709 

Hanot's,  710 

hypertrophic,  710 

Laennec's,  710 

monolobular,  710 

multilobular,  710 

of  hver,  709 

portal,  710 

ventricuU,  627 
Cladothricosis,  171 
Cleithrophobia,  895,  903 
Clergj'men's  sore  throat,  603 
Coal  miner's  disease,  554 
Cocaine  habit,  293 
Coccidiaria,  174 
Coccidioidal  granuloma,  172 
Coccygodynia,  809 
Cochlear  nerve,  819 
Coeliac  disease,  664 
Cold,  common,  512 
Colic,  lead,  295 

mucous,  654 

painter's,  295 
CoUtis,  mucous,  654 
Collapse  of  lung,  547 
CoUes'  law,  181 
ColUer  de  ^'enus,  184 
Colon,  dilatation  of,  682 
Coloptosis,  685 

Combined  system  diseases,  857 
Complement,  21 
Completing  substance,  21 
Compression  of  lung,  547 
Congestion  of  kidneys,  770 

of  liver,  702,  703 

of  lungs,  541 

of  spleen,  407 
Constipation,  655 
Consumption,  92 
Conus  meduUaris,  880 
Convulsive  tics,  903 
CoprolaUa,  903 
Coprostasis,  677 
Corona  veneris,  184 
Coronary  arteries,  diseases  of,  444 
Corpora  quadrigemina,  lesions  of,  836 
Corrigan's  water-hammer  pulse,  465 
Coryza,  512 
Costiveness,  655 
Cough,  winter,  527 

Coughing  in  diseases  of  respiratory  sys- 
tem, 510 
Cowpox,  233 

Cramps,  occupation  or  professional,  897 
Cranial  nerves,  diseases  of,  814 
Craniotabes,  330 
Craw-craw,  224 
Cretinism,  336,  346 
Croup,  135 

false,  520 

membranous,  137 

spasmodic,  520 


INDEX 


929 


Croupous  or  diphtheritic  enteritis,  667 

pneumonia,  24,  71 
Crus,  lesions  of,  836 
Cryoscopy,  762 
Cryptogenetic  infections,  63 
Culex,  198 

Curschmann's  spirals,  535 
Cyanosis,  413,  510 

enterogenous,  304,  414 
Cyclic  albuminuria,  765 

or  periodic  vomiting,  615 
Cycloplegia,  816 
Cylindruria,  768 
Cynanche  gangrspnosa,  597 
Cystic  duct,  obstruction  of,  732 

kidneys,  congenital,  797 
Cysticercus  cellulosa,  218 
Cytase,  21 
Cytolysins,  21 
Cystinuria,  758 
Cystitis,  788 
Cysts  of  kidney,  797 

of  pancreas,  743 


Dalrymple's  sign  in  exophthalmic  goitre, 

343 
Dandy  fever,  265 

Dejerine's  interstitial  hypertrophic   and 
progressive  neuritis  of  infants,  814,  856 
Delhi  boil,  196 
Delire  de  toucher,  903 
Delirium  tremens,  290 
Dengue,  265 
Depression  of  conductivity,  420 

of  contractility,  421 
Dermatitis  coccidioides,  172 
Dermatomyositis,  912 
Deviation  of  the  complement,  28 
Diabetes  insipidus,  318 
mellitus,  305 

complications  of,  311 
diagnosis  of,  312 
diet  Ust  for,  314 
etiology  of,  305 
pathology  of,  305 
prognosis  of,  313 
symptoms  of,  308 
treatment  of,  313 
Diarrhoea  of  children,  661 
hill,  280 
nervous,  647 
tubular,  654 
Diarrhoeal  disorders  of  children,  661 
Dibothriocephalus  latus,  215 
Dicroccehasis,  212 
Diet  in  diabetes,  314 

in  typhoid  fever,  52 
Dietetic  albuminuria,  765 
Digestive  system,  diseases  of,  587 

tuberculosis  of,  117 
Dilatation  of  colon,  682 

59 


Diphtheria,  131 

avirulent,  135 

bacillus,  variation  in  virulence  of,  135 

complications  and  sequels  of,  138 

diagnosis  of,  139 

etiology  of,  131 

laryngeal,  137 

malignant,  137 

nasal,  137 

pathology  of,  132 

pharyngeal,  136 

prognosis  of,  140 

symptoms  of,  136 

treatment  of,  140 

wound,  138 
Dipht!ccroid  infections,  135 
Distomatosis,  211 
Distomiasis,  211 
Dittrich's  plugs,  528 
Diverticula  of  oesophagus,  606 

of  sigmoid,  672 
Diverticulitis,  sigmoid,  672 
Dourine,  174 
Dracunculosis,  223 
Dropsy,  epidemic,  277 

pericardial,  487 

peritoneal,  746 

pleural,  579 
Dry  mouth,  596 
Dubini's  electrical  chorea,  904 
Ductless  glands,  diseases  of,  337 
Duke's  so-called  fourth  disease,  251 
Dum-dum  fever,  195 
Durosiez's  sign  in  heart  disease,  466 
Dysentery,  bacillary,  145 

amoebic,  175 

infantile,  661 
Dyspepsia,  acute,  622 

chronic,  626 

intestinal,  650 

nervous,  621 
Dyspeptic  diarrhoea,  acute,  661 
Dyspnoea,  413,  508 
Dysthyreosis,  339 
Dystrophia  adiposo  genitalis,  328 
Dystrophy,  progressive  muscular,  912 

facio-scapulo-humeral  type 
of    Landouzy    and    De- 
jerine,  914 
Leyden-Mobius  form,  914 
pseudohypertrophic  form  of 

Duchenne,  913 
scapulo-humeral  form   of 
Erb,  914 
Dystrypsia,  650 


E 


Ebrtein's  sign  in  pericarditis,  481 
Echinococcus  cyst,  349 

granulosa,  217 
Echokinesis,  903 
Echolaha,  903 
Eczema  of  tongue,  595  <^ 


930 


INDEX 


Eelworm  infection,  219 
Egyptian  chlorosis,  218 
Electrical  conductivity  of  urine,  763 

reactions,  807 
Elephantiasis,  395 

of  leg,  223 
Ellis  and  Gariand,  S-shaped  curve  of,  568 
Elongation  of  uvula,  604 
Embolism  of  mesenteric  arteries,  682 
Emphysema,  555 

acute  vesicular,  558 

interalveolar,  558 

interlobular,  558 

interstitial,  558 

large  lunged,  555 

pseudohypertrophic,  555 

senile,  558 

subpleural,  558 

vicarious,  558 
Empyema,  574 

necessitatis,  575 

of  pericardium,  483 

pulsating,  575 
Encephahtis,  acute  hemorrhagic,  871 
suppurative,  371 

cerebellar,  871 
Encephalopathy,  lead,  295 
Endarteritis,  chronic  deforming,  489 
Endocardium,  diseases  of,  445 
Endocarditis,  acute,  445 

chronic,  450 

gonococcic,  91 
Endophlebitis,    chronic   obliterating   he- 
patic, 696 
portal,  697 
Endotheliolysins,  21 
Endothelioma,  397 

primitive,  of  spleen,  408 
Endotoxins,  21 
Enteralgia,  649 
Enteric  fever,  32 
Enteritis,  acute,  657 

chronic,  659 

croupous  or  diphtheritic,  667 

phlegmonous,  667 

pseudomembranous,  654 
EnterocoUtis,  661 
Enterodynia,  649 
Enteroptosis,  685 
Enterorrhagia,  652 
Enzyme,  fat-splitting,  609 
Eosinophilia,  364 
Epilepsy,  888 

Epileptiform  convulsions,  888 
Epistaxis,  511 

recurring,  511 
Epstein-Pel  disease,  400 
Epizootic  aphtha,  273 
Ergotism,  300 

Erb's   juvenile   form  of   muscular   dys- 
trophy, 914 

sign  in  tetany,  351 

upper  arm  type  of  brachial  paralysis, 
821 


Erni's  tapotage  sign  in   tuberculosis  of 

lungs,  114 
Erysipelas,  67 

Erysipeloid  of  Rosenbach,  69 
Erythema,  infectious,  251 

migrans,  69 
Erythremia,  385 
Erythrocytosis,  385 
Erythronielalgia,  907 
Estivo-autumnal  malarial  fever,  197 
infections,  203,  205 
parasite,  201 
Exanthematic  typhus  fever,  237 
Extrasystoles,  auricular,  417 

nodal,  418 

ventricular,  417 


Facial  nerve,  817 

paralysis,  central,  817 
peripheral,  818 

spasm,  818 
Famine  fever,  178,  237 
Farcy,  159 
Fascioliasis,  212 

Fatty  tumors,  multiple  symmetrical,  328 
Fauces,  diseases  of,  598 
Faucitis,  acute,  598 
Fecal  impaction,  677 
Fetid  bronchitis,  528 
Fever  in  infections,  25 
Fibrinous    bronchiolitis,     acute    obliter- 
ating, 531 

bronchitis,  530 

pneumonia,  71 

rhinitis,  137 
Fibrinuria,  758 
Fibroid  induration  of  lung,  552 

phthisis,  552 

pneumonia,  chronic,  552 

tuberculosis,  chronic,  115 
Fibrotic  nutmeg  liver,  703 
Filariasis,  223 
Fish  poisoning,  300 
Fisher's  sign  in  diseases  of  pericardium, 

487 
Flagellata,  173 
Flajani's  disease,  342 
Fleas,  225 

Flexner's  antimeningococcic  serum,  32 
Flint  murmur,  461,  466 
Fluke  infections,  211 
Folie  de  doute,  903 
Follicular  tonsilhtis,  599 
Foot-and-mouth  disease,  273 
Foot-drop,  812 
Food  poisoning,  299 
Fourth  disease,  Duke's  so-called,  251 
Fraentzel  murmur,  461 
Framboesia,  193 
Friedreich's  ataxia,  857 

sign  in  diseases  of  pericardium,  486 
in  tuberculosis  of  lungs,  114 


INDEX 


931 


Galactotoxism,  299 
Gall-bladder  and  biliary  ducts,  diseases 
of,  721 

carcinoma  of,  736 

inflammation  of,  726 
Gall  sickness,  174 
Gallstones,  728 
Galziekte,  174 
Gambian  horse  disease,  174 
Gangosa,  286 
Gangrene  of  cheek,  593 

of  lung,  561 

symmetrical,  908 
Gangrenous  proctitis,  281 
Gaseous  distention  of  the  parotid  duct, 

597 
Gastralgia,  617 
Gastrectasis,  630 
Gastric  catarrh,  acute,  622 
chronic,  626 

fever,  623 

neurasthenia,  621 
Gastritis,  acute,  622 

chronic,  626 

infectious,  625 

phlegmonous,  624 

simple,  622 

suppurative,  624 

toxic,  624 
Gastrodynia,  617 
Gastro-enteritis  of  children,  661 
Gastro-intestinal  auto-intoxication,   303, 
661 

catarrh,  661 
Gastroptosis,  685 
Gastrorrhagia,  613 
Gastrosuccorrhoea,  619 
Gastroxynsis,  619 

Gaucher  type  of  splenomegaly,  408 
Genito-urinary    system,    tuberculosis  of, 

120 
Gerhardt's  sign  in  tuberculosis  of  lungs, 

114 
Glanders,  159 
Glandular  fever,  252 
Glenard's  disease,  685 
Gliosis,  spinal,  884 
Glossitis,  594 

Glossopharyngeal  nerve,  819 
Glycosuric  test,  762 
Giliraltar  fever,  164 

Gilford's  sign  in  exophthalmic  goitre,  343 
Gigantism,  355 
Gilford's  cases  of  dwarfs,  336 
Gilles  de  la  Tourette's  disease,  903 
Goitre,  340 

exophthalmic,  342 
Gonococcic  bacteremia,  90 

endocarditis,  91 

infection,  90 

synovitis  and  arthritis,  91 
Goundou,  287 


Gout,  320 

acute,  323 

chronic,  324 

irregular,  325 

retrocedent,  324 

suppressed,  324 
Gouty  bronchitis,  528 
von  Graefe's  sign  in  exophthalmic  goitre, 

343 
Grain  poisoning,  300 
Grancher's  sign  in  tuberculosis  of  Ij^mph 

nodes,  101 
Granuloma  of  genitals,  ulcerating,  283 
Graves'  disease,  342 
Green  sickness,  369 
Grinder's  rot  or  asthma,  554 
Grip,  143 

Grocco's  triangle,  569 
Gruber-Widal  reaction,  21,  28,  47,  49 
Grubler's  tumor,  295 
Guinea- worm  infection,  223 


Hsemosporidia,  174 

Hall's  sign  in  aneurysm,  499 

Halteridium,  174 

Halzoun,  212 

Harrison's  groove,  330 

Hay  asthma  or  fever,  515 

Hay  garth's  nodosities,  920 

Headache,  biUous  or  sick,  886 

Heart,  absolutely  irregular,  419 

acute  dilatation  of,  438 

aneurysm  of,  443 

block,  420,  423 

chronic  dilatation  of,  438 

enlargement  of,  437 

fatty,  430 

fibroid,  434 

functional  capacity  of,  414 

hypertrophy  and  dilatation  of,  437 
438 

infectious  febrile,  431 

insufficient,  425 

irritable,  429 

neuromuscular  disorders  of,  415 

overstrained,  429 

palpitation  of,  416 

-pang,  493 

parasites  of,  444 

rupture  of,  444 

valvular  disease  of,  452 

weak,  424 
Heat  cramps,  905,  906 

exhaustion  or  prostration,  905 

stroke,  905 
Heberden's  nodes,  920 
Hectic  fever  in   pulmonary  tuberculosis, 

112 
Heel,  painful,  810 
Hemarthrosis,  391 
Hematemesis,  613 


932 


INDEX 


Hematomyelia,  876 
Hematoporphyrinuria,  758 
Hematuria,  769 

Bilharzian,  213 

Egyptian,  213 
Hemeralopia,  815 
Hemiatrophy,  facial,  923 
Hemiacrania,  886 
Hemiplegia,  862 

of  infants,  846 
Hemisystole,  418 
Hemogenesis,  deficient,  23,  362 
Hemoglobinuria,  epidemic,  387 

malarial,  208 
Hemoglobinuric  fever,  208 
Hemolymph  nodes,  393 
Hemolysins,  21 
Hemolysis,  21 

increased,  362 
Hemolytic  ictero-anemia,  692 
Hemopericardium,  487 
Hemophilia,  390 
Hemopneumothorax,  580 
Hemoptysis,  539 

parasitic,  211 
Hemothorax,  576,  580 
Henoch's  hysterical  chorea,  904 

purpura,  389 
Hemorrhage,  bronchopulmonary,  539 

cerebral,  862 

from  lenticulostriate  artery,  864 

from  stomach,  613 

in  newborn,  387 

into  cerebellum,  866 

into  crus,  865 

into  internal  capsule,  864 

into  pancreas,  737 

into  pons  and  medulla,  866 

into  spinal  cord,  876 

pulmonary,  539 
Hemorrhagic  cortical  encephalitis,  acute, 
871 

diseases,  387 

encephalitis,  acute,  871 

infarction  of  lung,  545 

pachymeningitis,  internal,  827 

pleuritis,  576 
Hemorrhoidal  phlebectasis,  683 
Hemorrhoids,  683 
Hepatargia,  688 
Hepatic  artery,  diseases  of,  696 

auto-intoxication,  688 

capsulitis,  709 

veins,  diseases  of,  696 
Hepatitis,  acute,  705 

non-suppurative,  705 

chronic  interstitial,  709 

suppurative,  707 
Hepatolysins,  21 
Hepatoptosis,  685 

partial,  695 
Hepatopulmonary  abscess,  709 
Hereditary  ataxia,  857 

cerebellar  ataxia,  857 


Hereditary     spastic     paraplegia,     847, 
857 

spinal  paralysis,  847 
Herpes  zoster,  813 
Hertel's  exophthalmometer,  343 
Hertoghe's  hypothyroidism,  336 
Hiccough,  510 
Hill  diarrhoea,  280 
Hippocratic  succussion  splash,  582 
Hirschsprung's  disease,  682 
Hodgkin's  disease,  397,  398 
Hoffmann's  sign  in  tetany,  351 
Hookworm  disease,  218 
Hormones,  338 
Hunterian  chancre,  182 
Huntington's  chorea,  902 
Hutchison's  teeth,  189 

triad  of  symptoms  in  syphilis,  189 
Hydatid  disease,  214 
Hydrargyrism,  297 
Hydrocephalic  cry,  830 
Hydrocephalus,  875 
Hydronephrosis,  793 
Hydropericardium,  487 
Hydroperitoneum,  746 
Hydrophobia,  266 
Hydrotherapy  in  treatment  of  typhoid 

fever,  53 
Hydrothorax,  579 
Hymenolepsis  nana,  216 
Hyperacidity,  618 
Hyperchlorhydria,  618 
Hyperemia  of  brain,  861 

of  kidneys,  771 

of  liver,  703 

of  lungs,  541 
Hyperesthesia  of  stomach,  616 
Hypermotihty  or  hyperkinesis  of  stomach, 

614 
Hypernephroma,  353,  798 
Hyperorexia,  617 
Hyperosmia,  814 
Hyperpituitarism,  355 
Hyperpncea,  508 
Hyperthyroidism,  339 

and  exophthalmic  goitre,  342 
Hypertrophic   pulmonary  osteo-arthrop- 
athy,  923 

stenosis  of  pylorus,  643 
Hypochlorhydria,  619 
Hypochylia  gastrica,  619 
Hypoepinephry,  353 
Hypoglossal  nerve,  820 
Hypoosmia,  814 
Hypoparathyreosis,  349 
Hypophysis  cerebri,  355 
Hypopituitarism,  355 
Hypostatic  congestion  of  lungs,  542 
Hypothyroidism,  339,  346 
Hypotonia  of  muscles  of  children,  general 

or  localized,  916 
Hypotonic    or   atonic    pseudoparalysis, 

congenital,  916 
Hysteria,  892 


INDEX 


933 


Ichthyosis  of  tongue.  595 
Ichthyotoxism,  300 
Icterus  gravis,  691,  699,  705 

melas,  692 

neonatorum,  691 
Idiopathic  hypertrophy  of  heart,  440 
IleocoUtis,  661,  663 
Ileus,  675 

paralytic,  675 
Immune  bodies,  71 
Impulsive  tic,  903 
Indian  liver-fluke  disease,  212 
Indigestion,  chronic,  626,  636 

intestinal,  650 
Indigo-carmine  test,  762 
Indurative  mediastinopericarditis,  485 
Infantile  dysentery,  661 
Infantilism,  335,  355 
Infarction  of  mesenteric  vessels,  682 
Infection  carriers,  19 
Infections,  concurrent,  20 

diagnosis  of,  28 

double,  20 

general,  63 

local,  63 

mixed,  20 

nature  and  lesions  of,  20 

of  unknown  or  doubtful  etiology,  226 

pathological  physiology  of,  23 

pathways  of,  19 

prophylaxis  of,  29 

pyogenic,  61 

secondary,  20,  64 

terminal,  64 

treatment  of,  31 
Infectious  and  contagious  diseases,  17 

chorea,  900 

diseases,  17 

febrile  heart,  431 

gastritis,  625 

lesions  of  biliary  tract  and  adjacent 
viscera,  733 

phlegmon  of  pharynx,  acute,  604 
Inflation,  compensatory,  of  lungs,  558 
Influenza,  143 
Infusoria,  174 
Insolation,  905 

Intellectual  centre  of  language,  843 
Intercortical  sensory  aphasia,  842 
Intermittent  albuminuria,  765 

claudication  or  lameness,  493 

fever,  197 
Internal  capsule  of  brain,  834 
Interstitial  hypertrophic  progressive  neu- 
ritis of  childhood,  814,  856 

nephritis,  chronic,  783 

pneumonitis,  chronic,  652 
Intestinal  catarrh,  657 

cohc,  649 

dyspepsia,  650 

-fluke  disease,  212 

hemorrhage,  652 


Intestinal  hemorrhage,  in  typhoid  fever, 
42 

indigestion,  650 

infantilism,  304,  336 

juice,  645 

neuralgia,  649 

obstruction,  674,  733 

pain,  649 

sand,  683 

teniasis,  214 

tormina,  647 
Intestine,  constriction  of,  675 

diminished  sensibility  of,  650 

functional  disorders  of,  646 

incarceration  of,  675 

intussusception  or  invagination   of, 
675 

motor  disorders  of,  648 

occlusion  of,  674 

paralysis  of,  648 

paresthesia  of,  650 

pathological  physiology  of,  643 

spasm  of,  648 

stenosis  of,  675 

strangulation  of,  675 

stricture  of,  675 

tuberculosis  of,  118 

tumors  of,  676 

ulceration  of,  673 
Intoxication,  acid,  304 

auto-,  304 

bacterial,  22 
Intoxications,  289 
Intrapleural  pressure,  505 
Intraspinal  hemorrhage,  876 
Iridoplegia,  816 
Ischemic  paralysis,  823 
Itch,  grain  or  straw-bed,  225 

sarcoptic,  224 
Ixodiasis,  224 


Jacksonian  epilepsy,  890 
von  Jaksch's  disease,  400 
Jail  fever,  237 
Japanese  liver-fluke  disease,  211 

river  fever,  278 
Jaundice,  689 

acholuric,  692 

acute  infectious,  272 

black,  692 

catarrhal,  722 

chronic  family,  692 

congenital  hemolytic,  692 

effects  of,  692 

emotional,  691 

epidemic,  691 

grave,  691 

nemohepatogenous,  690 

hemolytic,  690 

hereditary,  692 

infectious,  690 

mechanical,  689 


934 


INDEX 


Jaundice,  menstrual,  691 

obstructive,  689 

splenomegalic,  692 

toxic,  690 

types  of,  689 

urobilin,  493 
Joffroy's  sign  in  exophthalmic  goitre,  344 
June  cold,  515 
Juvenile  arrhythmia,  416 


Kahler's  disease,  401,  767 

Kakke,  275 

Kala-azar,  195 

Keratosis,  595 

Kidneys,  active  congestion  of,  770 

acute  hematogenous  infection  of,  779 

anomaUes  of  form  and  position  of,  770 

circulatory  disturbances  of,  770 

cysts  of,  797 

functional  capacity  of,  762 

inflamination  of,  772 

of  pregnancy,  774 

parasitic  cyst  of,  797 

passive  congestion  of,  771 

soUtary  cyst  of,  797 

tumors  of,  798 
Kinases,  338 

Klumpke's  paralysis,  822 
Kocher's  sign  in  exophthalmic  goitre,  343 
Kopp's  asthma,  404 
Koranyi's  triangle,  569 
Korsakoff's  psychosis,  290,  812 
Kreatoxism,  299 
Kubisagari,  285 
Kussmaul's  dyspnoea,  311,  509 

sign  in  disease  of  pericardium,  486 


La  grippe,  143 
La  perleche,  591 
Lacunar  tonsilhtis,  599 
Laennec,  perles  of,  535 
Lamblia  intestinalis,  174 
Lancet-fluke  infection,  212 
Landolfi-'s  sign  in  heart  disease,  466 
Landry's  paralysis,  881 
Lardaceous  disease,  334 
Laryngeal  catarrh,  521 

diphtheria,  137 

perichondritis,  522 

tuberculosis,  107 
Laryngismus  stridulus,  520 
Laryngitis,  acute,  517 

chronic,  521 

oedematous,  519 

sicca,  518 

spasmodic,  520 
Larynx,  diseases  of,  517 

tumors  of,  523 


Latent  and  masked  malarial  infection=, 

209 
Lateral  sclerosis,  845 
Lathyrism,  300 
Lead  cohc,  295 

poisoning,  294 
Leber's  disease,  815 
Leishmania,  174 
Leontiasis  ossea,  924 
Lepra  alba,  167 
Leprosy,  166 
Leptomeningitis,  828 
Leukanemia,  377 
Leukemia,  378 

atypical,  383 

lymphatic,  378 

Ij^mphocytic,  381 

lymphoid,  381 

medullary,  378 

myelocytic,  379 

myeloid,  379 

splenic,  378 
Leukocythemia,  378 
Leukocytosis,  362,  364 

pathological,  364 

physiological,  364 
Leukoma,  595 
Leukopenia,  362,  363 
Leukoplakia,  595 

oris  et  buccalis,  595 
Leukosarcoma,  397 
Levulosuria,  aUmentary,  688 
Lingual  tonsils,  604  ' 

Linguiform  lobe  of  the  liver,  695 
Lipase,  609 
Lipomatosis,  multiple,  328 

symmetrical,  327 
Lipuria,  758 
Lissauer's  tract,  853 
Little's  disease,  846 
Liver,  abscess  of,  707 

active  congestion  of,  702 

acute  yellow  atrophy  of,  698,  705 

anomalies  of  form  and  position,  695 

carcinoma  of,  719 

cardiac,  703 

cirrhosis  of,  709 
biliarv,  717 
portal,  710 

congested  nutmeg,  703 

corset  or  constricted,  695 

diseases  of,  687 

bloodvessels  of,  696 

fatty,  697 

-fluke  disease,  211 

functions  of,  687 

passive  congestion  of,  703 

pathological  pathology  of,  687 

red  atrophy  of,  703 

sarcoma  of,  720 

syphilis  of,  28,  186 

tropical,  702,  705 

tuberculosis  of,  119 

tumors  of,  719 


INDEX 


935 


Lobstein's  cancer,  799 

Local  infections,  63 

Lockjaw,  149 

Locomotor  ataxia,  853 

Lorain  type  of  infantilism,  335 

Ludwig's  angina,  137,  597 

Lues,  180 

Lumbago,  911 

Lumbar  mj^elitis,  transverse,  880 

plexus,  824 
Lung,  abscess  of,  559 

compression  of,  547 

fever,  71 

fibroid  induration  of,  552 

-fluke  disease,  211 

gangrene  of,  561 

pneumococcic  infection  of,  71 

sclerosis  of,  552 

tumors  of,  562 
Lungs,  congestion  of,  541 

diseases  of,  539 

cedema  of,  543 

hyperemia  of,  541 

tuberculosis  of,  108 
Lupinosis,  300 
Luschka's  tonsil,  601 
Lymph  nodes  and  lymph  vessels,  diseases 
of,  393 
tuberculosis  of,  100 
Lymphadenitis,  393 
Lymphadenoma,  397 
Lymphangiectasis,  395 
Lymphangioma,  397 
Lymphangiosarcoma,  397 
Lymphangitis,  393 

Lymphatic  system,  tuberculosis  of,  100 
Lymphatism,  403 
Lymphemia,  364,  378 
Lymphocytoma,  397 
Lymphocytosis,  364 
Lymphoma,  397 

mahgnant,  397 
Lymphomatosis,  397 
Lymphosarcoma,  397 
Lysins,  21 
Lyssa,  266 

M 

Macroglossia,  596 
Madura  foot,  170 
Maidism,  300 
Main-en-griffe,  823 
Mai  de  caderas,  174 
Maladie  de  Woillez,  541 

du  coit,  174 
Malarial  cachexia,  209 

infections,  197 

latent  and  masked,  209 
Malignant  pustule,  171 
Malleus  humidus,  159 
Malta  fever,  164 
Mania  a  potu,  290 
Marie's  ataxia,  857 


Marsh  fever,  197 
Mastigophora,  173 
Measles,  247 

German,  250 
Meat  poisoning,  299 
Median  nerve,  823 
Mediastinal  tumor,  501 
Mediastinitis,  584 

Mediastinopericarditis,  indurative,  750 
Mediastinum,  diseases  of,  584 

tumors  of,  585 
Mediterranean  fever,  164 
Medina-worm  infection,  223 
Medulla,  lesions  of,  836 
Megalosplenic  polycythemia  or  erythro- 

cythemia,  385 
Melanicterus,  692 
Membranous  croup,  137 
Meniere's  disease,  819 
Meningeal  breathing,  509 

hemorrhage,  825 
Meningitis,  cerebrospinal,  86 

external  pach}^-,  826 

internal  pachy-,  827 

lepto-,  828 

purulent,  829 

serous,  829 

suppurative,  829 

sj^philitic,  187 

tuberculous,  122 
Meningococcic  infection,  86 
Meralgia  para?sthetica,  810 
Mercurial  poisoning,  297 
Mesenteric  vessels,  infarction  of,  682 
Metabohc  type  of  infantihsm,  336 
Metabohsm,  disorders  of,  303 
MetalUc  tinkle  of  Laennec,  582 
Metatarsalgia,  810 
Metazoan  infections,  211 
Methylene  blue  test,  762 
Miasmatic  diseases,  17 
Micromegaly,  336 
Migraine,  886 
Mikulicz's  disease,  597 
Miliary  fever,  274 
Milk  poisoning,  299 

sickness,  274 
Millar's  asthma,  404 
Miller's  phthisis,  554 
Millstone-maker's  phthisis,  554 
Mind  deafness,  844 
Miner's  anemia,  218 
Mitchell's,  S.  Weir,  disease,  907 
Mitral  insufficiency,  455 

stenosis,  459 
Mocbius'  sign  in  exophthalmic  goitre,  343 
Mononeuritis,  811 
Mononuclear  leukocytosis,  364 
MorbiUi,  247 
Morlius  coxse  senilis,  920 

maculosus,  389 

neonatorum,  387 
Moro  cutaneous  reaction,  126 
Morphine  habit,  292 


936 


INDEX 


Morvan's  disease,  885 
Mosquito,  Plasmodium  malarise  in,  202 
Mosquitoes,  varieties  of,  198 
Motor  aphasia,  842 

disorders  of  intestine,  647 
of  stomach,  614 

neuron,  diseases  of  lower,  848 
of  upper,  845 

and  lower,  852 

neurons,  802 
Mouth  breathing,  601 

diseases  of,  587 

dry,  596 

tuberculous  ulceration  of,  117 
Moynihan's  appendix  dyspepsia,  670 
Mucous  coUc,  654 
Muguet,  592 

Miiller's  muscle,  paralysis  of,  824 
Multiple       progressive      hyaloserositis, 

750 
Mumps,  260 

Muscles,  diseases  of,  911 
Muscular  strain  of  heart,  427 
Musculospiral  nerve,  823 
Musset's   sign    in    aortic    insufficiency, 

464 
Myalgia,  911 
Myasthenia  gastrica,  616 

gravis,  851 
Myatonia,  congenital,  916 
Mycetoma,  170 
Mycoprotein,  21 
Mycosis  intestinalis,  161 

puLmonalis,  161 
Mycotic  stomatitis,  592 
Myelemia,  364,  378 
Myehtis,  879 

acute  ascending,  881 

chronic,  881 

compression,  882 

disseminated,  881 

transverse,  880 
Myelocytosis,  364 
Myeloma,  multiple,  401,  767 
Myelopathic  albumosuria,  401,  767 
Myiasis,  226 
Myocardial  degeneration,  431 

weakness  or  insufficiency,  424 
Myocarditis,  acute,  431 

chronic  interstitial,  434 
Myocardium,     congenital     weakness  of, 
424 

diseases  of,  423 

fibroid  degeneration  of,  434 

tuberculosis  of,  106 
Myoclonus,  914 
Myopathy,  primary,  912 
Myositis,  912 
Myotonia,  congenital,  915 
Mytilotoxism,  300 
Myxoedema  of  adults,  347 

postoperative,  348 
Myxoedematous  infantihsm,  or  cretinism, 
336 


N 


Nagana,  174 
Nakra  fever,  278 
Nasal  catarrh,  acute,  512 
chronic,  544 

diphtheria,  137 

mucous  membrane,  tuberculosis  of, 
106 
Nasha  fever,  278 

Nasopharyngeal  obstruction,  chronic,  601 
Neapolitan  fever,  164 
Necrosis,  fat,  739 
Nemathelminthiasis,  218 
Nephritis,  772 

acute  diffuse,  773 

parenchymatous,  773 
suppurative,  779 

cardiovascular,  changes  in,  760 

chronic  diffuse  indurative,  783 
non-indurative,  780 

interstitial,  783 

parenchymatous,  780 
Nephrolithiasis,  794 
Nephrolysins,  21 
Nephroptosis,  685,  770 
Nerve,  circumflex,  823 
Nerves,  diseases  of,  808 
Nervous  belching,  615 

debiUty  or  disability,  895 

diarrhoea,  647 

diseases  of  functional  or  unknown 
nature,  886 

dyspepsia,  621 

exhaustion,  895 

prostration,  895 

system,  diseases  of,  811 

pathological  physiology  of, 
801 
tuberculosis  of,  122 

vomiting,  615 
Neuralgia,  808 

cervicobrachial,  899 

cervicooccipital,  809 

intercostal,  809 

lumbar,  809 

paraesthetica,  824 

phrenic,  809 

plantar,  810 

red,  907 

trifacial,  808 

trigeminal,  808 
Neuralgias,  visceral,  810 
Neurasthenia  and  psychasthenia,  895 
Neuritis,  811 

alcoholic,  812 

arsenical,  812 

diphtheritic,  812 

multiple,  275,  811 
Neurofibromatosis,  generalized,  814 
Neuromas,  814 

amputation,  814 

plexiform,  814 
Neuromuscular  disorders  of  heart,  415 


INDEX 


937 


Neurons,  801 

motor,  802 

sensory,  803 
Neuroretinitis,  815 
Neuroses,  occupation,  897 

professional,  897 
Neurotic  stomatitis,  chronic,  591 
Newborn,  hemorrhage  in,  387 
Night  bUndness,  815 
Nigrities,  595 
Nocardiosis,  171 
Nodal  rhythm,  419 
Noma,  593 

Non-bacterial  fungus  infections,  168 
Nose,  diseases  of,  511 

-bleeding,  511 
Nothnagel's  vasomotor  angina,  416 
Nurse's  contracture,  350 
Nutmeg  liver,  703 
Nyctalopia,  815 


Obesity,  327 

Obliterative  pericarditis,  485 

peritonitis,  749 

pleuritis,  577 
Obstetrical  or  birth  paralysis,  821 
Obstructive  biUary  cirrhosis,  732 
Ochronosis,  758 
Oculomotor  nerve,  816 
CEdema,  acute  pulmonary,  543 

chronic  pulmonary,  543 

of  brain,  862 

of  cardiac  disease,  414 

of  glottis,  519 

of  larynx,  519 

of  lungs,  543 

of  tongue,  596 

pleural,  579 

recurrent  pulmonary,  543 

suffocative  pulmonary,  543 
QSdematous  laryngitis,  519 
CEsophagismus,  606 
OEsophagitis,  acute,  605 

chronic,  605 
OEsophagus,  carcinoma  of,  607 

diseases  of,  605 

dilatation  of,  606 

diverticula  of,  606 

paralysis  of,  607 

rupture  of,  606 

spasm  of,  606 

spasmodic  stricture  of,  606 

stenosis  of,  607 

tuberculosis  of,  117 

ulceration  of,  605 

varices  of,  606 
Oidiomycosis,  172 
Olfactory  nerve,  814 
Oligopnoea,  509 
OUver's  sign  in  aneurysm,  499 
Oliguria,  756 
Onomatomania,  903 


Oocyst,  174 
Ophthalmoplegia,  817,  851 

external,  852 

internal,  852 
Opium  habit,  292 
Oppenheim's  disease,  916 
Opsonins,  22 
Optic  atrophy,  815 

chiasm,  815 

nerve,  815 

neuritis,  815 

tract  and  centre,  816 
Optical  aphasia,  842 
Oriental  sere,  196 
Orthopnoea,  508 
Orthostatic  albuminuria,  765 
Osteitis  deformans,  922 
Osteo-arthritis,  chronic  hypertrophic,  920 
Osteogenesis  imperfecta,  923 
Osteomalacia,  921 

of  puberty,  329 
Oxyuriasis,  220 


Paget's  disease,  922 
Pachymeningitis,  external,  826 

internal,  827 
Painter's  colic,  295 
Palpitation  of  heart,  416 
Palsy,  bulbar,  850 

pseudobulbar,  851 

shaking,  898 
Paludism,  197 
Pancreas,  cysts  of,  743 

diseases  of,  737 

hemorrhages  into,  737 

tuberculosis  of,  119 

tumors  of,  744 
Pancreatic  calculi,  745 

juice,  644 
Pancreatitis,  acute,  738 

chronic,  741 

gangrenous,  738 

hemorrhagic,  738 

suppurative,  739 
Papillitis,  815 
Papilloedema,  815 
Paragonimiasis,  211 
Paralysis,  acute  ascending,  881 

agitans,  898 

bulbar,  850 

driver's,  878 

family  periodical,  904 

glosso-labio-laryngeal    and    pharyn- 
geal, 850 

lead,  295 

of  insane,  855 

of  intestine,  648 

of  oesophagus,  607 

unilateral  ascending  and  descending, 
848 
Paramyoclonus  multiplex,  914 


938 


INDEX 


Paranephritis,  792 
Paraphasia,  842 
Paraplegia,  846 

ataxic,  858 

spastic,  845 

hereditary,  847 
of  adults,  845 
of  infants,  846 
Parasites,  malarial,  199 

estivo-autumnal,  201 
quartan,  200 
tertian,  199 

metazoan,  211 

protozoan,  173 
Parasitic  insects,  225 

stomatitis,  592 
Parathyroid  glands,  diseases  of,  349 
Paratyphoid  fever,  60 
Parenchymatous  and  fatty  degeneration 
of  heart,  431 

hepatitis,  705 

nephritis,  subacute  and  chronic,  780 

tonsilhtis,  599 
Paresthesia  of  intestine,  650 
Parkinson's  disease,  898 
Parorexia,  617 
Parosmia,  814 
Parotid  bubo,  596 

gland,  inflammation  of,  596 
Parotitis,  596 

acute  symptomatic,  596 

chronic,  597 

epidemic,  260 

infectious,  260 
Paroxysmal  albuminuria,  765 

tachycardia,  422 
Parry's  disease,  342 
Pathways  of  infection,  19 
Pediculosis,  225 
Pellagra,  300 
Pemphigoid  purpura,  389 
Perforation  in  typhoid  fever,  42 
Pericardial  transudate,  487 
Pericarditic  pseudocirrhosis  of  liver,  750 
Pericarditis,  748 

chronic,  484 

external,  485 

fibrinous,  478 

purulent,  483 

serofibrinous,  480 

suppurative,  483 

with  effusion,  480 
Pericardium,  adherent,  485 

air  and  gas  in,  488 

blood  in,  487 

diseases  of,  478 

dropsy  of,  487 

empyema  of,  483 

tuberculosis  of,  103 
Pericholecystic  adhesion,  chronic,  733 
Perichondritis,  laryngeal,  522 
Perihepatitis,  704 
Perinephritic  abscess,  792 
Perinephritis,  792 


Peripheral  facial  paralysis,  818 
Perisigmoiditis,  672 
Peritoneum,  diseases  of,  746 

tuberculosis  of,  103 
Peritonitis,  acute,  748 

chronic,  749 

hyperplastic,  750 

deforming,  750 

hyaline,  750 
Pernicious  anemia,  373 

estivo-autumnal  malarial   infection, 
207 
algid  form,  208 
comatose  form,  207 
hemorrhagic  form,  208 
Peroneal  type   of   progressive  muscular 

atrophy,  849 
Perpetual  irregularity,  419 
Pertussis,  257 
Perverted  appetite,  617 
Pestis  ambulans,  158 

minor,  158 
Petruschky's  spinalgia,  101 
Pfeiffer  phenomenon,  21 
Phagedena,  tropical,  282 
Pharyngeal  tonsil,  601 

diphtheria,  136 
Pharyngitis,  598,  603 

acute,  603 

chronic,  603 
Pharyngocele,  606 

Pharynx,  acute  infectious  phlegmon  of, 
604 

diseases  of,  598 

tuberculosis  of,  117 

ulceration  of,  603 
Phlebectasis,  hemorrhoidal,  683 
Phlebitis,  hepatic,  696 
Phlegmonous  enteritis,  667 

laryngitis,  519 

tonsillitis,  599 
Phloridzin  test,  762 
Phthiriasis,  225 
Phthisis,  92 

fibroid,  552 

miller's,  554 

ventricuh,  627 
Piles,  683 

Pin  worm  infection,  220 
Piroplasmosis,  195 

von  Pirquet's  cutaneous  reaction,  125 
Pituitary  body,  diseases  of,  355 

tumors  of,  836 
Plague,  156 

Plasmodium  kochi,  174 
,-.'       malarias  in  man,  199 
in  mosquito,  202 
Plethora  and  polycythemia,  363 
Pleura,  diseases  of,  564 

tuberculosis  of,  102 

tumors  of,  584 
Pleural  dropsy,  579 

oedema,  579 
Pleurisy,  564  .,  i 


INDEX 


939 


Pleurisy,  chronic  adhesive,  577 

diaphragmatic,  570 

.dry,  plastic,  or  acute  adhesive,  564 

interlobar,  571 

suppurative,  574 

with  effusion,  566 
chronic,  577 
Pleuritis,  564 

Baccelli's  sign  in,  569,  575 

chronic,  577 

fibrinous,  564 

Grocco's  sign  in,  569 

hemorrhagic,  576 

purulent,  574 

serofibrinous,  566 
Pleurodynia,  911 
Pleuropericarditis,  485 
Plumbism,  294 
Pneumothorax,  580 
Polyorrhomenitis,  578 
Pneumaturia,  758 
Pneumococcic  infection,  70 
of  lungs,  24,  71 

septicemia,  70 
Pneumogastric  or  vagus  nerve,  819 
Pneumonokoniosis,  554 
Pneumonia,  71 

alcoholic,  79 

apical,  79 

asthenic  or  adynamic,  79 

basal,  79 

bilious  or  malarial,  80 

central,  79 

cUnical  varieties  of,  79 

complications  and  sequels  of,  81 

croupous,  24 

diagnosis  of,  82 

double,  79 

epidemic,  79 

ether,  80 

etiology  of,  71 

fever  in,  75 

in  aged,  80 

in  children  and  infants,  SO 

larval  or  abortive,  79 

latent,  79 

lobular,  549 

massive,  79 

migratory  or  creeping,  79 

pathology  of,  72 

physical  signs  of,  77 

postoperative,  80 

prognosis  of,  82 

secondary,  80 

symptoms  of,  73 

temperature  in,  74 

terminal,  80 

toxic,  80 

treatment  of,  82 

typhoid,  79 
Pneumonic  plague,  158 

tuberculosis,  acute,  109,  115 
Pneumonitis,  71 
Pneumopericardium,  488 


Pneumothorax,  582 

Podagra,  320 

Polioencephalitis,  inferior,  850,  871 

superior,  851,871 
Poliomyelitis,  acute,  270 
chronic  anterior,  841 
epidemic,  270 
Polyarthritis,   chronic,   atrophic  type  of 

Goldthwait,  918 
Polycythemia,  363 

with  cyanosis  and  enlarged  spleen,  385 
Polynuclear  leukocytosis,  364 
Polyorrhomenitis,  105,  750 
Polyphagia,  617 
Polypnoea,  508 
Polyserositis,  750 
Polyuria,  318,756 
Ponos,  279 
Pons,  lesions  of,  836 
Portal  vein,  696 
Postural  albuminuria,  765 
Potter's  rot  or  asthma,  554 
Preacher's  sore  throat,  521 
Precipitins,  21 
Proctitis,  gangrenous,  281 
Prof  eta's  law,  181 
Proteosoma,  174 
Protozoa,  173 

Protozoan  infections,  27,  173 
Protozoic  dermatitis,  172 
Progressive  muscular  atrophy,  852 

of  Charcot-Marie-tooth 

type,  849 
of  Duchenne-Aran  type,  848 
of  Vulpian  type,  848 
peroneal  type,  849 
dystrophy,  912 
neural  muscular  atrophy,  849 
spinal  muscular  atrophy,  848 
Pseudohypertrophic  muscular  paralysis, 

912 
Pseudoleukemia,  397 
Pseudomembranous  enteritis,  654 
Pseudotuberculosis,  171 
Psilosis,  281 
Psittacosis,  287 
Psoriasis  of  tongue,  595 
Psorospermiasis,  172 
Psychical  blindness,  844 

deafness,  844 

Ptomaine  poisoning,  299 

Ptyahsm,  591,  596 

Pulmonary  apoplexy,  545 

aspergillosis,  171 

congestion,  541 

embolism  and  thrombosis,  545 
hemorrhage,  539 
infarction,  545 
insufliciency,  470 
oedema,  543 
stenosis,  470 
Pulse,  alternating,  421 
Purpura,  387 

abdominal,  389 


940 


INDEX 


Purpura  fulminans,  390 

hemorrhagic,  389 

Henoch's,  388,  389 

idiopathic,  388 

rheumatica,  389 

symptomatic,  388 
Putrid  bronchitis,  528 
PyeUtis,  788 
Pyemia,  61 
Pyelonephritis,  788 
Pyelonephrosis,  788 
Pylephlebitis  adhesiva,  696 

suppurativ^e,  697 
Pylethrombosis,  696 

Pylorus,  insufficiency  or  incontinence  of, 
616 

spasm  of,  615 
Pyococcic  infection,  61 
Pyogenic  infections,  61 
Pyopneumopericardium,  488 
Pyopneumothorax,  580 

subphrenic,  749 
Pyuria,  769 


QUADRIGEMINAL  pulse,  418 

Quartan  malarial  infection,  203,  205 

parasite,  200 
Quincke,  penetrating  or  centripetal  pulse 
of,  465    _ 
serous  meningitis  of,  829 
Quincke's  disease,  907 
Quinquageminal  pulse,  418 
Quinsy,  599   _ 

Quotidian  estivo-autumnal  malarial  infec- 
tion, 206 


Rabies,  266 
Rachitic  rosary,  330 
Rachitis,  329 

tarda,  329 
Rag-picker's  disease,  161 
Railway  brain,  896 

spine,  896 
Ranula,  596 
Raynaud's  disease,  908 
von  Recklinghausen's  disease,  814 
Recurrent  pulmonarj^  oedema,  543 
Reichmann's  disease,  619 
Reflexes,  805 

Relapses  in  typhoid  fever,  48 
Relapsing  fever,  178,  224 
Renal  calculus,  794 

disease,  hypertrophy  of  heart  in,  439 

tuberculosis,  121 
Respiratory  system,  diseases  of,  505 

tuberculosis  of,  106 
Retropharyngeal  abscess,  604 
Rheumatic  fever,  253 
Rheumatism,  acute  and  subacute,  253 

articular,  253 


Rheumatism,  muscular,  911 
Rheumatoid  arthritis,  918 
Rhinitis,  acute,  512 

chronic,  544 

fibrinous,  137 
Rhizopoda,  173 
Rhythm  of  auricular  paralysis,  419 

nodal,  418,  419 
Remittent  fever,  197 
Rickets,  329 

acute,  330,  333 
Riedel's  lobe,  695 
Riga's  aphtha,  591 

disease,  591 
Ringworm  of  tongue,  595 
Rock  fever,  164 

Rocky  Mountain  spotted  fever,  224,  269 
Rosenbach,  erysipeloid  of,  69 
Rosenbach's  sign  in  exophthalmic  goitre, 

343 
Rose,  cephaHc  tetanus  of,  151 

cold,  515 
Roseola,  epidemic,  250 
Rotch's  sign  in  pericarditis,  481 
Rotheln,  250 

Roundworm  infection,  218 
Rubella,  250 

notha,  250 
Rubeola,  247 
Rupture  of  heart,  444 

of  oesophagus,  606 

of  spleen,  406 


S 


Sacral  plexus,  824 
Salivary  calculi,  597 

glands,  diseases  of,  596 
hypersecretion  of,  596 
Saltatory  spasm,  904 
Sand,  intestinal,  683 
Sapremia,  61 
Sarcodina,  173 
Sarcoma,  349,  798 
of  larynx,  523 
of  Uver,  720 
Sarcoptic  itch,  224 
Scarlet  fever,  240 

compUcations  and  sequels  of,  244 
diagnosis  of,  244 
etiologj'  of,  240 
pathology  of,  241 
prognosis  of,  245 
symptoms  of,  241 
treatment  of,  245 
varieties  of,  243 
Schmidt's  test  diet,  652 
Schnnlein's  disease,  389 
Sciatica,  809 

Sclerosis,  disseminated,  859 
insular,  859 
multiple,  859 
of  coronary  arteries,  434  _,    , 


INDEX 


941 


Sclerosis  of  lung,  552 

of  spinal  cord,   subacute   combined, 
858 

posterior,  853 

posterolateral,  858 

toxic  combined,  858 

ventriculi,  627 
Scorbutus,  331 
Screw-worm,  226 
Scrofula,  92 
Scurvy,  331 

infantile,  333 

-rickets,  333 
Seatworm  infection,  220 
Secondary  infection,  64 
Secretory  disorders  of  intestine,  650 

of  stomach,  618 
Senile  tremor,  900 
Sensory  disorders  of  intestine,  649 
of  stomach,  616 

neuron,  803 

diseases  of,  853 
Septic  infections,  61 
Septicemia,  61,  64 
Septicemic  plague,  158 
Septicopyemia,  61 

Septicopyemic  abscesses,  multiple,  708 
Serofibrinopneumothorax,  580 
Serositis,  multiple,  105,  578,  750 
Serous  membranes,  tuberculosis  of,  102 
Seven-day  fever,  178 
Ship  fever,  237 
Siberian  Uver-fluke  disease,  212 

opisthorchiasis,  212 
Siderosis,  554 
Sighing  in  diseases  of  respiratorj^  system, 

510 
Sigmoid  diverticulitis,  672 
Sinus  irregularity,  416 
Siriasis,  905 
Sitotoxism,  300 
Sleeping  sickness,  194 
Smallpox,  226 

complications  of,  231 

diagnosis  of,  231 

prognosis  of,  232 

treatment  of,  232 

varieties  of,  230 
Smith's   sign   in   tuberculosis   of    lymph 

nodes,  101 
Smoker's  tongue,  595 
Snake-venom  poisoning,  298 
Sneezing  in  diseases  of  respiratory  sys- 
tem, 510 
Snuffles,  188 

Sobbing  in  diseases  of  respiratory  sys- 
tem, 510 
Soldier's  heart,  427 
Somatic  teniasis,  217 
Soor,  592 
Sore  throat,  598 

clergymen's,  603 
preacher's,  521 
Sparganum  mansoni,  218 


Sparganum  proliferum,  218 
Spasm  habit,  901 

of  cardia,  615 

of  intestine,  648 

of  oesophagus,  606 

of  pylorus,  615 
Spastic  cerebral  paraplegia,  846 

diplegia,  846 

paralysis  of  infants,  846 

paraplegia,  845 

hereditary,  847 

spinal  paralysis,  845 

tabes,  845 
Spinal  accessory  nerve,  820 

cord,  837-840 

anemic  degeneration  of,  858 
compression  of,  882 
difTuse  and  focal  diseases  of,  876 
hemorrhage  into,  876 
secondary  degeneration  of,  858 
subtotal  transverse  lesion  of,  837 
total  transverse  lesion  of,  837 
tumors  of,  883 
unilateral  lesions  of,  838 

gliosis,  884 

meningeal  hemorrhage,  826 

nerves,  diseases  of,  821 
Spirillosis,  178 
Spirochsetfe,  173 
Spirochetosis,  178 
Splanchnoptosis,  685 
Spleen,  diseases  of,  405 

enlargement  of,  407 

floating,  406 

movable,  406 

rupture  of,  406 

tuberculosis  of,  102 
Splenic  anemia,  407,  408 

fever,  161 

pseudoleukemia,  400 

tumor,  acute,  407 
chronic,  407 
Splenomegaly,  407 

Gaucher  type  of,  408 

tropical,  195 
Splenoptosis,  406,  685 
Spondylose  rhizomeUque,  921 
Sporozoa,  174 
Spotted  fever,  86,  237 
Sprue,  281 

S-shaped  curve  of  Ellis  and  Garland,  568 
St.  Anthony's  fire,  67 
St.  Vitus'  dance,  900 
Staphylolysin,.21 
Status  epilepticus,  890 

lymphaticns,  403 
Steatorrhoea,  737 

Stellwag's  sign  in  exophthalmic  goitre,  343 
Stenocardia,  493 
Stenosis,  607 

aortic,  466 

mitral,  459 

of  intestine,  674 

of  cEsophagus,  607 


942 


INDEX 


Stenosis  of  pylorus,  630,  643 

pulmonary,  470 

tricuspid,  469 
Stokes,  bellows  murmur  of,  465 
Stomach,  acute  dilatation  of,  629 

atony  of,  616 

carcinoma  of,  638 

chronic  dilatation  of,  630 

diseases  of,  608 

loss  or  impairment  of  appetite 

in,  610 
nausea  and  vomiting  in,  612 
thirst  in,  611 

excessive  amount  of  gases  in,  611 

hemorrhage  from,  613 

hyperesthesia  of,  616 

motor  disorders  of,  614 

non-carcinomatous  tumors  of,  643 

peristaltic  unrest  of,  615 

secretory  disorders  of,  618 

sensory  disorders  of,  616 

symptomatic  disorders  of,  610 

tuberculosis  of,  117 

ulcer  of,  632 
Stomatitis,  587 

aphthous,  589 

catarrhal,  589 

croupous,  591 

epidemic,  273 

gangrenous,  593 

infectious,  587 

mechanical,  588 

membranous,  591 

mercurial,  591 

thermic,  588 

toxic,  588 

ulcerative,  590 
Stonecutter's  phthisis,  554 
Streptolysin,  21 
Streptothricosis,  171 
Stricture  of  oesophagus,  606 
Stridulus  laryngitis,  520 
Stroke,  862 
Strongyloidosis,  219 
Struma,  340 
Subinfection,  25 
Succus  entericus,  645 
Sudoral  typhoid,  40 
Suffocation,  510 

Summer  diarrhoea  of  children,  661 
Sunstroke,  905 
Superacidity,  618 
Surra,  174 
Swamp  fever,  197 
Sweating  sickness,  274 
Sydenham's  chorea,  900 
Syncope,  local,  908 
Synovitis,  gonococcic,  91 
SyphiUs,  180 

acquired,  180 

bones,  joints,  bursse,  and  muscles  in, 
187 

circulatory  system  in,  185 

congenital,  181 


Syphilis,  cutaneous  lesions  of,  186 

diagnosis  of,  189 

digestive  system  in,  186 

etiology  of,  180 

general  symptoms  of,  183 

genito-urinary  system  in,  186 

mucous  membrane  lesions  of,  184 

nervous  system  in,  187 

of  liver,  186 

pathology  of,  181 

prognosis  of,  189 

respiratory  system  in,  185 

treatment  of,  190 
Syphilitic  bursopathy  of  Verneuil,  188 

Uver,  28 
Syringomyelia,  884 


Tabardillo,  237 
Tabes  dorsalis,  853 

arthropathies  in,  855 
etiology  of,  853 
pathology  of,  853 
symptoms  of,  854 
treatment  of,  856 
Tabo-paralysis,  855 
Tachycardia,  421 

paroxysmal,  418,  422 
Tachypnoea,  508 
Taenia  echinococcus,  217 
mediocanellata,  214 
saginata,  214 
solium,  215 
Tapeworm,  beef,  214 
dwarf,  216 
fish,  215 
infection,  214 
pork-measly,  215 
Tay-Sachs  disease,  847 
Telangiectasis  of  skin  and  mucous  mem- 
brane, multiple,  511 
Tellais'  sign  in  exophthalmic  goitre,  344 
Teniasis,  214 

diagnosis  of,  216 
intestinal,  214 
somatic,  217 
symptoms  of,  216 
treatment  of,  216 
Terminal  or  secondary  infections,  64 
Tertian  estivo-autumnal  malarial  infec- 
tion, 205 
malarial  infection,  203 
parasite,  199 
Tetanolysin,  21 
Tetanus,  149 

hydrophobicus,  151 
idiopathic,  149 
traumatic,  149 
Tetany,  350 
Texas  fever,  224 
Thalamus,  lesions  of,  836 
Thermic  fever,  905 


INDEX 


943 


Thirst  in  diseases  of  stomach,  611 
Thomsen's  disease,  915 
Thoracic  duct,  disease  of,  401 

myeUtis,  transverse,  880 

nerve,  long  or  posterior,  823 
Threadworm  infection,  220 
Thrombosis  of  cavernous  sinus,  870 

of  cerebral  sinuses,  870 

of  kidney,  771 

of  lateral  sinus,  870 

of  longitudinal  sinus,  870 

of  lung,  545 

of  mesenteric  veins,  682 

of  spleen,  406 
Thrush,  592 

Thymic  tracheostenosis,  403 
Thymus  body,  diseases  of,  402 

enlargement  of,  403 
Thyroid,  diseases  of,  339 
Thyroiditis,  acute,  340 
Thyroids,  aberrant  or  accessory,  349 
Tic  convulsif,  903 

impulsive,  903 
habit,  901 

douloureux,  808 
Tick  fever,  224,  269 

infection,  224 
Tongue,  acute  oedema  of,  596 

black,  595 

diseases  of,  594 

eczema  of,  595 

geographical,  595 

ichthyosis  of,  595 

leukoplakia  of,  595 

psoriasis  of,  595 

ringworm  of,  595 

smoker's,  595 

tylosis  of,  595 

wandering  rash  of,  595 
Tonsil,  lingual,  604 

Luschka's,  601 

pharyngeal,  601 
Tonsillar  abscess,  599 
Tonsillitis,  598 

acute,  598 

chronic,  601 
Tonsils,  diseases  of,  598 

enlarged,  601 

hypertrophied,  601 

tuberculosis  of,  117 
Torticollis,  820,  912 
Toxemia,  22,  61 
Toxins  and  antibodies,  20 

extracellular,  20 

intracellular,  21 
Trachea  and  bronchi,  diseases  of,  524 

tuberculous  ulceration  of,  108 
Tracheal  and  bronchial  obstruction,  537 
Tracheitis,  acute,  524 
Tracheobronchitis,  acute,  524 
Traumatic  neuroses  and  psychoses,  896 
Transcortical  aphasia,  842 
Transmission  of  infectious  diseases,  18 
Traube's  sign  in  aortic  insufficiency,  464 


Trematode  infections,  211 
Trembles,  274 
Treponema^,  173 
Trichiniasis,  221 
Trichinosis,  221 
TrichocephaUasis,  221 
Trichomonas,  174 
Tricuspid  insufficiency,  468 

stenosis,  469 
Trigeminal  nerve,  817 

pulse,  418 
Trismus  neonatorum,  150 
Trochlear  nerve,  816 
Tropical  abscess  of  liver,  708 

phagedena,  282 
Trousseau's  sign  in  tetany,  351 
Trypanosomse,  174 
Trypanosomiasis,  194 
Tsetse-fly  disease,  194 
Tubercula  dolorosa,  814 
Tuberculin  in  treatment  of  tuberculosis, 
129 

tests,  125 
Tuberculosis,  92 

acute  miliary,  96 
pneumonic,  109 

bloodvessels  in,  106 

chronic  fibroid,  110 
ulcerative,  109 

etiology  of,  92 

fresh  air,  nutritious  food,  rest,  and 
exercise  in,  127 

general  diagnosis  of,  125 

laryngeal,  107 

medicinal  treatment  of,  130 

miliary,  102 

of  bones  and  joints,  124 

of  cerebral  meninges,  122 

of  circulatory  system,  106 

of  digestive  system,  117 

of  female  genitalia,  120 

of  genito-urinary  system,  120 

of  intestines,  118 

of  liver,  119 

of  lungs,  108 

classification  of,  116 
diagnosis  of,  115 
pathology  of,  109 
prognosis  of,  115 
symptoms  of,  110 

of  lymph  nodes,  102 

of  lymphatic  system,  100 

of  meninges,  829 

of  myocardium,  106 

of  nasal  mucous  membrane,  106 

of  nervous  system,  122 

of  a>sophagus,  117 

of  pancreas,  119 

of  pericardium,  103 

of  peritoneum,  103 

of  pharynx,  117  ' 

of  pleura,  102 

of  respiratory  system,  106 

of  serous  membranes,  102 


944 


INDEX 


Tuberculosis    of    several    serous    mem- 
branes, 105 
of  stomach,  117 
of  testicle,  120 
of  tonsils,  117 
of  urinary  system,  121 
pathology  of,  94 
peritoneal,  104 

prophylactic  measures  in,  126 
pulmonary,  108 

special  forms  of,  treatment  of,  131 
specific  remedies  in  treatment  of,  129 
surgical  intervention  in,  131 
treatment  of,  127 
tuberculin  in  treatment  of,  129 
Tubular  diarrhoea,  654 
Tufnell's  treatment  in  aneurysm,  502 
Tumors   and    tumor-like    formations   of 
lymph  nodes,  397 
of  bladder,  799 
of  brain,  873 
of  heart,  444 
of  intestine,  676 
of  kidney,  798 
of  larynx,  523 
of  liver,  719 
of  lungs,  562 
of  mediastinum,  585 
of  pancreas,  744 
of  pleura,  584 
of  spleen,  410 
of  thyroid,  349 
Tunica  vaginalis,  chylous  dropsy  of,  223 
Tylosis  of  tongue,  595 
Typhoid  carriers,  34,  37 
cholera,  154 
fever,  32 

characteristic  lesions  of,  36 

chills  in,  40 

circulatory  system  in,  44 

color  of  skin  in,  40 

diagnosis  of,  49 

diarrhoea  in,  41 

diet  in,  52 

digestive  system  in,  41 

epistaxis  in  early  stages  of,  43 

eruptions  in,  40 

etiology  of,  33 

general  management  of,  51 

genito-urinary  system  in,  46 

hemorrhage  in,  59 

hydrotherapy  in  treatment  of, 
53 

intestinal  hemorrhage  in,  42 

leukopenia  in,  44 

Uver  in,  43 

nervous  system  in,  45 

pathology  of,  34 

perforation  in,  42,  59 

peritonitis  in,  43 

prognosis  of,  50 

recurrence  in,  49 

relapses  in,  48 

respiratory  system  in,  43 


Typhoid  fever,  symptoms  of,  37 
temperature  in,  38 
treatment  of,  50 
tympanites  in,  41 
varieties  of,  47 
pneumonia,  79 
pneumonitis,  34 
sudoral,  40 
Typhus  fever,  237 

of  Mexico,  237 
Tyrotoxism,  299 


Ulcer  of  stomach  and  duodenum,  632 
etiology  of,  432 
pathology  of,  633 
symptoms  of,  634 
treatment  of,  636 
of  intestine,  673 
of  oesophagus,  605 
of  pharynx,  603 
tropical,  196 
Ulcerating  granuloma  of  genitals,  283 
Ulcerative  tuberculosis,  chronic,  109,  115 
Ulnar  nerve,  823 
Uncinariasis,  218 
Undulant  fever,  164 
Uremia,  759 
Ureteritis,  788 
Urethra,  tuberculosis  of,  14 
Urinary  system,  diseases  of,  755 

tuberculosis  of,  121 
Urine,  abnormal  constituents  in,  757 
abnormally  colored,  758 
electrical  conductivity  of,  763 
variations  in  normal  constituents  of, 
756 
Uvula,  elongation  of,  604 


Vaccination,  method  of,  233 

Vaccines,  bacterial,  32 

Vaccinia,  233 

Valvular  disease  of  heart,  chronic,  452 
diagnosis  of,  472 
prognosis  of,  472 
treatment  of,  473 
lesions,  combined,  471 

Vaquez's  disease,  385 

Varicella,  235 

Varices,  606 

Varicose  axillary  glands,  223 
groin  glands,  223 

Variola,  226 

Vasomotor  and  trophic  disorders,  907 

Varix,   cutaneous  and  deep  lymphatic, 
223 

Vegetable  poisoning,  301 

Venal  distomatosis,  213 

Ventricle,  hvpertrophy  and  dilatation  of 
left,  442  " 


INDEX 


945 


Ventricle,  hypertrophy  and  dilatation  of, 

right,  442 
Ventricular  extrasystoles,  417 

rhythm,  419 
Verneuil,  syphilitic  bursopathy  of,  188 
Verruga,  284 
Vertigo,  paralytica,  285 
Vestibular  nerve,  819 
Vincent's  angina,  139 
Virchow's  giant  growth  of  colon,  682 

smooth  atrophy  of  base  of  tongue,  185 
Visceroptosis,  685 
VitiUgoidea,  693 
Volkmann's  contracture,  823 
Vomiting,  cyclic  or  periodic,  615 

nervous,  615 

primary  periodic,  615 


W 


Wassermann  complement-binding  test, 
28 
deviation-of-the-complement  test,28 
reaction  in  syphilis,  189 
Waxy  or  bacony  degeneration,  334 
Weil's  disease,  272,  691 
Wernicke's  hemiopic  pupillary  reaction, 

816 
Whipwerm  infection,  221 
White  patches  or  milk  spots  on  pericar- 
dium, 484 
Whooping  cough,  257 
Winckel's  disease,  387 
Winter  cough,  527 

chronic,  528 


Wintrich's  sign  in  tuberculosis  of  lungs, 

114 
Wolff-Eisner  conjunctival  test,  126 
Wooden  tongue,  169 
Wool-sorter's  disease,  161 
Word-bUndness,  841 
Word-deafness,  841 
Wound  diphtheria,  138 
Wrist-drop,  812 
Writer's  cramp,  897 
Wry-neck,  912 


X-RAYS,  use  of,  in  pneumonia,  86 
Xanthelasma,  693 
Xanthoma,  693 
Xerostomia,  596 


Yawning  in  diseases  of  respiratory  sys- 
tem, 510 
Yaws,  193 
Yellow  fever,  261 


Zenker's  degeneration  in  typhoid  fever, 

36 
Zooparasites,  20 
Zooparasitic  infections,  173 
Zuckergussleber,  578,  750 
Zuckergusslunge,  750 
Zuckergussmilz,  750 
Zuckerkandl's  bodies,  351 


60 


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